Human Anatomy & Physiology

Second Edition

Chapter 11
Introduction to the
Nervous System and
Nervous Tissue

PowerPoint® Lectures created by Suzanne Pundt, University of Texas at Tyler

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 Review
1. Know the difference between neurons and neuroglia; the central and peripheral nervous systems;
receptors and effectors; and afferent and efferent divisions.

2. Learn about structure and functional differences between the different parts of a neuron

3. Learn about construction of a synapse and type of Synapses based on junctions.

4. How do we structurally and functionally classify neurons?

5. Know the basics about the different types of neuroglia; where they are found and what they do. What
is ganglia?

6. What is myelin? What is its function and how does it work?

7. What are the types of membrane channels, how become activated?

8. What is Sodium–potassium ATPase , How many sodium potassium exchanged?

9. What are the main process in neural activity

10.What is transmembrane potential?

11. What is electrical gradient and chemical gradient and the electrochemicalgradient.

12.What is resting potential, Know how a resting potential established? Where is more sodium and
more potassium?

13.What types of channels cause changes in the resting membrane potential?

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15.What is graded potential? How do graded potentials differ from action potentials.

16.Do you see graded potential in any other cells besides neurons.

17.What is the difference between depolarization, repolarization and

18.hyperpolarization? Know the channels that affect each of those three types of

19.polarization.

20.What is threshold? Know the numbers in millivolts of resting membrane

21.potential and threshold.

22.Know the sequence of events for generating an action potential and the location of

23.these events. What is All-or-none principle?

24.Know the two types of refractory periods.

25.How do the two types of conduction of action potentials differ?

26.Beside myelination what property of a nerve cell affects speed of propagation? What is

27.the difference between Type A, B, C nerves.

28. Know the two types of synapses and understand the sequence of events that lead to

29.release of neurotransmitters at a chemical synapse.

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31.How do the two synapses differ in terms of speed? How do the number of chemical synapses affect the
speed of transmission? Know the two types of summation and understand the difference between IPSPs
and EPSPs.

32. Know the two types of synapses (chemical, electrical). How they transmit nerve impulses .

33.Understand the sequence of events that lead to release of neurotransmitters at a chemical synapse.

34.How do the two synapses differ in terms of speed? How do the number of chemical

35.synapses affect the speed of transmission?

36.What are Classes of Neurotransmitters

37.Learn about events at a Cholinergic Synapse

38.What is synaptic delay, synaptic fatigue

39.What are other Neurotransmitters (only those mentioned in power point) besides Ach.

40.What are Neuromodulators, example?

41.Learn about post synaptic potentials

42.Know the two types of summation and understand the difference between IPSPs and EPSPs.

43.What is facilitation, example?

44.What are axoaxonic synapses

45.Know the effect of frequency of action potential on the information processing

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Useful links

http://www.youtube.com/watch?v=6R2-AFcJrhs ……………….sodium potassium pump

https://www.youtube.com/watch?v=SdUUP2pMmQ4 ..Nerve Impulse Molecular Mechanism

http://www.youtube.com/watch?v=U0NpTdge3aw...................... action potential

http://www.youtube.com/watch?v=7EyhsOewnH4 ……………….Depolarization

http://www.youtube.com/watch?v=ifD1YG07fB8 ……………….action potential (refractory)

http://www.youtube.com/watch?v=SyJgz4P-Omo …………………. vesicle transport

http://www.youtube.com/watch?v=7MSDS6jKJSA........................ Ach synapses

http://sites.sinauer.com/neuroscience5e/animations05.02.html ...............Summation of

Postsynaptic Potentials

https://www.youtube.com/watch?v=Tqwo9dmIXAQ...................... Cocaine in the human brain

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MODULE 11.1 OVERVIEW OF THE
NERVOUS SYSTEM

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Overview of the Nervous System
Nervous system – controls perception and experience of world
– Directs voluntary movement
– Seat of consciousness, personality, learning, and memory
– Regulates many aspects of homeostasis with endocrine
system:
 respiratory rate
 blood pressure
 body temperature
 sleep/wake cycle
 blood pH

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Anatomical Divisions of the Nervous System
CNS – brain and spinal cord
Brain – billions of nerve cells (neurons); protected by bones of skull
Spinal cord – begins at foramen magnum; continues through vertebral
foramina of first cervical to first or second lumbar vertebra
Millions of neurons; much fewer than brain
Enables brain to communicate with most of body below head and neck
PNS – all nerves in body outside protection of skull and vertebral
column

Nerves – axons of neurons bundled together with blood vessels and

connective tissue; carry signals to and from CNS; classified by origin or
destination
Cranial nerves – 12 pairs of nerves traveling to or from brain
Spinal nerves – 1 pairs of nerves traveling to or from spinal cord
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Anatomical Divisions of the Nervous System
Divided anatomically into:

Central nervous system (CNS)

Peripheral nervous system (PNS)

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Anatomical Divisions of the Nervous System

Figure 11.1 Structure of the nervous system.

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Imagine when your mouth is dry

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• Three Functional Classifications of Neurons
1. Sensory neurons
• Afferent neurons of PNS
carry impulses to the center; detect
changes inside and outside the body;
begin in any organ and end in CNS

2. Motor neurons
• Efferent neurons of PNS
carry messages away from CNS;
employ peripheral neurons to carry
message form brain to the effector
Ganglia : Masses of
3. Interneurons neuron cell bodies,
• Association neurons surrounded by
neuroglia
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Functional Divisions of the Nervous System

Figure 11.3 Summary of the structural and functional divisions of the nervous system.

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An Overview of the Nervous System.
Central Nervous System (CNS)
Information processing
(brain and spinal cord)
integrates, processes, and
coordinates sensory input
and motor commands.

Peripheral Nervous
Sensory information Motor commands within
System (PNS) within efferent division
(nervous tissue afferent division
outside the CNS
and the ENS)

Somatic nervous Autonomic

system (SNS) nervous system (ANS)

Parasympathetic Sympathetic
division division

• Smooth
muscle
Special sensory Visceral sensory Somatic sensory
receptors receptors receptors • Cardiac
monitor smell, monitor internal monitor skeletal muscle
taste, vision, organs muscles, joints, • Glands
balance, and and skin surface Skeletal • Adipose
hearing muscle tissue

Receptors Effectors

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 Functional Divisions of the Nervous System
Nervous system functional categories: sensory, integrative, or motor:

– Sensory – sensory (afferent) division of PNS gathers information

about internal and external environments; input from both subdivisions
(below) carried from receptors to spinal cord and/or brain by spinal and
cranial nerves
 Special sensory division:

– Vision, hearing, taste, smell, and balance

 Somatic sensory division–

– carry signals from skeletal muscles, bones, joints, and skin

 Visceral sensory division – transmit signals from

– viscera (heart, lungs, stomach, kidneys, and urinary bladder)

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Functional Divisions of the Nervous System
Nervous system functional categories: sensory, integrative, or
motor:

Figure 11.2 Functions of the nervous system.

