Readings

Sunday, 29 May 2022 4:04 PM

[11, 12, 16, 17, 20, 27, 33]

Lectures Page 1
1 - Basic Principles of Brain Organisation and Neuroanatomy
Tuesday, 15 February 2022 2:25 AM

Cellular Components of the Nervous System

Chapter 1 Reading
Focus on these sections (pp. 2-16):
• Cellular components of the nervous system
• Neurons
• Glial cells
• Cellular diversity in the nervous system
• Neural circuits
• Other ways to study neural circuits
• Organisation of the human nervous system

What kind of thing is the brain?

• Seemingly silly question today. We now know the human brain is a complex system made up
of ~86 billion individual neurons (roughly the same number of neurons as there are stars in the
Milky Way) linked by ~100 trillion connections

• But a little over than a century ago, there was a vigorous debate about this question.

• Many early theories of brain organisation posited a system of neighbouring elements fused in
a giant, continuous, net-like arrangement or reticulum. This is known as reticular theory.

• One of the most famous proponents was Italian neuroanatomist Camillo Golgi (1843-1926),
who developed a ground-breaking staining method that selectively stains neurons and their
dendritic trees and axons so they can be observed under a microscope.

• Using Golgi's staining method, the Spanish neuroanatomist Santiago Ramon y Cajal
(1852-1934), produced detail images of neurons and their processes. He arrived at a very
different conclusion from that of Golgi. According to Ramon y Cajal, neurons were individual,
discrete elements that could make contact with one another, but are not continuously fused.
This is known as neuron theory.

• At the time of Golgi and Ramon y Cajal, synapses couldn't be observed directly, so decisive
evidence in favour of the reticular or neuron theory was unavailable.

• It was only with the invention of the electron microscope (1930s) that neuroscientists
discovered tiny gaps in the synapses - now known as the synaptic cleft - that connect neurons.

• Figure: Electron microscope image of an excitatory synapse. The white arrows indicate the

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 • Figure: Electron microscope image of an excitatory synapse. The white arrows indicate the
synaptic cleft - the gap between the pre- and post-synaptic neurons. The scale bar represents
400 nm.

What is a neuron?
• Neurons or cells that are specialised for long-distance electrical signalling and intercellular
communication.

• Composed of a cell body or soma, dendrites, and axon.

• Dendrites are branched projections of neurons that receive signals or electrical impulses
(known as action potentials or spikes) from other neurons and propagate these signals to the
cell body, or soma, of the neuron.

• Axons are long, slender projections of neurons that conducts electrical impulses away from
the cell body or soma.

---> Right: myelinated axon, which is a sheath, a lipid layer that coats or surrounds the axon and
facilitates faster transmission of electrical signals, like rubber plastic coating on electrical wires.
• An insulating kind of cable for electrical signals to be more efficiently conducted along the
length of an axon.

Cellular components of the nervous system

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Neural Circuits

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Organisation of the Human Nervous System

Axes of the Nervous System

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Surface Anatomy of the Cerebral Hemisphere

Lateral View of the Human Brain

Dorsal View of the Human Brain

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Dorsal View of the Human Brain

Ventral View of the Human Brain

Midsagittal View of the Human Brain

Major Internal Structures of the Brain

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Coronal View of the Human Brain

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2 - Electrical Signals of Nerve Cells
Sunday, 13 March 2022 5:06 PM

• Cell body with a dendritic tree in different shapes. These particular trees reach out to the
upper layers of the cortex and every neurons has axons, with particular axons going out of the
cortex to other places in the brain, e.g. basal ganglia, brain stem etc. This is a projection
neuron as it is projecting out of cortex.

• Dendrite tree attached to the cell body, with axons which extend away from the cell body.
There are little sheaths of fat which are called Myelin sheaths that improve its electrical

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 There are little sheaths of fat which are called Myelin sheaths that improve its electrical
characteristics.

• The inside of the neuron had overall quite a negative charge which is an electricity concept
and negative electrical charge, with the outside of the neuron having quite a positive charge.

• Cell wall which is made up of a lipid bilayer, which is a biochemical figure on how to heat
things that are inside the cell inside the cell, and things outside the cell, outside the cell.

• Brackets ( [K+] ) indicate concentration; ( -> ) indicates force, e.g. electric force or diffusion
force

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• Diffusion is the force on molecules to move from areas of high concentration to areas of low
concentration and fill the empty space.

• At t = 0, tightly formed. By t = 5, it's all spread out.

○ t = time

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• How does the flow differ when you have a large and wide open channel as compared to the
narrow channel on the left?

• Diffusion force depends on the concentration gradients and channel permeability. The
diffusion force tends to push things from high concentrations to lower concentrations, and the
greater the concentration disparity, the more diffusion that will occur, the quicker the
diffusion will occur.

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• Asking basically what is the charge of the inside relative to the outside? In this regard, the
voltage will be less than zero, as it will be negative. The inside is less positive than the outside,
therefore it's a negative number.

• V ~ (what's the overall charge on the inside and what's the overall charge on the outside and
what's the different between those overall charges and the answer to that question will be
voltage)

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• Diffusion force likes to have an equal number of things on the left as there are on the right.
But every time a positive charge moves across the membrane, it likes it because it's got more
space to roam and is more spread out.

• However, it's further away from these negative charges and we know that positive things like
negative things.

• So, where the diffusion forces are trying to pull the positive charges out of the cell, the electric
force is trying to pull positive charges into the cell and that's characteristic of real cells.

• At t = infinity, at a certain point, the electric force is equal and opposite to the diffusion force.
This means that you are in a state of equilibrium with no net flow.

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• A person came up with an equation that asked at what point did the flow of a particular ion
stop, and what is the value of E that causes that flow to stop. What is the potential where all
these things stopped flowing from one side to the other?

• This person said that the resulting membrane potential is proportional to 1/Z, where Z is the
charge of the thing you're looking at flowing across a particular membrane, which in this case
is a plus charge.

• If you assume in this example that Z > 0, and if you further assume the concentration of the
thing that's carrying those positive chargers, X, is greater than the concentration of X on the
outside, it means that the fraction Xin is divided by Xout, it means that this is greater than 1,
which leads to a voltage greater than 0.

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• Equilibrium is dominated by the ion with the most permeability. In this example, the ion with
the greatest permeability is Blue, as it has a larger channel than Yellow. When t = infinity, due
to the Blue channel being larger, more Blue ions will move from the inside to the outside,
whereas a small amount of Yellow ions will move outside, with most staying on the inside.

• Diffusion forces equals electric forces is about the entire system, and not about any particular
ion species alone.

• Diffusion does not know that the Blue ions and Yellow ions are different, and want to get to
where there is space. Similarly, the electric force does not know about identity either. It wants
to move away from charges that are similar and wants to move towards charges that are
different.

• In this example, because Blue has much more ability to travel across this membrane, it ends up
filling the empty space more than Yellow.

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• Due to the permeability of K+ being greater than the permeability of Na+ - which is true in the
actual cell, at least at rest - we ought to have a situation where more K+ ends up on the
outside than Na+.

• This is what we should observe in theory, however this does not occur in reality.

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• An active transporter does biochemical work against the forces that may be.

• In this particular case, it will take three Na+ ions in the inside of the cell when they get close to
it, it's going to bundle them all up and it's going to move them from the inside of the cell to the
outside of the cell. In doing so, it's going to trade two K+ cells and move them in the other
direction.

• This is not something that happens in accordance with the electric forces or with diffusion
forces. This is something that happens by biomechanical work being done to make this
happen.

