Appendix 2: Communication Central Nervous System Podcast Transcript

Hey everyone Sydney and Hanna again. This podcast we’ll be talking about the Central Nervous System. We recommend that if you haven’t listened to the first podcast that you go back and do that, or at least review some of the concepts, as there is a lot of carry over into this unit.

The big themes of this subunit are segregation and integration of information within the Central Nervous System, which we call the CNS. Segregation and integration will remain important themes throughout the chapter. Segregation is when things are separated or kept separately. When we look at Integration, we are thinking about things coming in together or intertwining. You’ll see some examples of segregation and integration throughout the podcast so see if you can identify which concept is represented as we go through.

An example of segregation can be seen with the three ganglion cell types, M, W, and P. These cells have different conducting speeds, so they carry information at different speeds. M and W are also responsible for carrying intensity info, while P cells carry wavelength. When you look at the LGN, we see this example of segregation. LGN stands for later geniculate nucleus but you can just learn it as the LGN. So these different types of information are being brought to different layers of the LGN. So we are keeping this type of information separate or segregated. Try to look through your notes and see if you can find other situations where we see this type of segregation, and try to find some integration as well.

Okay so some more terminology for you is neurons and glial cells. You saw lots of neurons in the last unit, talking about muscles and synapses. Basically neurons are sending nerve impulses to different places in the body. When we look at glial cells, these cells are not sending any nerve impulses, instead, they are working to protect and support neurons. They can even provide nourishment to neurons. So there are a lot more of them present in the body than there are neurons.

Now we’ll talk about vision. This is the one section of this unit that you’ll likely want to spend a bit more time on as it can be tricky, and there’s a lot of content.

One big concept of vision is the pathways of photoreceptors. The notes from the lectures should walk you through the two pathways pretty easily but there’s a few points I’d like to point out. So basically the goal of reacting to a photon is to decrease the number of Na+ channels open, so sodium channels open. These channels are cGMP dependent. This was always something I found weird because it made more sense in my head for the stimulus, or light, to be triggering these channels and reaching a threshold and depolarizing, but in fact that’s the way it works in the dark.

And that’s because in this unstimulated state, there is always sodium ions exiting the cell through the sodium potassium pump, creating a cycle of sodium ions entering and exiting. This is known as the ‘dark current’. This keeps the membrane potential at about -40mV, which is depolarized. Since it is depolarized, the neurotransmitter, glutamate, is being released. Think about how this is likely due to a similar mechanism that releases neurotransmitters from a neuron using calcium ions to promote fusion of vesicles to the membrane into the synaptic cleft. So this increase in the neurotransmitter glutamate causes a depolarization in the ‘off’ bipolar cell in the eye.

The other thing to remember is that there are “on” cells and “off” cells. And those names aren’t representative of what they’re doing. So one cell doesn’t just turn on or off depending on whether there’s light or not. In a stimulated state, off bipolar cells hyperpolarize and on bipolar cells depolarize. Both of these are a response to a decrease in glutamate. In an unstimulated state, the opposite occurs. So those are things you just need to memorize. Through a series of steps which you should make sure to walk yourself through, we see an increase in glutamate which hyperpolarizes on bipolar cells and depolarizes off bipolar cells.

So the key take away to remember this is that when a photon hits a photoreceptor it will always hyperpolarize and release less glutamate.

We’re about to talk about receptors. Photoreceptors in the retina will pick up photons and create a signal which will be passed down to other neurons throughout the body. But the important part here is the “receptive field”. The only photoreceptors that are considered to be in the neuron’s receptive fields are the ones connected through neurons that are directly on the surface of the retina. Any other neurons connected or not connected are not considered to be on the field.

Ok, so another type of cells where we’re seeing “on” and “off” in the name. This is where we’re looking at on-centre off-surround and off-centre on-surround. This is also one of the most complicated topics of this unit so we have a lot of questions to address in regards to this as well.

Here are some key things you need to remember about photoreceptors. When a photon hits a photoreceptor, it ALWAYS has the same effect – the photoreceptor will hyperpolarize, and will decrease its glutamate release.

When talking about on-centre off-surround and off-centre on-surround bipolar cell receptive fields, it helps to associate “on” with “depolarize” – for example: on-centre means that the centre depolarizes in response to light and on-surround means the surround depolarizes in response to light – the same association can be made between “off” and hyperpolarize.

“On” bipolar cells always depolarize in response to a decrease in glutamate and “off” bipolar cells hyperpolarize in response to a decrease in glutamate – there is no real trick to remember this, so take the time to work it all out in a way that works for you.

Now we can put all that information together and describe the steps involved when a photon of light stimulates a bipolar cell receptive field. Here we will use the example of stimulating the centre of an on-centre, off-surround bipolar cell.

So the photon hits a photoreceptor, causing it to hyperpolarize and decrease glutamate release. Next, we need to decide, what type of bipolar cell are we dealing with? Heads up: this step is the most complicated step so it will take some practice! We know from the question that we are stimulating the centre of an on-centre bipolar cell, so according to the above logic we already know that the bipolar cell MUST depolarize. We can now work backwards to decide the type of bipolar cell that the glutamate from the photoreceptor is being released on. Since “on” bipolar cells are the ones that depolarize in response to a decrease in glutamate release from a photoreceptor, we can determine that we must be dealing with an “on” bipolar cell.