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 Functional Divisions of the Nervous System
– Integrative functions – analyze and interpret incoming sensory
information; determine an appropriate response
 99% of integrated sensory information is subconsciously disregarded
as unimportant
 Remaining sensory stimuli that CNS does respond to leads to motor
response

– Motor functions – actions performed in response to integration by

motor (efferent) division of PNS;
 Motor/efferent division –

– Motor neurons carry out motor functions; travel

• from brain and spinal cord via cranial and spinal nerves

– Effectors – organs that carry out effects of nervous system

(subdivisions on next slide…)
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 Functional Divisions of the Nervous System
Motor division subdivided into somatic and autonomic divisions, by organs
that neurons contact

– Somatic motor division (SNS) – neurons transmit signals to

 skeletal muscle; voluntary control (aka voluntary motor division)

– Autonomic nervous system (ANS) or visceral motor division

 Regulates secretion of certain glands, contraction of smooth muscle,

and contraction of cardiac muscle; involuntary (aka involuntary
motor division)

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• Motor Neurons
– Two groups of efferent axons in ANS vs. one in SNS
 Signals from CNS motor neurons to visceral effectors pass synapses at
autonomic ganglia dividing axons into:
– Preganglionic fibers
– Postganglionic fibers

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 MODULE 11.2 NERVOUS TISSUE
Central canal
Gray matter
White matter

CENTRAL CANAL

Neuroglia in the CNS

Ependymal cell
Ependymal cells are
simple cuboidal epithelial
Neuron cells that line fluid-filled
Gray
matter passageways within the
brain and spinal cord.
Neuron Microglial cell
Microglia are phagocytes
that move through
nervous tissue removing
unwanted substances.

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• Neurons and Neuroglia
– Neurons perform:
 All communication, information processing, and control functions
of the nervous system

– Neuroglia preserve:
 Physical and biochemical structure of neural tissue

 Neuroglia are essential to:

 Survival and function of neurons

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Neurons
Neurons – excitable cells responsible for sending
and receiving signals as action potentials; most

Perikaryon

Dendrites
Nucleus
consist of three parts (Figures 11.4, 11.5):

Axon
Cell Body (Soma)

Cell body
Dendrites: Short branched processes

Axon: Long single process

Telodendria

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Neurons
Dendritic branches

Nissl bodies (RER

and free ribosomes)

Mitochondrion

Axon hillock

Initial segment
of axon Axolemma
Telodendria

Golgi apparatus Axon

Neurofilament Synaptic
Nucleus terminals

Nucleolus
Dendrite See Figure 12–2

PRESYNAPTIC CELL An understanding of neuron POSTSYNAPTIC

function requires knowing its CELL
structural components.

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Neurons
Neurons – excitable cells responsible for sending and receiving signals as action
potentials; most consist of three parts (Figures 11.4, 11.5):

Cell body (soma) – most metabolically active region; manufactures all proteins
needed for whole neuron; organelles support high level of biosynthetic activity:

– Both free ribosomes and rough endoplasmic reticulum (protein synthesis);

RER visible with microscope (Nissl bodies)

– Golgi apparatus (vesicular transport)

– Large or multiple nucleoli (ribosomal RNA)

– Mitochondria supply energy required

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Neurons
Cell body organelles (continued)

– Cytoskeleton – microtubules; structural support and chemical

transportation between cell body and axon

– Neurofibrils – intermediate filaments of cytoskeleton; structural support

extending into neuron processes

Dendrites – short, branched processes; receive input from other neurons,

which they transmit toward cell body as electrical impulses; each neuron may
have multiple dendrites

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 Neurons
Each neuron has only one axon (nerve fiber); can generate and conduct action
potentials; distinct regions of axon:

– Axon hillock – where axon originates from cell body

– Axon collaterals – branches extending from main axon

– Telodendria – small branches arising from axon and axon collaterals near
where extensions end

– Axon terminals or synaptic bulbs – arise from telodendria; components

that communicate with target cell

– Axolemma – plasma membrane surrounding axon and its cytoplasm

(axoplasm)
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 Neurons
Substances travel through axoplasm by two types of axonal transport (flow):

– Slow axonal transport – transports substances (cytoskeleton proteins) from

cell body through axon; rate of 1–3 mm/day

– Fast axonal transport – requires motor proteins and consumes ATP; vesicles
and membrane-bound organelles travel back toward (retrograde) or away
from (anterograde) cell body; maximum rate of 200 mm/day and 400
mm/day respectively

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 Poliovirus and Retrograde Axonal
Transport
• Poliomyelitis – caused by poliovirus; infection impacts CNS and especially spinal
cord; can result in deformity and paralysis

• No cure exists, but polio can be easily prevented by vaccination

• Virus accesses CNS by first entering muscle cells; passes into motor neurons at
neuromuscular junction; travels length of axon by retrograde axonal transport
until reaching spinal cord

• Other viruses (herpes simplex, rabies) and

• toxins (tetanus) also have ability to invade via this method

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Neurons

Figure 11.5 Neuron structure.

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Neurons
• Neurons have three main functional regions:

– Receptive region – dendrites and cell body

– Conducting region – axon

– Secretory region – axon terminal

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Neurons
Neurons can be classified according to structural features (Table 11.1):

– Multipolar – single axon and multiple dendrites; over 99% of all neurons

– Bipolar – one axon and one dendrite and cell body between them; eye
and olfactory epithelium (nasal cavity)

– Pseudounipolar – only one fused axon; extends from cell body; divides
into two processes: one carries sensory information from sensory
receptors to cell body; other carries sensory information (pain, touch,
and pressure) from cell body to spinal cord;

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Neurons

Table 11.1 Neuron Classification

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Neurons
Neurons can also be classified into three functional groups (Table 11.1):

– Sensory (afferent) neurons – carry information toward CNS; neuron cell

bodies in PNS receive information from sensory receptors and relay
information via axons to brain or spinal cord; usually pseudounipolar or
bipolar

– Interneurons (association) neurons – relay information within CNS

between sensory and motor neurons; most neurons in body; multipolar;
communicate with many other neurons

– Motor (efferent) neurons – carry information away from cell body in

CNS to muscles and glands; mostly multipolar

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Neurons
Specific neuron components group together:
– CNS:
 Nuclei – clusters of neuron cell bodies
 Tracts – bundles of axons

– PNS:
 Ganglia – clusters of neuron cell bodies
 Nerves – bundles of axons

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Neuroglia (1 of 9)

Neuroglia (neuroglial) cells –

– Half the volume of the nervous system

– provide structural support and protection for neurons; also

maintain their environment (Figures 11.6, 11.7)

– Able to divide and fill in space left behind when neuron dies

– Form of each type of neuroglial cell is specialized for function;

Structure-Function Core Principle

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Neuroglia (2 of 9)
Neuroglia or neuroglial cells (continued)

– 4 types reside in CNS:

 Astrocytes

 Oligodendrocytes

 Microglia

 Ependymal cells

– 2 types reside in PNS:

 Schwann cells

 Satellite cells
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 Neuroglia
Many types of neuroglia in CNS

Figure 11.6 Neuroglial cells of the CNS.

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Neuroglia
Many types of neuroglia in PNS

Figure 11.7 Neuroglial cells of the PNS.

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Neuroglia (4 of 9)
• Neuroglia or neuroglial cells (continued)

– Oligodendrocytes – also in CNS; radiating processes with flattened sacs;

wrap around axons of nearby neurons to form myelin

Figure 11.6 Neuroglial cells of the CNS.

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Neuroglia (3 of 9)
Astrocytes – large star-shaped cells; many processes terminating in end-feet;
function to:
 Anchor neurons and blood vessels in place;
 help define and maintain three-dimensional structure of brain
 Transport of nutrients and gases between blood vessels and neurons;
regulate extracellular environment of brain
Figure 11.6 Neuroglial cells of
 Formation of blood-brain barrier; the CNS.
protective structure; surrounds
capillary endothelial cells; makes them
impenetrable to most polar
compounds and proteins
 Repair damaged brain tissue by rapid
cell division

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 Neuroglia (5 of 9)
– Microglia – small, scarce cells; activated by injury into wandering
phagocytic cells within CNS; ingest disease-causing microorganisms,
dead neurons, and cellular debris

Figure 11.6 Neuroglial cells of the CNS.