• Even though this K+ channel is much better than this Na+, as more K+ gets out from the inside
to the outside, this pump pushes it back in and pulls Na+ out, and that's how you end with the
situation we see in the real world.

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• Diffusion pulls K+ from the inside to the outside, but the electric force pulls it back in the other
direction

• Diffusion pulls Na+ from the outside to the inside, as does the electric force

• Diffusion pulls Cl- into the cell, electric forces pushed it out because it's negative and it doesn't
like negative inside the cell

• Diffusion would - if it could - pull these negative proteins (A-) out and the electric force would
as well, but they're stuck and cannot move because they're too big to fit through any of the
channels in the membrane and there's no selective channels for them or are very few.

• The Goldman equation tells us that the equilibrium potential of neuron will depend on all of

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• The Goldman equation tells us that the equilibrium potential of neuron will depend on all of
the ion species and their conductivities for their permeability.

• The bigger the concentration gradient, the more diffusion will tend to push things apart and
the more similar those concentrations, the less those things will tend to come apart.

• Relative permeability - the overall potential in equilibrium will be determined by the

concentrations of the ion species under considerations on the inside.

• Voltage gated - change with the membrane potential itself.

• At rest, PK is doing most of the work to decide what the membrane potentials look like, what
the resting membrane potential is. But if a cell is strongly stimulated by the current injection
from us using the battery from another cell injecting its neurotransmitters.

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• From injection from the battery of another cell injecting its neurotransmitters, it starts at cell,
becomes excited and increases, comes down and returns to baseline.

• The permeability of Na+ starts small, becomes exponential, and falls really quickly, not lasting
long. It's pretty sharp and that corresponds to the P of the action potential.

• If you look at the permeability of K+, it starts out a little higher, with more conductivity or
permeability in general.

• This action potential is driven by an opening by an increase of Na+ transaction or flow and then
a relatively slower increase in K+ flow. And then that Na+ flow shuts down really quick and goes
back up to what it was and the K+ flow takes a little longer to shut down since K+ is a bit
sluggish.

• Baseline phase ---> rising phase ---> overshoot phase ---> declining phase ---> undershoot
phase ---> baseline phase

• The baseline phase is characterised by both permeability of Na+ and K+ being the default
baseline level, that the rising phase is characterised by a very small increase in K+ transduction
and a much greater increase in Na+.

• Na+ does most of the work and the rising phase becomes very dominant, with K+ doing
relatively little compared to what Na+ is doing.

• In the declining phase Na+ is reversing, but it's also that K+ has reached a point where it's
contributing a little more to the game here and balancing out that Na+ is doing.

• The undershoot phase is where Na+ is going back to its normal level, which doesn't explain

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• The undershoot phase is where Na+ is going back to its normal level, which doesn't explain
why it would make the cell membrane go even more negative than it used to be. What's
happening is that it's taken a while for K+ to return to baseline. K+ is still pushing things out
with a positive charge out of the cell which makes the cell negative.

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3 - Voltage-Dependent Membrane Permeability
Sunday, 13 March 2022 5:11 PM

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• Hyperpolarisation - going from a polarized negative state to an even more negative state.

• To hyperpolarizing inputs, nothing interesting happens. Whatever state the cell is in at its
resting potential of -65 mV, it's satisfied being there. You can go further negative and nothing
happens.

• If you go from negative to positive, that is where the interesting behaviour occurs. Most of the
action here occurs for depolarizing inputs.

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• As you progress further along by increasing the membrane potential, the transient inward
current gradually becomes smaller, and ultimately disappears.

• If you take the increasing peak values and plot them as a function of the clamped membrane
potential, what you observe is that for very negative clamp values, there's not much of a dip
and not as much of a delayed outward current.

• As you get to appreciably less negative and eventually positive values, you see that the
delayed late component keeps growing with no sign of slowing down, whereas the early
component grows and then tapers off.

• Apparently, a membrane potential of 52 mV kills that component of the current, 52 mV is the

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• Apparently, a membrane potential of 52 mV kills that component of the current, 52 mV is the
reversal potential of Na+. Another way of saying that this is the equilibrium potential of Na+.
It's the potential at which it would stop flowing across the membrane, or it's very close to the
potential which it would stop flowing across the membrane given its concentration on the
inside and the outside of the cell.

• If you have a normal amount of Na+ on the outside then you get a normal response. If you take
that Na+ away you do not get much of a response. You can change the behaviour of this early
response by manipulating the Na+ concentration. This provides stronger evidence that the
early component is Na+ oriented.

• Another way we can reason that the component is K+ related is by using clever chemistry.
Tetrodotoxin will block the flow of Na+ which disable the Na+ channels from working. Or you
could add tetraethylammonium (TEA).

• If you block Na+ channels, you end up with no early component. If you block K+ channels, you
get the early component but no late component. Now we can clearly associated Na+ with the
early and K+ with the late.

• Manipulating the levels of Na+ manipulates the amplitude and behaviour of the early
component and blocking Na+ blocks the early component and blocking K+ blocks the late
component.

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• g = conductance

• The question now is how do we express these conductivity ease selective for Na+ or selective
for K+ as a function of the membrane potential and time.

• The conductivity of Na+ rises quickly. The rise starts at the very beginning of the clamp, and it
happens very fast, and it keeps growing but it doesn't sustain so it reaches higher and higher
peak values but always decays. This means that there is an activation component and an
inactivation component. We're increasing conductivity but it's a transient increase and it shuts
down quickly.

• Whereas for K+ you get more of a sluggish response, and it's much less peaky than the Na+ but
it sustains itself for much longer and lasts longer. In these plots they show no evidence of
decaying.

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• We're examining how the conduction of Na+ and K+ behave at membrane potential regimes
experienced during an action potential. If you take all that together, what you observe is that
both Na+ on the left and K+ on the right, you find that they both have a sigmoidal shape.

• This means that at very negative membrane potentials, the conduction is incredibly small. This
goes a long way towards understanding equilibrium because at negative potentials which the
cell is at equilibrium, K+ is much more permeable than Na+, but both of those things are very,
very small in the grand scheme.

• That is, you do not have very permeable ions or very permeable channels near equilibrium
potentials. But as you start to excite that neuron and give it sufficient input, then you get this
regime here.

• The first thing to do is understand conceptually what an action potential is from the
perspective of Na+ permeability and K+ permeability.

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 perspective of Na+ permeability and K+ permeability.

• That initial fast rise is driven primarily by this Na+ conductivity. At the peak, the Na+
conductivity turns back off and Na+ stops rushing into the cell pretty quickly.

• You have an initial activation of Na+ and that drives the upshoot of this action potential and
then a few things drive this downshoot and the undershoot, and that's going to be the
deactivation of Na+ and an activation K+.

• You give your neuron some current, and what happens is that causes Na+ conductivity to
increase, i.e. opening Na+ channels. Na+ current increases, which is a depolarizing effect. This is
going to drive your neuron into the action potential, and as that's happening you are opening
K+ channels at a slower time scale and that's going to increase K+ current outside of the cell.

• You have a fast depolarizing effect and a slow hyperpolarizing effect, which is going to give you
an undershoot that is going to take a while to get back to its normal state.

• Hodgkin and Huxley built a model that said that an action potential is coming completely from
Na+ and K+ conductance changes.

• After Na+ enters and K+ exits, how do these concentrations return to equilibrium? There's
going to be some flow naturally back through the ion channels, but then you have the Na+ and
K+ pump which has a significant role in returning to equilibrium.