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Neuroglia (6 of 9)
– Ependymal cells – ciliated cells; line hollow
spaces within CNS (brain and
spinal cord); manufacture
and circulate cerebrospinal
fluid (CSF)

– Schwann cells – encircle axons in PNS to

provide them with myelination (Figure
11.7)

– Satellite cells – surround cell bodies of

neurons in PNS; provide supportive
Figure 11.6 Neuroglial cells of
functions (still not well defined)
the CNS.
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 The Myelin Sheath
Myelin Sheath – layers of plasma membrane of Schwann cell or
oligodendrocyte in PNS and CNS respectively (Figures 11.8, 11.9):

Myelination – neuroglial cells wrap multiple layers of membrane (myelin)

around axon

– Lipid content of myelin sheath insulates axon (prevents ion

movements) like rubber around copper wire; increases speed of action
potential conduction

– Makes nerves appear white

– Myelinated axons conduct action potentials about 15–20 times faster

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 Myelin

Myelinated
axons

Internode

Myelin Oligodendrocyte
(cut) Astrocyte
Axon Axolemma
White
matter
Node

Unmyelinated
axon

Basement
membrane

Capillary

A diagrammatic view of neural tissue in the CNS, showing relationships between

neuroglia and neurons
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 The Myelin Sheath (2 of 6)
Differences between myelination in PNS and CNS:
Neurolemma – on outer surface of myelinated axons in
PNS; Schwann cell nucleus, organelles, and cytoplasm;
not present in CNS (Figure 11.8a, b)

Number of axons myelinated – oligodendrocytes have

multiple processes that myelinate multiple axons in CNS;

Schwann cell only myelinates one axon in PNS

Timing of myelination – myelination begins early in fetal

development in PNS and much later in CNS;

– very little myelin in brain of newborn

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The Myelin Sheath (3 of 6)

Figure 11.8a The myelin sheath in the PNS and CNS.

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The Myelin Sheath (5 of 6)
Axons in both CNS and PNS are generally longer than neuroglial cells so
multiple cells must provide complete myelin sheath

– Internodes – segments of axon covered by neuroglia

– Node of Ranvier – gap between adjacent neuroglia; where myelin

sheath is absent

Small axons in CNS and PNS are usually unmyelinated

White matter – composed of myelinated axons; appear white

Gray matter – composed of neuron cell bodies,

unmyelinated dendrites and axons; appear gray

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Regeneration of Nervous Tissue (1 of 3)
• Regeneration or replacement of damaged tissue

– is nearly nonexistent in CNS;

– limited in PNS; neural tissue can regenerate only if cell body remains
intact

Figure 11.10 Repair of axon damage in the PNS.

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Regeneration of Nervous Tissue (2 of 3)
Regeneration steps (Figure 11.10):

– Axon and myelin sheath degenerate distal to injury (Wallerian

degeneration); facilitated by phagocytes

– Growth processes form from proximal end of axon

– Schwann cells and basal lamina form regeneration tube

– Single growth process grows into regeneration tube; directs new

axon toward its target cell

– New axon reconnects to its target cell

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 Site of injury

Fragmentation of Axon Myelin Proximal stump Distal stump

axon and myelin
occurs in distal
stump.

Schwann cells Macrophage

form cord, grow
into cut, and
unite stumps.
Macrophages
engulf degener-
ating axon and Cord of proliferating Schwann cells
myelin.
Axon sends buds
into network of
Schwann cells
and then starts
growing along
cord of Schwann
cells.

Axon continues
to grow into
distal stump and
is enclosed by
Schwann cells.

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Gliomas and Astrocytomas
• Primary brain tumors – originate
in brain; most are gliomas (caused
by abnormally high rate of division
of glial cells)

• Predisposing conditions –
exposure to ionizing radiation and certain diseases

• Astrocyte – most commonly affected cell; tumor is

astrocytoma
– Range in severity from mild (good prognosis) to
highly aggressive (very poor prognosis)

– Treatment – varies with tumor type, age, and

health of patient; generally involves surgical
removal of mass with chemotherapy and perhaps
radiation therapy
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 MODULE 11.3
ELECTROPHYSIOLOGY OF
NEURONS

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Our activities are relying on neurons

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 For activities you need stimulation and
excitability

Excitability: Ability of an organism or a specific tissue to r

eact to the environment.
You become excited when you are stimulated enough

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Neurons are cells that send and receive signals

Receive Information Spread Passing

Information Processing & Information
through & propagate Synaptic activity
stimulation Excitability information

Changes in transmembrane potential

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Introduction to Electrophysiology of Neurons
All neurons are excitable (responsive) in presence of various stimuli: chemical
signals, local electrical signals, and mechanical deformation

Stimuli generate electrical changes across neuron plasma membrane; rapidly

conducted (conductivity) along entire length of membrane

Two forms of electrical changes occur in neurons:

– Local potentials (graded potential) – travel short distances

– Action potentials – travel entire length of axon

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Neurons become excited through changes
in transmembrane potential
Changes with plasma membrane permeability in response
to chemical or physical stimuli

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In molecular level changes in transmembrane
potential occur through channels and pumps in
plasma membrane

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 Ion Channels and Gradients

• Passive Channels (Leak Channels)

– Are always open
– Permeability changes with conditions

• Active Channels (Gated Channels)

– Open and close in response to stimuli
– At resting potential, most gated
channels are closed

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Ion Channels and Gradients
Gated channel types:

– Ligand-gated channels – open in response to binding of specific

chemical (ligand) to specific receptor

– Voltage-gated channels – open in response to changes in voltage across

membrane

– Mechanically-gated channels – open or close in response to mechanical

stimulation (pressure, stretch, or vibration)

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 Ion Channels and Gradients
Mechanically gated channel Voltage-gated channel Chemically gated channel

–70 mV

Inactivation
Channel closed Channel closed gate Resting state

–60 mV Presence of ACh

Applied Binding
pressure ACh site

Channel open Channel open Gated

Channel closed channel
Pressure +30 mV
removed

Channel inactivated
Channel closed Channel open
A chemically gated Na+ channel that
opens in response to the presence of
ACh at a binding site.

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 Ion Channels and Gradients
Sodium-potassium ion pump (Na+/K+ ATPase)

Ions moving against electrochemical gradients move via

ATP-consuming pumps; one of most important is
sodium-potassium ion pump (Na+/K+ ATPase)

– Moves three Na+ ions out and two K+ions into cell,
per ATP hydrolyzed

– Maintains (and to some extent creates) high

concentration of Na+ in extracellular fluid and
lower concentration in cytosol; opposite true for
K+

– Gradients Core Principle

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 Main Processes in Neural Activities
1.Changes in transmembrane potential

• Resting potential : The transmembrane potential of resting cell

• Graded potential : Temporary, localized change in resting potential,

• Action potential : An electrical impulse produced by graded potential,

does not diminish as it moves, propagates along surface of axon to
synapse

2. Synaptic activity : Releases neurotransmitters at presynaptic membrane,

Produces graded potentials in postsynaptic membrane

3. Information processing : The integration of stimuli at the level of individual

cells and Response of postsynaptic cell

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The Resting Membrane Potential
Thin layer of negatively charged ions exists in cytosol on inside of cell; thin
layer of positively charged ions exists on outside of cell

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The Resting Membrane Potential (2 of 3)
Voltage – electrical gradient established by separation of charges between two
locations (across plasma membrane)

Membrane potential – electrical potential across cell membrane; source of

potential energy for cell

Typical neuron has resting membrane potential (RMP) of 70 mV (Figure

11.11a)

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All plasma (cell) membranes produce resting potential
(Transmembrane Potential of an Undisturbed Cell)
EXTRACELLULAR FLUID
Cl–
–30 0
–70
+30
mV
3 Na+
Na+ leak
K leak
+
channel
channel

Sodium–
Plasma potassium
membrane exchange
pump

CYTOSOL

Protein 2 K+

Protein Protein

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The Resting Membrane Potential (3 of 3)

– RMP is slightly negative because leakage channels favor gradient

where more K+leaks out, than Na+leaks in (there are more K+channels

than Na+ channels)

– RMP of neuron is less negative at –70 mV than that of skeletal muscle

fiber at –90 mV; largely due to number of potassium ion leak channels

in skeletal muscle fiber

– Cell is polarized when voltage difference across plasma membrane

does not equal 0 mV

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 Principles of Electrophysiology

Figure 11.11a Ion movements leading to changes in the membrane potential.

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A&P Flix: Resting Membrane Potential

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Changes in Membrane Potential: Ion
Movements
Cell starts with negative resting membrane potential, (negative with respect
to extracellular fluid)

Unequal distribution of ions across plasma membrane exists; gradients are

maintained by gated channels and pumps (Na+/K+ pump)

When gated channels for specific ion open, ions will follow electrochemical
gradient into or out of cell

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Changes in Membrane Potential: Ion
Movements
Can alter cell’s membrane potential by opening gated channels and causing

ions to flow into or out of cell

– Figure 11.11a shows membrane at rest (not being stimulated); gated ion

channel is closed

– In Figure 11.11b ligand binds ligand-gated cation channel, and cations

(such as sodium ions) follow electrochemical gradient into cell;

– Depolarization; influx of positive charges makes membrane

potential less negative

– Cell becomes less polarized as membrane potential approaches 0 mV

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 Changes in Membrane Potential: Ion
Movements
– Repolarization: When cell returns to resting membrane potential
– In Figure 11.11c, ligand binds to cation channel (such as a K+ channel)
for which electrochemical gradient is reversed;

– cations flow out of cell into extracellular fluid

– Hyperpolarization ; As cell loses positive charges, membrane

potential becomes more negative than at rest

 Hyperpolarization may also result from opening of channels for

anions (chloride ions);

– would allow negatively charged ions to flow into cell

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Changes in Membrane Potential: Ion
Movements

Figure 11.11 Ion movements leading to changes in the membrane potential.

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 Local Potentials
Local changes in transmembrane potential that cannot spread far from
site of stimulation
Stimulus that opens a chemically gated channel produces a graded
potential
– May cause one of two effects

– Depolarization – positive charges enter cytosol; make membrane potential

less negative (change from 70 to 60 mV)

– Hyperpolarization – either positive charges exit or negative charges enter

cytosol; makes membrane potential more negative (change from 70 to 80
mV)
Chemical
stimulus
Chemical removed ChemicalChemical
stimulus stimulus stimulus
applied Repolarization applied removed

Transmembrane Resting potential

potential (mV)
Depolarization
Hyperpolarization
Return to
resting potential
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Local Potentials (2 of 2)
Graded potentials; vary greatly in

– size; degree of change in membrane potential depends on length of

stimulation, number of ion channels open, and type(s) of ion channels
open

– Reversible – when stimulus stops, neuron quickly returns to resting

potential

– Decremental – changes in membrane potential produced are small;

current is lost across membrane over few millimeters; cannot send
signals over great distances; useful for short-distance signaling only
(local potentials)

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 Resting State
Initial Resting membrane with closed chemically gated sodium ion channels
segment
EXTRA-
CELLULAR
–70 mV FLUID

Graded Potentials
CYTOSOL

Stimulus
applied Stimulation
here
Membrane exposed to chemical that opens the sodium ion channels

–65 mV

Graded Potential
Spread of sodium ions inside plasma membrane produces a local current
that depolarizes adjacent portions of the plasma membrane

Local –60 mV –65 mV –70 mV

current

Local current
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Big Picture Animation: Local Potentials

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Action Potentials (1 of 11)
Small local changes in potential of neuron’s plasma membrane; triggers for
long-distance action potentials

Action potential –
uniform, rapid depolarization and repolarization of membrane potential

Via voltage gated channels

Only generated in trigger zones (axolemma, axon hillock, and initial segment
of axon)

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 Action Potentials (1 of 11)
States of voltage–gated channels –

Two types of voltage-gated channels involved in action potentials

– One for sodium ions and one for potassium ions

Why only axons have action potentials? (Figure 11.12)

Voltage gated channels are most abundant in axolemma of neuron;

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 Action Potentials
– Voltage-gated potassium channels have
two possible states: resting (closed) and
activated (open) (Figure 11.12a)

 Resting state – channels are closed; no

potassium ions are able to cross
plasma membrane

 Activated state – channels are open;

potassium ions are able to flow down
concentration gradients

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Action Potentials
Voltage-gated sodium channels have two gates
(activation and inactivation gates) with three
states (Figure 15.12b):

– Resting state – inactivation gate is open

and activation is closed; no sodium ions
are able to move

– Activated state – voltage change opens

activation gate; both activation and
inactivation gates are open when an
action potential is initiated
– Inactivated state – inactivation gate is
closed and activation gate is open;
channel no longer allows sodium ions to
move through; once action potential is
over, channel returns to resting state
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 Action Potentials
Neuronal action potential has three general phases;
lasts only few milliseconds:

– Depolarization phase – membrane potential

rises toward zero; then becomes positive briefly

– Repolarization phase – membrane potential

returns to negative value

– Hyperpolarization phase – membrane potential

temporarily becomes more negative than
resting membrane potential

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 Generation of an Action Potential
ABSOLUTE REFRACTORY RELATIVE REFRACTORY
PERIOD PERIOD

3 Sodium channels close,

+30
voltage-gated potassium
channels open, and potassium
ions move out of the cell.
Repolarization begins.
0
D E P OL A R IZATION R E P OL A R IZATION
Membrane potential (mV)

Resting
membrane 2
potential
Voltage-gated sodium Potassium channels
−40 channels open and close, and both sodium
sodium ions move into the and potassium channels
Threshold cell. The membrane return to their
−60
potential rises to +30 mV. normal states.
−70 1
4
A graded depolarization
brings an area of excitable
membrane to threshold
(−60 mV).
During the absolute refractory During the relative refractory
period, the membrane cannot period, the membrane can
respond to further stimulation. respond only to a larger-
than-normal stimulus.

0 1 2
Time (msec)

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 Action Potentials (7 of 11)
Action potential proceeds through following steps (Figure 11.13):

1. Local potential must be able to depolarize axon strongly

enough to reach level called threshold (usually 55 mV)

2. Once threshold reached, voltage-gated sodium channels activate and

sodium ions flow into axon causing depolarization

 Positive Feedback loop – initial input (activation of sodium ion

channels and depolarization) amplifies output (more sodium ion
channels are activated and axolemma depolarizes further)

 Feedback Loops Core Principle

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Action Potentials (9 of 11)

Action potential steps (continued):

3. Sodium ion channels inactivate and voltage-gated potassium ion

channels activate: sodium ions stop flowing into axon; potassium begins
exiting axon as repolarization begins

4. Sodium ion channels return to resting state and repolarization

continues

5. Axolemma may hyperpolarize before potassium ion channels return to

resting state; then axolemma returns to resting membrane potential

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Action Potentials (8 of 11)

Figure 11.13 Events of an action potential.

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Action Potentials (10 of 11)

Figure 11.13 Events of an action potential.

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 Refractory Period
Refractory period – period after neuron has generated action potential;
cannot be stimulated to generate another action potential; divided into two
phases (Figure 11.14):

Absolute refractory period – when no additional stimulus (no matter how

strong) is able to produce additional action potential

– Coincides with voltage-gated sodium channels being activated and

inactivated

– Sodium channels may not be activated until they return to resting states
(activation gates closed and inactivation gates open)

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Refractory Period

Relative refractory period – follows immediately after absolute refractory

period; only strong stimulus can produce action potential

– Voltage-gated sodium channels returned to resting state; able to open

again

– Potassium channels are activated and membrane is repolarizing or

hyperpolarizing; takes much larger stimulus to trigger action potential

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Refractory Period

Figure 11.14 Refractory periods of an action potential.