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• When Na+ rushes into the cell to depolarize it, there some bleed over. Some passive current is
going to flow to the right and it's going to activate the next sodium channel and then repeats.
It sort of activates its neighbours by virtue of passive flow.

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• Oligodendrocytes reach out with some fatty sheath and they wrap up the axons of other
neurons.

• Nodes of Ranvier are gaps in the myelin

• If you have an action potential at Point A, that local bleed over gets all the way to Point B
because there is no leak. The action potential starts there and does not go to its neighbour
because this neighbour has this Myelin sheath without any Na+ channels, so it immediately
gets pushed to the next possible node.

• With this structure, it lets action potentials propagate more quickly when you have a
myelinated axon compared to when you do not.

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 • Myelinated axons are going to have, on average, higher conduction velocities, which means
how fast does the action potential get from Point A to Point B than their unmyelinated
counterparts.

• There are two ways you can make action potentials faster. You can make the axons big, or you
can myelinate them.

Beyond this part for quiz advice

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• Action potential is sufficient input to a neuron to make these concentrations of ions change
very quickly due to a very quick change in the conductivity of the ion channels that dictate
their flow. The key players here are the Na+ channel and the K+ channel.

• An intrinsic property of an ion channel is its permeability to a particular ion, or its conductivity
to a particular ion.

• An action potential is associated with a fast rise in sodium conductivity, and the decline in
membrane potential is associated with a decline in Na+ conductivity and an increase in K+
conductivity.

• The basic idea is that when you get current that's injected into a cell, you're going to generate
an action potential. It opens Na+ channels as it happens. As that occurs, more Na+ rushes
inside the cell. This is what generates this depolarizing effect. Eventually, this change in the
Na+ conductance catches up, and Na+ begins rushing out of the cell. So, in one case, you have
positive charge in the form of Na+ going into the cell, and then eventually you have positive
charge in the form of K+ going out of the cell.

• This balances the effect an in fact overwhelms the effect of Na+ eventually and pulls back
down, and the fact that you get pulled down further than you initially started is just the way it
works.

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 works.

• What we have here is first the demonstration that there's always a transient aspect to the
response that goes negative. This would be an inward current and you have a later aspect
that's less transient and more stable, and that would be an outward current.

• The early dip in the graphs is all about Na+. We know this because the early dip disappears at
the +52mV mark, which is very close to the reversal potential for Na+.

• The rise and fall means that there is an activation aspect to Na+ activation and a deactivation
aspect to it.

• Na+ has an activation time, and K+ does not.

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• Voltage clamp - a constant electrical potential applied to a cell membrane, typically in order to
measure ionic currents.

• A refractory period is this period immediately after an action potential where the cell
membrane potential is lower than it's resting potential. That means the cell is going to be
more difficult to make that cell fire an action potential than it normally would because it's
hyperpolarized.

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4 - Ion Channels and Transporters
Thursday, 17 March 2022 3:29 PM

• Can expose different faces of the transport to the pipette and control and measure it in
different ways. Look into the textbook for patch clamp and write them here

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• Saw a transient activation and then a subsequent inactivation of Na+ currents in response to a
sustained input.

• If you look at the Na+ channels, you get the same one under the different conditions a few
times.

• (C) represents the micro whereas (D) represents the macro. (C) is at the individual level, but
once you average them you got (D).

• (E) says that if you average all of these things together and that corresponds to the
macroscopic level and then you look at the peak value of that current as a function of the
amplitude of your voltage, you get this shape in terms of how open is your channel or what's
the probability of getting some current flow as a function of how negative or positive your
memory potential is.

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• Comparison of Na+ channel (left) and K+ channel (right). You have the clamp, the microscopic
different ions being measured or one ion channel being measured repeatedly in different
channels, the sum or average of those behaviours and then you've got the macroscopic thing
that you would get from a voltage clamp and then you've got the response the likelihood of
ion permeability or channel being open as a function of member potential on the bottom.

• We again see a sustained activation, a sustained opening, a sustained conductance of K+ that

matches the observations taken at a macroscopic level and you can see the effects of noise or
randomness.

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• For the middle diagram: when at rest or when you're sufficiently depolarized, the channel is
closed. But once you turn on that clamp voltage, the channel opens and is permeable or
conductive to Na+. As it stays on for a bit longer, the paddle flips over and blocks the channel.
The channel is open but inactive.

• Underneath the middle diagram: a depiction for how channels initially allow Na+ to cross in
and then gradually close Na+ off. The K+ version, it stays closed, and then the current comes on
and it's slow and stays closed. But eventually the current is on long enough, it begins to open
and then it stays open until the current turns off. When the current turns off, then the paddle
closes.

• Another way of reinforcing that Na+ is a quick response but then inactivates. Whereas K+ does
not inactivate, just has a slower activation response.

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• These ion specific channels are made up of these protein ribbons that are all coiled up and
different protein coils are embedded in different parts of the cell membrane.

• The wires are called pore loops which create a little cavity inside the cell wall. You would
expect that because with a cavity, things can get through that cavity.

• The way that these structures become ion specific or selective for particular ions, it's largely
structural in nature. It's largely controlling how narrow or wide. But, there are optimal channel
size for specific ions.

• This diagram is voltage dependent, i.e. how do these channels display voltage dependence?

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• You do have things out here in the cell wall that have charged and therefore will move in
response to potential differences between the inside or the outside. That's how you can get
the geometry of these complicated proteins to change. And it's the geometry of these proteins
that allow things into or out of them.

• This figures shows how do the various ion species selective channels compare to each other in
terms of their biochemical organic chemistry makeup.

• They all have pore loops that allow specific ions to be in the middle of them, and whether this
pore is Na+ specific, Ca+ specific or K+ specific is going to have to do with the structural
properties of that pore. So how big is the pore and therefore what's the optimal size ion that
can survive in it, that can not only pass through it but it's stable without being attached to a
bunch of water molecules.

• Overall the structure is quite similar but they're pointing to the heterogeneity and saying that
you can get a lot of different specificities out of this heterogeneity.

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• This figure demonstrates the K+ is by far the most diverse. With a hyperpolarizing clamp and a
depolarizing clamp, what you'll see is that each of these is a different type of K+ channel, and
some of them behave like we've seen before, which they are opened in response to a positive
clamp and they don't do anything in response to a negative clamp.

• Getting you to notice that not all K+ ion channels look like the standard model. This is how they
operate in a giant squid axon, but these ion channels are expressed in many areas and
locations within cells and neural tissue and they have a great variety of behaviours and
something similar is true for the other ion channels.

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• These diagrams show that there's many more types of sensitivities in these ion channels than
just voltage. They can be sensitive to other molecules, so neurotransmitters for instance, so
things that come from other axons and are released after an action potential. Molecules enter
this nest of subunits stuck onto your channel, in this case a glutamate molecule, which binds
to this complex and changes the confirmations of the transmembrane pore and allow Na+ or K+
ions to go through it.

• The point is that there are ways to make a molecule across the membrane and have the shape
about those molecules and the pores that they define be sensitive to temperature just as you
can with mechanical force.

• Active transporters. Reinforce the idea that they are energy dependent. Energy is usually
exchanged or has to do with phosphoryl or dephosphoryl relation or particular molecules.

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 exchanged or has to do with phosphoryl or dephosphoryl relation or particular molecules.

• To get an ion transfer against its concentration gradient you need to actively transport it, and
that just means it costs energy, you have to find some way of dealing with this energy cost.