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Big Picture Animation: Action Potentials

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Local and Action Potentials Compared
Graded local potentials produce variable changes in membrane potentials
while actions potentials cause maximum depolarization to +30 mV

All-or-none principle refers to event (action potential) that either happens

completely or does not occur at all

– If neuron does not depolarize to threshold then no action potential

will occur

– Action potentials are not dependent on strength, frequency, or length

of stimulus like local potentials

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Local and Action Potentials Compared

Local potentials are reversible; when stimulus ends neuron returns to resting
membrane potential; action potentials are irreversible; once threshold is
reached it cannot be stopped; will proceed to completion (all-or-none)

Signal distance is greater for action potentials versus “local” potentials:

– Local potentials are decremental; decrease in strength over short

distance

– Action potentials are nondecremental; signal strength does not

decrease despite traveling long distances

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 Local Anesthetic Drugs
• Local anesthetics – (lidocaine) commonly administered agents for surgical
or dental procedures; produce temporary numbness in specific area

• Block voltage-gated sodium channels of neurons in treated area;

• prohibits depolarization; action potentials relaying pain are not

transmitted to CNS

• Nonselective; also affect sodium channels in muscles of area; causes

temporary paralysis; reason for crooked smiles and drooling following
dental work

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Propagation of Action Potentials (1 of 8)
Action potentials must be conducted (propagated) along entire length of axon
to serve as long-distance signaling service (Figures 11.15, 11.16):

Action potentials – self-propagating; travel in only one direction:

– Each action potential triggers another in next section of axon, usually

starting at trigger zone and ending at axon terminals (like dominoes)

– Action potentials travel in one direction as sodium ion channels of each

successive section of axon go into refractory period as next section
depolarizes

– Action potential propagation down axon is nerve impulse

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Propagation of Action Potentials (2 of 8)
• Events of Propagation – action potential is propagated down axon in
following sequence of events:

Figure 11.15 Propagation of an action potential.

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Propagation of Action Potentials (3 of 8)
• Events of Propagation (continued):

Figure 11.15 Propagation of an action potential.

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Big Picture Animation: Propagation of Action
Potentials

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 Propagation of Action Potentials (5 of 8)
Conduction speed – rate of propagation;
– Influenced by both axon diameter and myelination;
determines how rapidly signaling can occur within
nervous system

– Axons with larger diameter have faster conduction

speeds because larger axons have lower resistance
to conduction (current flows through them more
easily)

– Presence of absence of myelination gives rise to

two types of conduction:

 saltatory and continuous conduction

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Propagation of Action Potentials (7 of 8)
– Continuous conduction – in unmyelinated axons; every section of
axolemma from trigger zone to axon terminal must propagate action
potential; slows conduction speed as each successive section of axon
must depolarize

Figure 11.16 Comparison of saltatory and continuous conduction.

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Propagation of Action Potentials (6 of 8)
– Saltatory conduction – in myelinated axons where insulating properties
of myelin sheath increase efficiency and speed of signal conduction;
action potentials only depolarize nodes of Ranvier; “jumps” from node
to node

Figure 11.16 Comparison of saltatory and continuous conduction.

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Propagation of Action Potentials (8 of 8)

Figure 11.16 Comparison of saltatory and continuous conduction.

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 Propagation of Action Potentials (10 of 19)
Classification of Axons by Conduction Speed:

– Type A fibers – fastest conduction speeds (120 m/sec or 250 mi/h); largest
diameter (5–20 m) and myelinated; sensory and motor axons associated
with skeletal muscle and joints

– Type B fibers – slower conduction speeds (15 m/sec or 32 mi/hr); mostly

myelinated with intermediate diameter axons
(2–3 m); efferent fibers of autonomic nervous system (ANS) and some
sensory axons

– Type C fibers – slowest conduction speeds (0.5–2 m/sec or 1–5 mi/hr);

smallest diameter fibers (0.5–1.5 m); unmyelinated axons include efferent
fibers of ANS and sensory axons; transmit pain, temperature, and certain
pressure sensations Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved
 Multiple Sclerosis
• Multiple sclerosis (MS) – certain cells of immune system attack
myelin sheaths within CNS; type of autoimmune disorder (patient’s
own immune system attacks part of body)

• Causes progressive loss of myelin sheath; in turn causes loss of

current from neurons

• Symptoms – result from progressive slowing of action potential

propagation; depend on region of CNS affected; most exhibit
changes in sensation (e.g., numbness), alterations in behavior and
cognitive abilities, and motor dysfunction, including paralysis

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Putting It All Together: The Big Picture of
Action Potentials

Figure 11.17 The Big Picture of Action Potentials.

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MODULE 11.4 NEURONAL
SYNAPSES

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Overview of Neuronal Synapses (1 of 4)
Neurons must communicate with other cells, including other neurons, in
order to carry out their functions

Synapse – where neuron meets target cell (neuronal synapse if another

neuron); can be electrical or chemical (Figure 11.21):

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 Overview of Neuronal Synapses (2 of 4)
– Axodendritic synapse – between axon of one neuron and dendrite of
another

– Axosomatic synapse – between axon of one neuron and cell body of

another

– Axoaxonic synapse – between axon of one neuron and axon of another

Figure 11.18 Structural types of synapses.

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 Overview of Neuronal Synapses (3 of 4)
Terms used to describe which neuron is sending and which is receiving

message, regardless of type of synapse:

– Presynaptic neuron – neuron sending message from its axon terminals

– Postsynaptic neuron – neuron receiving message from presynaptic

Telodendrion
neuron at its cell body, axon, or dendrites
Synaptic terminal
Endoplasmic
Mitochondrion reticulum

Synaptic
vesicles
Presynaptic
membrane
Postsynaptic Synaptic
membrane cleft
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 Overview of Neuronal Synapses (4 of 4)
Synaptic transmission – transfer of chemical or
electrical signals between neurons at synapse;
fundamental process for most functions of nervous
system

– Allows for voluntary movement, cognition,

sensation, and emotions

– Average presynaptic neuron forms

synapses with about 1000 postsynaptic
neurons

– Postsynaptic neuron can have as many as

10,000 synaptic connections with different
presynaptic neurons Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved
 Electrical Synapses (1 of 3)
Electrical synapse – occurs between cells electrically coupled via gap junctions
(Figure 11.19a):
– Axolemmas of each cell in synapse are nearly touching; gap junctions
align channels forming pores that ions or other small substances can flow
through

– In areas of brain responsible for programmed, automatic behaviors

(breathing)

– In cardiac and visceral smooth muscle to allow for coordinated muscle

activity

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 Electrical Synapses (2 of 3)
– Electrical current can flow directly from axoplasm of one
neuron to next; creates two unique features of electrical
synapses:

 Transmission is bidirectional – either neuron can be pre

or postsynaptic; depends on direction current flows
between them

 Transmission is nearly instantaneous – only delay is time

for presynaptic neuron to depolarize (less than 0.1
milliseconds); much faster than chemical synapses (1 or
more milliseconds) Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved
Chemical Synapses (1 of 6)
Chemical Synapses (Figures 11.19,
11.20):

– Make up majority of synapses in

nervous system

– More efficient than electrical

synapses; convert electrical signals
into chemical signals; no signal
strength is lost (as at electrical
synapses)

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• Chemical Synapses
– Are found in most synapses between neurons and all synapses between
neurons and other cells

– Cells not in direct contact

– Activity may tuned by many factors

 Action potential may or may not be propagated to postsynaptic
cell

depending on:
 Amount of neurotransmitter released

 Sensitivity of postsynaptic cell

 Frequency of action potential

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Chemical Synapses (2 of 6)
– Synaptic vesicles – filled with chemical messengers (neurotransmitters);
transmit signals from presynaptic to postsynaptic neurons at chemical
synapses