• This figure is explaining to you is that these active transports depend on energy (trough).
They're saying how much Na+ is going through this active transport, how much Na+ is being
transported and if you disrupt ATP synthesis (taking energy away from the system), less Na+
gets through, costing you energy. You need ATP to do this (2) and also K+, because without K+
you lose Na+ transport as well.

• Geometry = function

• When we see a confirmation of change, what we're doing is that we're changing the geometry
and therefore changing its function or functional properties.

• Here you bound a Na+ and then there's a conformational change and you can release the Na+
that you had bound up, but in releasing the Na+ that's bound up, you have to bind up K+ for
that to happen. Once K+ gets wrapped up, it comes back through the other way and will
eventually get you back to this fissure where you release the K+. You can only release the K+ if
you grab more Na+.

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 • This is an ion exchanger.

• Here you're grabbing Na+ and K+ together and there's this bundle up and careful exchange
with an ATP being consumed. If permeable to one positive charge going in this direction and a
different positive charge going in the other direction, the identity of those charges can be
different.

• If ions are going in different directions they are called antiporters. If ions are going in the same
direction across the membrane in or out, they're called co-transporters.

Review
• A great variety of mechanistic functions and that great variety comes about by geometric
properties/functional properties of these transmembrane proteins and how they manifest
across the cell. Should deeply understand the patch clamp and should understand the figures
associated with the patch clamp and how the probabilistic average of microscopic currents is
what generates macroscopic observations.

• Geometry = function and how ion specificity comes from pore width. There's an optimal width,
an optimal channel size that conspires with the properties of the proteins that are forming
that channel to dictate whether it's going to permit Na+, K+, Ca+, Cl- or whatever.

• How voltage dependence occurs (nothing beyond what is discussed in the chapter)

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6 - Vision: The Eye
Saturday, 2 April 2022 2:04 AM

Anatomy of the Human Eye

• Fluid-filled sphere

• 3 layers of tissue

• Only the retina contains neurons

• Ciliary body encircles the lens

○ Ciliary muscle adjusts the lens
○ Ciliary processes supply eye with fluid

• Iris: Coloured region that contains two sets of muscles to adjust pupil size

• Pupil: The opening in the centre

• Sclera: Outer most tissue layer

• Cornea: Transparent tissue that permits light rays to enter the eye

Accommodation in the Human Eye

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Myopia and Other Refractive Errors

• Emmetropia (Normal): relaxed ciliary muscles result in focused image in the distance

• Myopia (Nearsighted): light rays are focused in front of the retina

• Hyperopia (Farsighted): light rays are focused beyond the retina

The inner surface of the retina, viewed with an ophthalmoscope

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 • Fovea - has the photoreceptors that detect different wavelengths of light, called cones and
that's what results in our perception of colour.

The blind spot

Structure of the Retina I

• Five basic classes of neurons:
○ Photoreceptors
○ Bipolar cells
○ Ganglion cells
○ Horizontal cells
○ Amacrine cells

• Two types of photoreceptors:

○ Rods
○ Cones

• The retina is at the back of the eyeball, and light has to travel through all of these layers before
it arrives at the photoreceptors that detect it. The signals then travel backwards from the
photoreceptors to the bipolar cells to the ganglion cells, all still within the retina.

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Structure of the Retina II

Structure of the Retina III

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---> The physiological scotoma is a blind region where the ganglion cell axons leave the retina in the
optic nerve

Why are the photoreceptors in the deepest layer?

• Key points:
1. Photoreceptor disks 'wear out' and so continuously move up the photoreceptor until
they reach the top, are pinched off, and the then recycled (phagocytosed) (12 days)

2. Pigment epithelium regenerates the photopigment after exposure to light

3. Blood flow in pigment epithelium supplies photoreceptors

Phototransduction: Absorption of light by the photopigment results in change in membrane

potential
• Photoreceptors do not exhibit action potentials - graded response

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 • Light activation causes a graded change in membrane potential

• Shining a light on a photoreceptor results in hyperpolarization (less transmitter released) -

does not require as much activation, since when in the dark, the receptor is naturally
depolarized and so it transmits at a quite high rate

What changes the membrane polarisation?

• In the dark you have a lot of cyclic GMP and therefore these channels that depend on it are
open, which allows these positive ions to come in which depolarizes the outer segment. At the
same time, you've got some flow of K+ out which hyperpolarizes. But overall, you get a
depolarized cell which releases lots of neurotransmitters in the dark.

• In the light, all of a sudden the photon has decreased your cyclic GMP. These channels that
depend on it can't do anything anymore, and so the positive ions can't get into the cell. But
you've still got this flow out because that's not affected by the amount of cyclic GMP because
these channels don't depend on it. The net effect is a hyperpolarized cell that released less
neurotransmitters.

What happens when a photon is absorbed?

Lectures Page 53
 • Photon ---> absorbed by retina ---> changes the configuration ---> causes change to opsin --->
activates transducin (intracellular messenger) ---> activates phosphodiesterase (PDE) --->
hydrolyses cGMP ---> less cGMP

• When you've adapted to low light, your vision gradually improves because the settings
become more optimal for the particular illumination. Then someone turns on a torch, briefly
saturates your rods, and you have to go through adaptation again.

And then it's all reset so it can happen again!

Rods and Cones Differ In…

1. Shape - rod-like vs cone-like
2. Photopigment - and therefore their response characteristics

Lectures Page 54
 ○ Each photon makes a relatively small change in membrane potential, so you need about
100 photons to make a cone change as much as one photon for a rod. Cones can cope
with a lot more light before they saturate.

○ About rods and cones, cones do not saturate at high levels of steady illumination, so
adaptation is more efficient in cones than rods. Cones actually recover about four times
faster than rods, that's why they don't saturate in high, steady illumination.

3. Pattern of synaptic connections - which determines spatial acuity

• Rods:
○ Convergence from rods to rod bipolar cells: pools the signal (hence, low light vision)
▪ Rod bipolar cells synapse on amacrine cells
▪ These amacrine cells synapse on cone bipolar cells and in turn on the ganglion
cells

• Cones:
○ One cone to one cone bipolar cell - and then straight to ganglion cells: less sensitive but
high spatial acuity

Lectures Page 55
 ○ You do not know where that photon of light was, because with this distribution, all these
cells have different receptor fields. Because you're pulling all of that information, you
lose some of that acuity. Whereas for a cone, if this cone gets stimulated, you exactly
where it is.

4. Distribution across retina - rods in the periphery, cones in the fovea

• Cones:
○ Throughout at low density
○ Packed into fovea/foveola
○ High spatial acuity

• Rods:
○ Throughout periphery, none in the centre
○ Low spatial acuity

No photoreceptors in region of optic disc

Lectures Page 56
 ○ This distribution of different cell types explains that you don't have colour vision in the
periphery because you don't have anything that can tell you information about colour
vision. Your brain makes it up.

○ Eccentricities are distance from a centre point. When you're fixating centrally, that's the
central point. And then as you move out, you get greater and greater eccentricity. It's in
degrees of visual angle.

---> Photopic vision is vision supported by cone photoreception.

---> The fovea is a region of the retina packed densely with cones that supports high acuity colour
vision

Lectures Page 57
Cones and Colour Vision
• Rods detect a single photopigment (rhodopsin)

• Cones can contain 3 different types of photopigment (3 opsins)

• Normal human colour vision is trichromatic

• Opsin is bound to the retina inside that disc membrane of the photoreceptor, and it's crucial in
determining what that photoreceptor is sensitive to.

• Colour is always a perception based on the relative reflection of wavelengths of light, not the
absolute values.