– Synaptic cleft – small ECF-filled space; separates presynaptic and

postsynaptic neurons in chemical synapses (gap junctions connect neurons
in electrical synapses)

– Postsynaptic neuron has neurotransmitter receptors; bind neurotransmitter

secreted from presynaptic neuron

– Synaptic delay – time gap between arrival of action potential at axon

terminal and effect on postsynaptic membrane

– Chemical synapses are unidirectional (unlike electrical); allow for variable

signal intensities; more neurotransmitter released from presynaptic neuron
leads to stronger response at postsynaptic neuron
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 Chemical Synapses (5 of 6)
Events at Chemical Synapse –multiple neurons secreting many different
types of excitatory or inhibitory neurotransmitters (Figure 11.20):

1. Action potential in presynaptic neuron triggers opening of voltage-

gated calcium ion channels in axon terminal

2. Influx of calcium ions causes synaptic vesicles to release

neurotransmitter into synaptic cleft

3. Neurotransmitters bind to receptors on postsynaptic neuron

4. Ion channels open, leading to local potential and possibly action

potential if threshold reached

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 Chemical Synapses (6 of 6)

Figure 11.20 Events at a chemical synapse: synaptic transmission.

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An action potential arrives and
depolarizes the synaptic terminal

Presynaptic neuron Action potential

Synaptic vesicles EXTRACELLULAR
FLUID
ER
Synaptic
terminal
Initial
segment
AChE

POSTSYNAPTIC
NEURON

Extracellular Ca2+ enters the synaptic

terminal, triggering the exocytosis of ACh

ACh

Ca2+ Ca2+
Synaptic cleft

Chemically gated
sodium ion channels

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ACh binds to receptors and depolarizes
the postsynaptic membrane

Initiation of
action potential
if threshold is
reached at the
initial segment

Na+
Na+ Na +
Na +
Na+

ACh is removed by AChE

Propagation of
action potential
(if generated)

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 Mitochondrion

Acetylcholine
Synaptic
vesicle

SYNAPTIC
TERMINAL

SYNAPTIC
Choline
Acetylcholinesterase CLEFT

Acetate (AChE)

POSTSYNAPTIC ACh
MEMBRANE receptor

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Big Picture Animation: Synaptic
Transmission

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Neurotransmitters
Nearly all neurotransmitters undergo similar pattern of use despite that there
are over 100 known; share similar features:

– Made in cell body or axon terminal and packaged into synaptic vesicles

– Released from axon terminals of presynaptic neurons; cross synaptic

cleft; bind to specific receptors on postsynaptic membrane

– Effects are often rapidly terminated through removal and/or

degradation

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 Chemical Synapses
Synaptic transmission may be terminated by ending effects of
neurotransmitter (Figure 11.23):

– Neurotransmitters diffuse away from synaptic cleft in ECF; can be

reabsorbed into neuron or astrocyte

– Neurotransmitter broken down in synaptic cleft by enzymes; by-

products of reaction reabsorbed by presynaptic membrane for
reassembly

– Some neurotransmitters are reabsorbed into presynaptic neuron

(reuptake)

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Chemical Synapses

Figure 11.23 Methods of termination of synaptic transmission.

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Big Picture Animation: Termination of
Synaptic Transmission

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Concept Boost: Sorting out Different Types
of Channels and Pumps in Membrane of a
Neuron (1 of 3)
Distribution of protein channels and pumps is predictable if functions are
considered:

Ligand-gated ion channels bind neurotransmitters from another neuron (to

receive signals); so ligand-gated ion channels will be located on receptive
regions of neuron (dendrites and cell body)

Voltage-gated sodium and potassium ion channels open or close during

action potential to send signal to another cell; located on part of neuron that
sends signals to other cells via action potentials (axon)

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Concept Boost: Sorting out Different Types
of Channels and Pumps in Membrane of a
Neuron (2 of 3)
Voltage-gated calcium ion channels trigger exocytosis of synaptic vesicles;
only one place in neuron where synaptic vesicles are located (axon terminal)

Leak channels and Na+/K+ pump generate and maintain resting membrane
potential; RMP applies to entire neuron, so leak channels and Na+/K+ pumps
are located throughout every part of neuron’s membrane

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Concept Boost: Sorting out Different Types
of Channels and Pumps in Membrane of a
Neuron (3 of 3)

Figure 11.24 Types of channels and pumps in different parts of the neuron membrane.

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Putting It All Together: The Big Picture of
Chemical Synaptic Transmission

Figure 11.25 The Big Picture of Chemical Synaptic Transmission.

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 MODULE 11.5
NEUROTRANSMITTERS

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Postsynaptic Potentials
Binding of neurotransmitter to receptor leads to an EPSP (excitatory effects)
or an IPSP (inhibitory effects)

Most neurotransmitters can have both effects; depends on which

postsynaptic neuron receptors they bind;

Single neurotransmitter may have several receptor types

Major neurotransmitters are classified into four groups based on chemical

structure (Table 11.3)

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Major Neurotransmitters (2 of 7)

Table 11.3 Major Neurotransmitters

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Major Neurotransmitters (3 of 7)
Acetylcholine (ACh) – small molecule neurotransmitter widely used by
nervous system

– Cholinergic synapses bind ACh; in neuromuscular junction, within brain

and spinal cord and within autonomic nervous system

– Largely excitatory; does exhibit some inhibitory effects in PNS

– Synthesized from choline and acetyl-CoA; packed into synaptic vesicles

– Quickly degraded by acetylcholinesterase (AChE); enzyme in synaptic

cleft; by-products taken back into presynaptic neuron for recycling and
reuse
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 Major Neurotransmitters (4 of 7)
Biogenic amines (monoamines); five neurotransmitters synthesized from
amino acids; used throughout CNS and PNS for regulation of homeostasis and
cognition; first three form catecholamine subgroup (made from amino acid
tyrosine); mostly excitatory:

– Norepinephrine (catecholamine; noradrenalin) – mainly in ANS;

influences heart rate, blood pressure, and digestion; in CNS regulates
sleep/wake cycle, attention, and feeding behaviors

– Epinephrine (catecholamine; adrenalin) – also in ANS; similar functions

as norepinephrine; more widely used as hormone by endocrine system.

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 Major Neurotransmitters (5 of 7)
Biogenic amines (continued):

– Dopamine (catecholamine) – used extensively by CNS; movement

coordination, emotion and motivation

– Serotonin – synthesized from amino acid tryptophan; most serotonin-

secreting neurons are in brainstem; axons project into multiple areas of
brain; functions include mood regulation, emotions, attention, feeding
behaviors, and daily rhythms

– Histamine – synthesized from amino acid histidine; regulation of

arousal and attention

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Major Neurotransmitters (6 of 7)
Three main amino acid neurotransmitters:

– Glutamate – most important excitatory neurotransmitter in CNS;

generate EPSPs in postsynaptic neuron

– Glycine and GABA – both major inhibitory neurotransmitters;

induce IPSPs on postsynaptic neurons by opening chloride ion
channels; hyperpolarize axolemma

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 Major Neurotransmitters (7 of 7)
Neuropeptides – group of neurotransmitters with wide variety of functions;
must be synthesized in cell body and transported to axon

– Substance P – released from type C sensory afferents that carry

information about pain and temperature; also released by other
neurons in brain, spinal cord, and gut

– Opioids – group of more than 20 neuropeptides; include endorphins,

enkephalins, and dynorphins; all elicit pain relief; nervous system
depressants

– Neuropeptide Y – feeding behaviors; may mediate hunger or feeling full

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• The Effect of a Neurotransmitter
– On a postsynaptic membrane
 Depends on the receptor, even for the same neurotransmitter

– For example, acetylcholine (ACh)

 Usually promotes action potentials

 But inhibits cardiac neuromuscular junctions

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Neurotransmitter Receptor (1 of 3)
Type of neurotransmitter receptor on postsynaptic membrane determines
response:

– Ionotropic receptors – components of ligand-gated ion channels;

directly control movement of ions into or out of neuron when bind to
neurotransmitter (Figure 11.26a)

– Metabotropic receptors – within plasma membrane; associated with

separate ion channel; connected to metabolic processes initiated when
neurotransmitter binds (Figure 11.26b)

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Neurotransmitter Receptor (2 of 3)
– Metabotropic receptors (continued):

– G-proteins – group of intracellular enzymes associated with many

metabotropic receptors; activate cascade of enzyme-catalyzed reactions; form
intracellular chemical messenger molecules called second messengers
(neurotransmitter is “first messenger”)

– Second messengers – open or close ion channels in postsynaptic membrane

 Cyclic adenosine monophosphate (cAMP) – common second messenger

derived from ATP; multiple functions in neurons

 cAMP binds to group of enzymes; add phosphate groups to ion channels;

triggers channel to open or close
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Neurotransmitter Receptor (3 of 3)

Figure 11.26 Types of neurotransmitter receptors.

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 Chemical Synapses (1 of 3)

• Postsynaptic potentials – local

potentials in membranes of postsynaptic
neuron (Figure 11.21):

– Excitatory postsynaptic
potential (EPSP) :Membrane
potential of postsynaptic neuron
moves closer to threshold; caused
by small local depolarization
(sodium or calcium channels open)

Figure 11.21a Postsynaptic potentials.

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 Chemical Synapses (2 of 3)

• Postsynaptic Potentials (continued):

– inhibitory postsynaptic
potential (IPSP): Membrane
potential of postsynaptic neuron
moves farther away from
threshold; caused by small local
hyperpolarization (potassium or
chloride ion channels open)

Figure 11.21b Postsynaptic potentials.

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 Chemical Synapses (3 of 3)

Figure 11.21 Postsynaptic potentials.

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 Neural Integration
Neurons receive input, both inhibitory
and excitatory, from multiple neurons,
each of which influences whether action
potential is generated

Neural integration – process in which

postsynaptic neuron integrates all
incoming information into single effect

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Neural Integration

Summation – all input from several postsynaptic potentials are added

together (EPSPs + IPSPs) to affect membrane potential at trigger zone

– Action potential will only be generated if threshold is reached;

sum of EPSPs must be enough to overcome sum of IPSPs

– If sum of IPSPs is greater than EPSPs, membrane will

hyperpolarize; threshold will not be reached and action
potential will not be generated

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 Neural Integration

Types of summation:

– Temporal summation – neurotransmitter released repeatedly from

axon terminal of single presynaptic neuron; each local potential (EPSP) is
short-lived; must be generated quickly to reach threshold and create
action potential (Figure 11.22a)

– Spatial summation – simultaneous release of neurotransmitters from

axon terminals of many presynaptic neurons (Figure 11.22b)

– IPSPs are also subject to both temporal and spatial summation but have
inhibitory effects; make it less likely to reach threshold with subsequent
action potential generation
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Temporal Summation
Multiple times
Rapid, repeated stimuli at one synapse

Second stimulus arrives

First stimulus arrives and is added to the Action potential is
first stimulus generated

ACTION
FIRST SECOND POTENTIAL
STIMULUS STIMULUS PROPAGATION

Initial Threshold
segment reached

Temporal Summation. Temporal summation occurs on a membrane that receives two

depolarizing stimuli from thesame source in rapid succession. The effects of the second
stimulus are added to those of the first.

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Spatial Summation
Multiple locations
Many stimuli, arrive at multiple synapses

Two stimuli arrive simultaneously Action potential is generated

TWO
SIMULTANEOUS ACTION
STIMULI POTENTIAL
PROPAGATION

Threshold
reached

Spatial Summation. Spatial summation occurs when sources of stimulation

arrive simultaneously, but at different locations. Local currents spread the
depolarizing effects, and areas of overlap experience the combined effects.
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 Neural Integration

Figure 11.22 Temporal and spatial summation of excitatory postsynaptic potentials (EPSPs).

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Summation of EPSPs and IPSPs
Neuromodulators and hormones
Can change membrane sensitivity to neurotransmitters
Shifting balance between EPSPs and IPSPs

Time 2: Time 3:
Hyperpolarizing Stimulus Hyperpolarizing
stimulus applied removed stimulus applied

EPSP Resting potential Resting potential EPSP

IPSP IPSP

Time 1: Stimulus Time 3: Stimuli

Depolarizing removed Depolarizing removed
stimulus stimulus
applied applied

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Big Picture Animation: Postsynaptic
Potentials

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• Neuromodulators
– Can alter either the rate of neurotransmitter release or the response of a
postsynaptic neuron to specific neurotransmitters

– Released by synaptic terminals

– Released alone or with a neurotransmitter

– Trigger responses involve multiple steps, or intermediary compounds

– Affect presynaptic membrane, postsynaptic membrane, or both

– Long term effect

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• Presynaptic inhibition (example : GABA effect)

– Action of an axoaxonic synapse at a synaptic terminal that decreases the

neurotransmitter released by presynaptic membrane

• Presynaptic facilitation (example: Serotonin effect)

– Action of an axoaxonic synapse at a synaptic terminal that increases the

neurotransmitter released by presynaptic membrane

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 Action
potential GABA
arrives release Inactivation of
calcium channels

Ca2+
2. Less calcium
enters
1. Action
potential 3. Less 4. Reduced
arrives neurotransmitter effect on
released postsynaptic
membrane

Presynaptic inhibition Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved
 Action
potential Serotonin
arrives Activation of
release
calcium channels

Ca2+
Ca2+
2. More calcium
enters
1. Action
potential
arrives 3. More 4. Increased
neurotransmitter effect on
released postsynaptic
membrane

Presynaptic facilitation Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved
• Facilitation
– A process in which one neuron enhance the effect of another one

– A neuron becomes facilitated as EPSPs accumulate

– Exposure of neurons to certain drugs in exteracellular fluid

 Raising transmembrane potential closer to threshold

 Until a small stimulus can trigger action potential

Coffee & Cola ~ caffeine

Cocoa ~ theobromine

Tea ~ theophylline

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– Opioids : Neuromodulators in the CNS
 Bind to the same receptors as opium or morphine

 Relieve pain

 Four Classes of Opioids

1. Endorphins

2. Enkephalins

3. Endomorphins

4. Dynorphins

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MODULE 11.6 FUNCTIONAL
GROUPS OF NEURONS

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Neuronal Pools (1 of 2)

Neuronal pools – groups of interneurons within CNS (Figure 11.27):

– Composed of neuroglial cells, dendrites, and axons in one location and

cell bodies in another location

– Type of information processed by pool is defined by synaptic

connections of pool

– Connections between pools allow for complex mental activity

(planned movement, cognition, and personality)

– Input neurons initiate series of signals that starts activity of pool

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Neuronal Pools (2 of 2)

Figure 11.27 A neuronal pool.

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 Neuronal Circuits (1 of 5)
Neural circuits – patterns of synaptic connection between neural pools; two
basic types of neural circuits (Figure 11.28):

– Diverging circuits begin with single input neuron axon; branches out to
make contact with multiple postsynaptic neurons that follow same
pattern (Figure 11.28a)

 Allow single neuron to communicate with multiple parts of brain

and/or body

 Characteristic of those transmitting incoming sensory information

sent from spinal cord to different neuronal pools in brain for
processing
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Neuronal Circuits (2 of 5)

Figure 11.28a Types of neural circuits.