'Red-green colour blindness'

Lectures Page 58
 • The reason that you most often like a lack of one of these is because the genes that encode for
the opsins that absorb medium and long wavelength are quite similar and are next to each
other on the X chromosome.

• Anomalous trichromats have three different opsins, but they have a different distribution or a
different numbers of the different opsins.

The brain 'makes up' colour too!

• The different wavelengths of light are absorbed by opsins in your cones at different
frequencies, and it's the relative resulting response that drives your perception.

• We have really complex context effects that demonstrate that the colours we experience can
be either a different colour. When the wavelength of light being reflected are identical or they
can be the same experience even though they're different wavelengths of light.

Lectures Page 59
 can be the same experience even though they're different wavelengths of light.

• Basically, what colour we perceive depends on the assumptions that your brain is making
about the illumination, combined with the wavelengths of light that are being reflected from
surrounding areas.

A reminder…

Responses of Retinal Ganglion Cells

• These ganglion cells responds to changes in illumination in specific locations of space. It's the
change, not the absolute value of light.

What leads to the centre-surround receptive fields of retinal ganglion cells?

• Remember: Photoreceptors reduce release of transmitter when photons are absorbed (i.e. in

Lectures Page 60
• Remember: Photoreceptors reduce release of transmitter when photons are absorbed (i.e. in
light)

• Bipolar cells are ON-centre or OFF-centre

○ Photoreceptor transmitter (glutamate) has opposite effects on these.

• When some bipolar cells have lots of glutamate, they hyperpolarize, so they are less likely to
release glutamate themselves. And then you have some bipolar cells that, like glutamate,
activates them, they depolarize and so they release more glutamate.

• If you are an ON-centre ganglion cell, bipolar cell sends you more glutamate, then you fire off
centre ganglion cells. If you're OFF-centre ganglion cells and your OFF-centre bipolar cell
hyperpolarizes, it's not going to release much glutamate, so you're not going to release much
glutamate and you're not going to fire off any action potentials.

Lectures Page 61
The effect of illumination - how our ganglion cells adapt

• Our ganglion cells have to be able to detect changes over a broad range of general
illumination. They cannot work in isolation and have to work together.

• For Image 2: within your retina, there are circuits that are essentially adjust the gain of
ganglion cells depending on the illumination to make sure they're still sensitive. So if you get
an increase in background luminescence (e.g. the sun comes out on a cloudy day), you get an
adaptive shift in the ganglion cells so that you need more photons to result in the same
number of action potentials heading to the brain.

• Ganglion cell firing therefore reflects the general luminous conditions as well as the specific
stimulation within that receptive field.

Ganglion cells signal luminance contrast - they like edges & boundaries!

Lectures Page 62
t1: Cone with an ON-centre ganglion cell: Light in centre hyperpolarises cell
---> less transmitter released on bipolar cell
---> ON-centre bipolar cell depolarizes (more activity)
---> releases more transmitter
---> ganglion cell fires action potentials

t2: Cones in surround also absorb light - hyperpolarizes cells

---> less transmitter release
---> hyperpolarizes horizontal cells

Lectures Page 63
---> hyperpolarizes horizontal cells
---> reduces activity on synapses with central photoreceptor
---> depolarizes centre cone
---> increases transmitter release
---> ON-centre bipolar cell hyperpolarizes (less activity)
---> ganglion cell fires less action potentials

Net effect: stimulation of the surround counteracts the stimulation of the centre = overall less
ganglion response to the light

• The amount of transmitter released by that centre cone cell is not just determined by its own
photoreceptor, but also what's happening in the surrounding photoreceptors through the
modulation by the horizontal cells.

The perception of light intensity

• Not only do our ganglion cells have to modulate depending on kind of illumination, but our
brain is interpreting that information based on the context.

Lectures Page 64
Summary
• Anatomy of the eye
• Accommodation & refractive errors
• The structure of the retina
• The cells types in the retina
• Photoreceptors - rods & cones
• Phototransduction & the biochemical interactions
• Colour (a start anyway…)
• Receptive fields & the centre-surround of ganglion cells
• Adaptation to different levels of illumination

Lectures Page 65
7 - Central Visual Pathways
Wednesday, 6 April 2022 2:33 AM

Central projections of retinal ganglion cells

• Ventral projection of the brain

Why a decussation at the optic chiasm?

Peripheral (outer) locations fall only on one retina

---> L periphery -> nasal L retina (A) -> R occipital
---> R periphery -> nasal R retina (D) -> L occipital

Lectures Page 66
---> R periphery -> nasal R retina (D) -> L occipital

More central (inner) locations fall on both retina (B, C)

---> Each eye therefore has a slightly different view

• There's a monocular portion of visual field on both sides, because your nose blocks part of the
input from the outer periphery as part of space. Then there's the inner region that's seen by
both eyes

What matters most is where the stimulus is in space (not which eye it's being registered by)
---> Need to keep signals from the same location together

Contralateral representation of space: L visual field is represented in R occipital cortex

---> Nasal retina on L has to cross to join temporal retina on R
---> nasal retina on R has to cross to join temporal retina

What goes where #2

Image on retina is flipped vertically and horizontally

Each eye registers a different region of space

---> Left retina has more of the left periphery
---> Right retina has more of the right periphery
---> Both register central regions

Active learning platform #2, #3

Lectures Page 67
Primary Visual Pathway

Course of the optic radiation to the striate cortex

Lectures Page 68
Visuotopic organisation

Let's review what you now know…by thinking about what happens with different lesions

Lectures Page 69
The other targets of retinal ganglion cells

Pupillary light reflex circuit

Lectures Page 70
Active learning platform #4

---> You shine a light in the left eye, which constricts the pupil, but the right eye doesn't change. This
suggests that there is damage:
• Between the left pretectum and the right Edinger-Westphal nucleus or the right ciliary
ganglion or the right pupillary constrictor muscle

Input for circadian rhythms

Lectures Page 71
Orienting responses

Interim Summary
• Your two eyes have slightly different views

• Information partially crosses at optic chiasm to keep information about a side of space
together, regardless of eye

• Representation of visual space is contralateral and inverted

• We can work out location of damage by looking at the pattern of visual deficits

• Primary visual pathway is retina-thalamus (LGN)-V1

• Offshoots to pretectum (pupil response), hypothalamus (circadian rhythms) and superior

colliculus (orienting)

Lectures Page 72
The layers of the cortex

Primary visual cortex (V1)

Neural Responses in V1

Lectures Page 73
Functional maps: neurons are clustered by receptive field and selectivity

Functional imaging reveals orderly mapping of orientation preference in the primary visual cortex

Lectures Page 74
Neurons responding to stimulation of both eyes first occur in primary visual cortex

Illustrating your stereopsis

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Magno-, parvo-, and koniocellular pathways

What information do they convey?