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Neuronal Circuits (3 of 5)

Neural Circuits (continued)

– Converging circuits – opposite configuration of diverging circuits;

axon terminals from multiple input neurons converge onto single
postsynaptic neuron (Figure 11.28b)

 Control of skeletal muscle movement

 Allow nervous system to respond to sensory information that it

collects and processes

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Neuronal Circuits (4 of 5)

Figure 11.28b Types of neural circuits.

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Neuronal Circuits (5 of 5)
CNS has two mechanisms that stabilize neural circuits; prevent electrical
activity from becoming chaotic:

– Inhibitory circuits – provide negative feedback mechanism to control

activity of other neural circuits

– Synaptic fatigue – synaptic transmission becomes progressively

weaker with prolonged and intense excitation

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Psychiatric Disorders and Treatments
(1 of 3)
• Psychiatric disorders affect thought processes; generally treated by
modifying synaptic transmission to change how neurons
communicate

• Psychopharmacology (study of drugs that affect higher brain functions)

targets either action potential generation or some aspect of
neurotransmitter physiology (next slide)

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Psychiatric Disorders and Treatments
(2 of 3)
– Schizophrenia – repetitive psychotic episodes (periods during
which patient is unable to appropriately test beliefs and
perceptions against reality); thought to result from excessive
release of dopamine; management involves blocking postsynaptic
dopamine receptors

– Depressive disorders – disturbances in mood; thought to result

from deficiency in synaptic transmission of serotonin,
norepinephrine, and/or dopamine; most widely used
antidepressants are selective serotonin reuptake inhibitors
(SSRIs); block serotonin transporter (only), preventing reuptake by
presynaptic neuron Copyright © 2019, 2016 Pearson Education, Inc. All Rights Reserved
Psychiatric Disorders and Treatments
(3 of 3)
– Anxiety disorders – exaggerated and inappropriate fear
responses; believed to stem from abnormalities in norepinephrine,
serotonin, and GABA transmission; treated with antidepressants,
GABA activity enhancers, and others that modulate norepinephrine
transmission

– Bipolar disorders – characterized by episodes of abnormal elevated

mood (mania) followed by depression; treatments involve decreasing
ease of action potential generation; generally block sodium channels
in axolemma

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Many Drugs
Affect nervous system by stimulating receptors that respond to

neurotransmitters,

Can have complex effects on perception, motor control, and emotional

states

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 Neurotransmitter Distribution in the Functions Affected Drugs That Affect It
Central Nervous System
Dopamine Midbrain, Ventral Pleasure and reward Cocaine,
tegmental area (VTA), Movement, Attention, Methamphetamine,
Cerebral cortex, Memory Amphetamine. In
Hypothalamus addition, virtually all
drugs of abuse directly
or indirectly augment
dopamine in the reward
pathway
Serotonin Midbrain, VTA, Cerebral Mood, Sleep, Sexual MDMA (ecstasy), LSD,
cortex, Hypothalamus desire, Appetite Cocaine
Norepinephrine Midbrain, VTA, Cerebral Sensory processing, Cocaine,
cortex, Hypothalamus Movement, Sleep, Methamphetamine,
Mood, Memory, Anxiety Amphetamine

Endogenous opioids Widely distributed in Analgesia, Sedation, Heroin, Morphine,

(endorphin and enkephalin) brain but regions vary Rate of bodily Prescription painkillers
in type of receptors, functions, Mood (Oxycodone)
Spinal cord

Acetylcholine Hippocampus, Cerebral Memory, Arousal, Nicotine

cortex, Thalamus, Basal Attention, Mood
ganglia, Cerebellum

Endogenous cannabinoids Cerebral cortex, Movement, Cognition Marijuana

(anandamide) Hippocampus, and memory
Thalamus, Basal ganglia
Glutamate Widely distributed in Neuron activity Ketamine,
brain (increased rate), Phencyclidine, Alcohol
Learning, Cognition,
Memory
Gamma-aminobutyric acid Widely distributed in Neuron activity Sedatives,
(GABA) brain (slowed), Anxiety, Tranquilizers, Alcohol
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Memory, Anesthesia
Serotonin: Released in brain ~ CNS
Shortages of Serotonin affect persons attention & emotion 
chemical imbalances and depression

Prozac, paxil, Zoloft, inhibit reabsorption of serotonin,

increase concentration at synapses relieve the symptoms

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Serotonin

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Dopamine
Released in brain ~ CNS

Both inhibitory and excitatory affects ~ mostly a downer

Involved in Parkinson’s disease and cocaine use

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Cocaine; inhibits removal of
dopamine  “cocaine high”
(produce feeling of pleasure and
reward leading to addiction)

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Nicotine: Stimulate postsynaptic Ach receptors, producing
prolonged EPSPs that facilitate CNS neurons, increase release
of dopamine (produce feeling of pleasure and reward leading to
addiction)

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Heroin is a highly
addictive drug derived
from morphine, which is
obtained from the opium
poppy

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Drugs interfere with synaptic function

1) Interfere with neurotransmitter synthesis

2) Alter rate of neurotransmitter release

Botulism toxin blocks release of ACH

Home-canned vegetables are the most common cause of botulism
outbreaks in the United State
This toxin can affect your nerves, paralyze you, and even cause death.
Even taking a small taste of food containing this toxin can be deadly.

3) Prevents neurotransmitter inactivation  excess of ACh

Cholinesterase Inhibitors ~ Insecticides &

Nerve Gas

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Arthropod Venom

• Venomous arthropods (in US) include spiders and scorpions; many

venoms affect neuronal synapses; termed neurotoxins

– Female black widow (Latrodectus mactans) – toxin causes massive

release of neurotransmitter; causes repetitive stimulation of
postsynaptic neuron
– Bark scorpion – most lethal of 40 species in US; venom prevents
postsynaptic sodium channels from closing; membrane remains
polarized; continues to fire action potentials

• Common symptoms – muscle hyperexcitability, sweating, nausea and

vomiting, and difficulty breathing

• Treatment and prognosis – depends on amount of venom received and

availability of medical care; severe cases usually require antivenin to
block effects of toxin
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Epileptic Seizures (1 of 2)

Epilepsy – recurrent episodes of abnormal, disorganized electrical activity in

brain (seizures)

• Result from sudden bursts of excitatory electrical activity within neuronal

pool; may be triggered by instability in membrane potential of single neuron

• Excess excitation overwhelms inhibitory circuits that normally prevent

overexcitation

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Epileptic Seizures (2 of 2)

• Continuous wave of excitation spreads over part of brain (partial seizure) or

entire brain (generalized seizure); no meaningful signals can be transmitted;
ends due to synaptic fatigue

• Symptoms – mild sensory disturbances to loss of consciousness to

characteristic jerking movements

• Therapy – medications aimed at preventing seizures and allowing inhibitory

circuits to function properly

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Neural Function ~ Homeostatic Imbalances
Changes in Extracellular Environment
Changes in pH ~ normal range 7.35 – 7.45
Increase pH  facilitation
Decrease pH  inhibition
> 7.8  spontaneous action potentials  convulse (involuntary
contraction of the muscles)
< 7.0  unresponsiveness  coma
Changes in ion concentration ~ Na+ and K+
Hyperkalemia ~ increase K+  reduced gradient for K+ to move out
of cell to repolarize  depolarized condition
Slight hyperkalemia  facilitation
Extreme hyperkalemia  inhibits repolarization suppresses
action potentials muscle paralysis  death by cardiac arrest
Changes in body temperature
Increased temperature  excitable neurons
Large increase  hallucinations, confusion and convulsions
Falling temperature  neuron inhibition
Large decrease  lethargy, confusion, unconsciousness
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