• Magnocellular pathway
○ M ganglion cells = larger receptive fields, faster conduction velocities, transient
responses, insensitive to different wavelengths of light
▪ Motion, not colour

• Parvocellular pathway
○ P ganglion cells = smaller receptive fields, slower conduction, sustained responses,
sensitive to differences in wavelengths
▪ Colour, not motion

• Koniocellular pathway
○ Some role in colour vision (short-wavelength-sensitive cones particularly)

Lectures Page 76
"Seeing" what your magno and parvocellular pathways are showing you…

V1 is just the start

Human brains have similar specialisation

Lectures Page 77
Let's have a look at that in 'real life'

Beyond striate cortex…the 'what' and 'where' pathways

Lectures Page 78
Example of specialisation in the 'what' (ventral) pathway

Lectures Page 79
Summary
• What does where from the retina to primary visual cortex
○ The decussation at the optic chiasm
○ Retinotopic map of space

• Anatomy of the central visual pathways

○ Major targets for retinal ganglion cells
▪ LGN (thalamus) for the primary visual pathway
▪ Pretectum for the pupillary light reflex
▪ SCN for the circadian rhythm
▪ Superior colliculus for head/eye orienting

• Primary visual cortex lies on the calcarine sulcus

○ Layers of V1
○ Contralateral representation of space; systematic mapping maintained
○ Cortical magnification - lots more cortex devoted to fovea than to the periphery
○ Orientation selectivity and ocular dominance columns
○ Stereopsis (binocular vision)
○ Magnocellular and parvocellular pathways
○ Functional organisation in the visual cortex

Lectures Page 80
8 - Lower Motor Neuron Circuits and Motor Control
Tuesday, 26 April 2022 9:28 PM

Preview
• Chapter 16 - LMN

• Electrical foundations of movement

• Action potential and neuromuscular junction

• Motor Units and the development of force

• Reflex control of muscle length and tension

LMN - Lower Motor Neuron

Lectures Page 81
Electrical Foundations of Movement

Nervous Control of Movement

Electrical Control of Movement

Lectures Page 82
Head Transplant

Nervous Control of Movement

• The basic unit of electrical communication within the nervous system is the action potential

Action Potential

Lectures Page 83
Action Potential

Neuromuscular Junction

Lectures Page 84
 • Lower motor neurons are those motor neurons that connect with other motor neurons so
they're either coming out of the brain stem and projecting out towards muscle. These α motor
neurons axons that connect to muscle fibres are what cause movements to occur, and it's this
connection that we call the neuromuscular junction.

Contraction

Development of Muscle Tension

Lectures Page 85
The Motor Unit

Dealing with Different Force Demands

Motor Units

Lectures Page 86
Force and Fatigability

Medial gastrocnemius muscle under different behavioural conditions

Lectures Page 87
Motor Unit Plasticity

Lectures Page 88
MU Summary

Turning it on

Reflex

Lectures Page 89
Stretch Reflex

Stretch Reflex Circuitry

Lectures Page 90
γ Motor Neurons

Golgi tendon organs

Lectures Page 91
Muscle Spindles and Golgi Tendon Organs

Lectures Page 92
Negative Feedback from Golgi Tendon Organs

Flexion-Crossed Extension Reflex

Summary

Lectures Page 93
Lectures Page 94
9 - Upper Motor Neuron Control of the Brainstem and Spinal
Cord
Sunday, 15 May 2022 1:56 PM

Preview
• Review: Basic brain terminology and anatomy

• Descending motor control

• Primary motor cortex

• Premotor cortex

• Brainstem circuits for balance and posture

Brain Terminology and Anatomy

Brain Axes

Lobes of the Cerebral Cortex

Lectures Page 95
Brain Landmarks

Descending Motor Control

Lectures Page 96
Sensorimotor Control Loop

Spinal Cord

Lectures Page 97
Descending Tracts

Lectures Page 98
Primary Motor Cortex

Functional Organisation of the Primary Motor Cortex

Lectures Page 99
Lectures Page 100
What do motor maps represent?

M1 represents movements, not muscles

Spike-triggered averaging

Lectures Page 101

Directional tuning in the primary motor cortex

Lectures Page 102

Tuning at the population level

Putting all this knowledge to work

Lectures Page 103

Brain-computer interfaces

Lectures Page 104

Premotor Cortex

Lectures Page 105

Visually guided instructed delay reaching task

Preparatory activity in PMd

Premotor Cortex

Lectures Page 106

Mirror Neurons

Broca's Area

Putting it all together

Lectures Page 107

Brainstem Circuits

Brainstem circuits supporting posture maintenance and control

Anticipatory Feedforward control

Lectures Page 108

Lectures Page 109
10 - Eye Movements and Sensory-Motor Integration
Sunday, 15 May 2022 2:10 PM

Preview
• Overview of sensorimotor integration and the functional role of eye movements in vision

• Extraocular muscles and brainstem connectivity

• Different types of eye movements

○ Gaze stabilising eye movements
○ Gaze shifting eye movements

• Neural control of saccadic eye movements

Sensorimotor Integration

Why study eye movements?

Lectures Page 110

What eye movements accomplish

Lectures Page 111

Extraocular Muscles and Brainstem Connectivity

Extraocular Muscles

Lectures Page 112

Abduction vs Adduction

Brainstem and Spinal Cord

Brainstem motor neuron innervation of extraocular muscles

Lectures Page 113

Different Types of Eye Movements

Stabilising vs. Shifting Gaze

Vestibulo-ocular reflex

Lectures Page 114

Optokinetic eye movements

Lectures Page 115

Sensitivities of VOR and optokinetic systems are complementary

Lectures Page 116

Smooth Pursuit Movements

Metrics of Smooth Pursuit Movements

Lectures Page 117

Vergence Eye Movements

Saccadic Eye Movements

Lectures Page 118

Metrics of Saccades

Saccades are ballistic

Lectures Page 119

Neural Control of Saccadic Eye Movements

Motor neuron activity related to saccade generation

Neural control of saccades

Lectures Page 120

Superior Colliculus

Lectures Page 121

Frontal eye fields

Lectures Page 122

Transformation of visual target information into saccade command

Sensory motor integration in the superior colliculus

Lectures Page 123

Saccades are encoded in movement, not retinotopic coordinates in SC

Frontal eye fields

Lectures Page 124

Neural responses in FEF

Lectures Page 125

11 - Cognitive Functions and the Organisation of the
Cerebral Cortex
Sunday, 15 May 2022 2:25 PM

What is Cognition?

Sensory input is integrated with knowledge: creates our experience

How does the brain do it?

Lectures Page 126

Identify the association cortices

---> Parietal, frontal and temporal

Neo cortex

Lectures Page 127

Neo cortex

Brodmann Areas

Example of layers in BA23

Unique Features

Lectures Page 128

How do we know what different brain areas do?

Subdivisions of the Association Cortex

Lectures Page 129

Clinical tests for Contralateral Neglect

Contralateral Neglect

Lectures Page 130

Left vs. right parietal damage

What does the asymmetry of neglect tell us about the neuroanatomy of attention?

---> The right parietal lobe is more important for attention than the left

Contralateral Neglect

Lectures Page 131

What if both parietal lobes are damaged?
•

Patient studies tell us…

"Attention Neurons"

Lectures Page 132

Effects of attention on other brain regions

Effects of attention on response to stimuli: vision

Lectures Page 133

Effects of attention on response to stimuli: vision

Effects of attention on response to stimuli: audition

Subdivisions of the Association Cortex

Lectures Page 134

The Temporal Lobe

What would you need to check before concluding a patient has a specific deficit for recognising
faces?
•

The Temporal Lobe

Lectures Page 135

"Recognition Neurons"

Lectures Page 136

A 'grandmother' cell?

"Recognition Neurons"

Lectures Page 137

Subdivisions of the Association Cortex

The Frontal Lobe

Lectures Page 138

Lectures Page 139
Frontal Lobe Damage

---> Selecting, planning and executing appropriate behaviour

The Frontal Lobe

Lectures Page 140

"Planning Neurons"

Lectures Page 141

The Association Cortices

Synaesthesia

Lectures Page 142

Types of Synaesthesia

Synaesthesia

Lectures Page 143

The Classic Stroop Effect

Synaesthesia Congruency Task

Lectures Page 144

Synaesthesia Congruency Effect

The Association Cortices

Summary

Lectures Page 145

Lectures Page 146
12 - Speech and Language
Saturday, 28 May 2022 10:52 PM

We Make Noises

Comprehension & Production

Lectures Page 147

When Language Doesn't Work

Characteristics of Aphasia

Major Language Areas

Lectures Page 148

When language doesn't work

Left is for language…

Probably…There's some better evidence

The typical brain

Lectures Page 149

Splitting the typical brain

The split brain

Lectures Page 150

Language and Handedness

Lectures Page 151

Left-handed prevalence

It's a right-handed world

Language and Handedness

Lectures Page 152

Lectures Page 153
Anatomical Asymmetries

Lectures Page 154

Mapping Language Functions

Lectures Page 155

Lectures Page 156
What about the right?

Lectures Page 157

Genes and Language

Sign Language

Lectures Page 158

A Critical Period

Lectures Page 159

Other animals and language

Lectures Page 160

Lectures Page 161
Summary

Lectures Page 162

Lectures Page 163
Content Review
Sunday, 5 June 2022 1:27 AM

1. Define α motor neurons, γ motor neurons, muscle spindles, and Golgi tendon organs.
• Larger motor neurons are called α motor neurons, whereas smaller motor neurons are called γ
motor neurons. Muscle spindles are specialised muscle fibres are sensory receptors arranged
in parallel with the force-generating striated muscle fibres. Golgi tendon organs are
encapsulated afferent nerve endings located at the junction of a muscle and a tendon. The
Golgi tendon circuit is this a negative feedback system that regulates muscle tension; it
decreases the activation of a muscle when exceptionally large forces are generated and, in this
way, protects the muscle.

2. What are the two types of lower motor neurons and how do they differ?
• Two types of lower motor neurons are found in the motor neuron pools of the ventral horn:
○ α motor neurons: relatively large motor neurons that innervate the striated muscle
fibres that actually generate the forces required for posture and movement (force-
producing)

○ γ motor neurons: relatively small motor neurons that innervate specialised (intrafusal)
muscle fibres and for part of the sensory receptors called muscle spindles. Muscle
spindles provide information about limb and body position, and are essential for
proprioception.

3. What is a motor unit?

• A motor unit is an alpha motor neuron and all the muscle fibres that it innervates.

• Most extrafusal skeletal muscle fibres are innervated by only a single motor neuron.

• Because there are many more muscle fibres than α motor neurons, individual axons branch
within muscles to synapse

Notes Page 164

Tutorial 11
Monday, 16 May 2022 6:00 PM

1. List some reasons we need eye movements and explain

a. Bring the high resolution fovea to features of interest in the visual field

2. Name the different extraocular muscles and describe/draw how each is responsible for
different eye movements
a. Superior rectus
b. Lateral rectus
c. Inferior rectus
d. Inferior oblique
e. Superior oblique

3. How do the VOIR and OKR relate?

a. Vestibulo-ocular movements and optokinetic eye movements operate together to move
the eyes and stabilise gaze relative to the external world, thus compensating for head
movements.
b. The Vestibulo-ocular reflex compensates nearly perfectly for rapid head movements at
frequencies around 1 Hz or above, but performance drops for lower frequencies. E.g., a
30 degree turn of the head to the right results in a 30 turn of the head to the right
results in a 30 degree rotation of the eyes to the left
c. The optokinetic system compensates nearly perfectly for global visual motion at lower
frequencies around 0.1 Hz, but performance drops for higher frequencies.

4. What is the latency of saccades and why are saccades described as ballistic?
a. After the onset of a target for a saccade it takes about 200 ms for eye movement to
begin. During this delay, the position of the target with respect to the fovea (i.e., how far
the eye has to move) is computed, and the difference between the initial and intended
position is converted into a motor command that activates the extraocular muscles to
move the eyes the correct distance in the appropriate direction.
b. A ballistic movement cannot be modified by new information once it is initiated. The
saccade-generating system doesn't respond to subsequent changes in target position
during a saccade. If the target moves again during this time (which is on the order of 15
to 100 ms), the saccade will miss the target, and a second saccade must be made to
correct the error.

5. Explain the separate neural control of saccade amplitude and direction

a. Two separate control tasks:
i. Controlling the amplitude of the movement (how far)
ii. Controlling the direction of the movement (which way)
b. Saccade amplitude is coded by the duration of activity in lower motor neurons in the
brainstem
c. Saccade direction determined by which eye muscles are activated
d. Oculomotor commands generated in the horizontal and vertical gaze centres in the
reticular formation in the brainstem

6. How does the alignment of visual and motor maps in the superior colliculus support sensor-
motor integration?
a. When an object appears at a particular location in the visual field, neurons are activated
in the corresponding part of the visual map
b. This triggers activity in subjacent neurons in the motor layer that activate upper motor
neurons that move the eye just the right amount to centre the fovea on the region of
visual space that provided the stimulation

Notes Page 165

Tutorial 12
Monday, 23 May 2022 6:14 PM

1. Describe the 4 main similarities in structure across neocortex areas, and note the major difference
between the association cortex and visual cortex.
• The circuitry of all cortical regions has some common features. First, each cortical layer has a
primary source of inputs and a primary output target. Second, each area has connections in
the vertical axis (called columnar or radial connections) and connections in the horizontal axis
(called lateral or horizontal connections). Third, cells with similar functions tend to be arrayed
in radially aligned groups that span all the cortical layers and receive inputs that are often
segregated into radial bands or columns. Finally, interneurons within specific cortical layers
give rise to extensive local axons that extend horizontally in the cortex, often linking
functionally similar groups of cells.

• The signals coming into the association cortices via the thalamus reflect sensory and motor
information that has already been processed in the primary sensory and motor areas of the
cerebral cortex and is being fed back to the association regions. The primary sensory cortices,
in contrast, receive thalamic information that is more directly related to peripheral sense
organs.

2. What are some of the distinctive features of associative areas?

•

3. What is contralateral neglect syndrome and where are you likely to find the damage responsible
for it?
• The hallmark of contralateral neglect syndrome is an ability to attend to objects, or even one's
own body, in a portion of space, despite the fact that visual acuity, somatic sensation, and
motor ability remain intact. Affected individuals fail to report, respond to, or even orient to
stimuli presented to the side of the body (or visual space) opposite the lesion.

• Importantly, contralateral neglect syndrome is typically associated with damage to the right
parietal cortex (see Chapter 29). The unequal distribution of this particular cognitive function
between the hemisphere is thought to arise because the right parietal cortex mediates
attention to both left and right halves of the body and extra personal space, whereas the left
hemisphere mediates attention primarily to the right; this hemispheric bias is thought to arise
from specialisation of the left hemisphere for language, thereby driving attentive functions
into the right hemisphere. This, left parietal lesions tend to be compensated by the intact right
hemisphere. In contrast, when the right parietal cortex is damaged, there is little or no
compensatory capacity in the left hemisphere to mediate attention to the left side of the body
or extrapersonal space.

4. What is prosopagnosia and where are you likely to find the damage responsible for it?
• One of the most thoroughly studied agnosia following damage to the temporal association
cortex in humans is the inability to recognise and identify faces. After damage to the inferior
temporal cortex, typically on the right, patients are often unable to identify familiar individuals
by their facial characteristics, and in some cases cannot recognise a face at all. Nonetheless,
such individuals are perfectly aware that some sort of visual stimulus is present and can
describe particular aspects or elements of it without difficulty.

5. What is the Wisconsin Card Sorting Task and where are you likely to find the damage in a patient
who struggles with this task?
• In this test, the examiner places four cards with symbols that differ in number, shape, or
colour before the subject, who is given a set of response cards with similar symbols on them.

Notes Page 166

 colour before the subject, who is given a set of response cards with similar symbols on them.
The subject is then asked to place an appropriate response card in front of the stimulus card
based on a sorting rule established, but not stated by the examiner (i.e. sort by either colour,
number, or shape). The examiner then indicates whether the response is "right" or "wrong".
After ten consecutive correct responses, the examiner changes the sorting rule simply by
saying "wrong". The subject must then ascertain the new sorting rule and perform ten correct
trials. The sorting rule is then changed again, until six cycles have been completed. In 1963, the
neuropsychologist Brenda Milner at the Montreal Neurological Institute showed that patients
with frontal lobe lesions have consistently poor performance in the Wisconsin Card Sorting
Task.

6. What is synaesthesia and how might you measure it?

• A remarkable sensory anomaly is evident in individuals who conflate experiences in one
sensory domain with those in another - a phenomenon called synaesthesia. The term means
literally "mixing of the senses", and its best understood expression is in individuals who see
specific numerals, letters, or similar shapes printed in black and white as being differently
coloured.

• On the basis of the synaesthetic colours they see, they can segregate targets from
backgrounds, they can group targets in apparent motion displays, and they show the Stroop
effect - the slowed reaction time that everyone exhibits when the printed ink and the spelling
of a colour word are at odds.

Notes Page 167

Tutorial 13
Monday, 30 May 2022 5:56 PM

1. The 4 lobes of the cerebral cortex

a. Frontal
b. Parietal
c. Occipital
d. Temporal

2. Feature separating the frontal and parietal lobes.

a. The central sulcus

3. The cells that supports the activity of neurons but do not themselves participate in electrical
signalling.
a. Glial cell

4. The endoplasmic reticulum is found in this part of the neuron.

a. The soma

5. A channel that becomes inactive during the overshoot phase of the action potential
a. Na+ voltage-gated channel

6. The structure responsible for ion selectivity in K+ channels.

a. The selectivity filter

7. This structure is thought to move across the membrane in response to depolarisation.

a. Voltage sensor

8. The slow opening of K+ voltage-gates channels during depolarisation allows for this type of
current.
a. A late outward current

9. A photoreceptor that has high spatial acuity

a. Cones

10. When light rays are focused in front of the retina

a. Myopia

11. The opposite of myopia

a. Hyperopia

12. A type of bipolar cell that hyperpolarises when light is shone on the centre of its receptive
field.
a. An OFF-centre bipolar cell

13. About 60% of fibers cross at this key location.

a. Optic chiasm

14. The lobe most associated with recognising/identifying objects.

a. Temporal lobe

15. A multisensory midbrain structure that coordinates head & eye movements towards targets.
a. The superior colliculus

16. Symptom of damage to the Edinger-Wetphal nucleus in the brainstem.

Notes Page 168

16. Symptom of damage to the Edinger-Wetphal nucleus in the brainstem.
a. No consensual eye response (i.e. one eye's pupil constricts in light, but not the other)

17. These neurons innervate skeletal muscle fibres.

a. Lower (alpha) motor neurons

18. The recruitment of motor units in size order based on the amount of force needed.
a. The size principle

19. When one muscle contracts, the other muscle relaxes.

a. Antagonistic muscle pairs

20. Percentage of pyramidal tract fibres that decussate to form the lateral corticospinal tract.
a. 90%

21. Upper motor neurons are found in these two locations.

a. The cortex and brainstem

22. Comprised of an alpha motor neuron and the muscle fibres it innervates.
a. A motor unit

23. Motor maps over-represent body parts responsible for finer movements (relative to larger
body parts responsible for coarser movements)
a. Cortical magnification

24. This mechanism prevents retinal adaptation

a. Tiny saccades to refresh the image on the retina

25. When the eye is adducted, this muscle is primarily responsible for elevating the eye
a. The inferior oblique

26. Neurons responsible for generating directional oculomotor commands

a. Local circuit neurons

27. A reflex that is limited to slow rotational movements ( <1 Hz)

a. The optokinetic system

28. A spinal injury on this area could cause paralysis in the hands
a. Lateral ventral horn

29. A disorder known as face blindness

a. Prosopagnosia

30. A region of the frontal lobe that mediates decision making and planning
a. The dorsolateral prefrontal cortex

31. This is where large-diameter pyramidal Betz cells are located.

a. Layer V of the primary motor cortex (M1)

32. This encodes the amplitude of saccadic eye movements.

a. The duration of activity in the lower motor neurons of the oculomotor nuclei

33. An area associated with the ability to produce language efficiently.

a. Broca's area

34. The emotional valence of speech, made using intensity, pitch, rhythm etc.
a. Prosody

Notes Page 169

35. Disordered syntax is a symptom of this condition.
a. Broca's aphasia

36. Tactile objects recognition in split-brain patients confirmed this feature of language control.
a. Language lateralisation

Notes Page 170

Short-Answer Questions (13)
Monday, 30 May 2022 5:59 PM

1. Explain the ionic basis of the action potential.

a. A stimulus affects the neuron potential. If it does not reach threshold it will dissipate
(passive current flow). If it does reach threshold the action potential is evoked (active
current flow).

b. Na+ conductance increases because the voltage-gated sodium channels have opened,
causing an influx of Na+.

c. K+ conductance increases because the voltage-gated potassium channels have opened,

and rapid repolarisation if caused by K + leaving the cell.

d. K+ conductance becomes temporarily higher than it usually is in the normal resting

condition. Then the voltage gated K+ channels close.

e. The cell returns to its usual resting membrane potential (because the K + in and out of
the cell find their electrochemical equilibrium again).

2. Explain the structural organisation of the retina. Then list some of the main
structural/functional differences between rods and cones.
○ Rods:
▪ There is only one type for shades from light to dark.
▪ Optimal in darker light conditions.
▪ Narrower than cones
▪ Majority of them are in the periphery
▪ Many rods connect to one bipolar cell
○ Cones:
▪ There are 3 different types that respond to different light frequencies, resulting in
colour vision.
▪ Optimal in brighter light conditions
▪ Wider than rods
▪ Majority in the foveal region
▪ They have a one-to-one connection with bipolar cells.

3. Explain the neural control of saccades.

○ Two separate control tasks:
▪ Controlling the amplitude of the movement (how far)
▪ Controlling the direction of the movement (which way)
○ Saccade amplitude is coded by the duration of activity in lower motor neurons in the
brainstem/abducens/oculomotor nuclei.
○ Saccade direction determined by which eye muscles are activated.
○ Oculomotor commands generated in the horizontal (paramedian pontine reticular
formation) and vertical (rostral interstitial nucleus) gaze centres in the reticular
formation of the brainstem.

4. What is feedforward postural control and what is predictive about it?

○ Feedforward postural control is when movements and motor commands are controlled
before any sensory feedback is available.
○ This mechanism is predicted because it anticipates disruptions to posture and
compensates before they can be sensed.
○ For example, when you pull open a heavy door this tends to pull the whole body
towards the door when you contract your bicep. But part of the motor plan is to predict
this and activate proximal leg muscles to compensate. So before you have engaged your
arm to pull the door, the feedforward mechanism predicts the instability and generates
an appropriate stabilising response.

Notes Page 171