Now we can finish the pathway! From here on, it is much more straight-forward or intuitive. The depolarization of the “on” bipolar cell will increase glutamate release onto a ganglion cell, causing the ganglion cell to depolarize, ultimately leading to an increase in action potential frequency.

Another common question we have about photo receptors is “If a photoreceptor always hyperpolarizes in response to light, how can we have increases AND decreases in glutamate release onto bipolar cells?” So since we know that the presence of light causes photoreceptors to hyperpolarize and decrease glutamate release onto a bipolar cell, we must introduce another cell type in between the photoreceptor and bipolar cell to act as a “signal switcher” in order to increase glutamate release onto a bipolar cell. This “signal switcher” is what we call a horizontal cell. So decreased glutamate release onto a horizontal cell causes it to depolarize, which increases glutamate release onto the bipolar cell.

So now we can talk some more about muscles and motor control. In the last little section, vision was an example of flow into the CNS, information coming to the CNS. In this section we are using muscles and motor control as an example of flow OUT of the CNS.

To start, we have both alpha and gamma neurons going towards muscle fibres. Alpha motor neurons control voluntary muscle contraction so any muscle contraction involved if I were to decide to take a step. Gamma motor neurons control muscle involuntary muscle contraction meaning a response to external forces acting on the muscle or a reflex.

Gamma neurons are activated at the same time that alpha motor neurons are activated. This is called alpha/gamma coactivation. This occurs in order to keep the intrafusal fibers taut, which allows the spindles to maintain sensitive to the stretch of a muscle.

Intrafusal fibers are fibers inside of the muscle that run parallel to the extrafusal fibers, but do not contain contractile mechanisms throughout. They only have contractile mechanisms at each end, so the top and the bottom. They are only there in order to keep the intrafusal fibers taut while the extrafusal fibers are being shortened. So if the intrafusal fibers are limp, then the spindles will send no APs to the brain which would not be very good.

One confusing part here is the common question: Which part is actually making up the muscle spindle? Would it be the actual intrafusal spindles or is it the neurons attached to the intrafusal fibers? In short, the answer is both. The muscle spindle encompasses the intrafusal fibers, which is the nuclear bag and chain, and also encompasses the sensory nerves.

Nuclear chain fibres and nuclear bag fibres are considered specialized sensory organs which as you know are making up the muscle spindles. The main differences between them that you need to know for this course are that nuclear bag fibres are the ones that appear to have the thicker centre that almost looks like a bag in the middle to help you remember. Also it’s the chain fibres that have the most secondary endings coming from it which respond mostly to absolute length/stretch.

There are also primary and secondary endings. This is pretty much a memory thing as well, but I’ll say it for you. Primary endings are annulospinal, so they wrap around the intrafusal fibres in a spiral shape. These sense the rate of change of length, so dynamic responses, as well as the absolute length, or the static responses. Secondary endings are flower spray endings which kind of look like roots attached to the intrafusal fibres. These sense the absolute length of the fibres, static responses again.

Note here that they can extend from both types of intrafusal fibres, nuclear bag and nuclear chain. Annulospinal also measure the rate of muscle stretch. The annulospinal and flower spray endings are both sensory afferents (remember the A in afferents). They are an important mechanism of communication between skeletal muscles and the brain. Two other key words here are afferent information carried by muscle spindles, and efferent information which is carried by gamma motor neurons. Afferent means that the information is going from the muscles to the CNS, A for Afferent and Away from the muscles. Then efferent is the opposite, from the CNS to the muscles.

So now we know what a muscle spindle is, “What is the difference between the muscle spindle and GTOs? And why do we need two receptors in the muscle?”

Muscle spindles and GTOs are both receptors in the muscle, but muscle spindles reside inside the muscle to detect its stretch whereas GTOs are within the tendon of the muscle to detect tension created by the muscle. Muscle spindles are in place to prevent overstretching so they send signals to shorten the muscle during stretch, and GTOs are in place to prevent over-contraction, so they send signals to lengthen the muscle during contraction.

It’s also important to note here that there are multiple GTOs within a muscle, so it helps if you understand that they are less than 1mm long and lie within the muscle tendons.

An area that many students struggle with is about how different areas are involved in motor control. I like to break this idea down into simpler steps. So first we know that the brain makes a plan, then the plan is implemented, and the plan is corrected if there are any errors throughout the process.

Error correction can be a confusing concept. An important thing to remember is that the cerebellum is always updated from many different motor areas. The cerebellum is where we receive these updates, which we can call feedback. If error correction is necessary, the cerebellum notifies the thalamus, which will communicate with the primary motor cortex to fix the problem. The basal ganglia is also involved in the error correction process, as it receives info from the motor cortex and cerebellum, and then sends information to the thalamus, which we know sends information to the motor cortex. This error correction isn’t just after our movement, it’s continuously happening before, during and after a movement.

This error correction leads to what we call motor memory. We often hear this called in our day to day lives as muscle memory, like a basketball player shooting free throws knows how to get it in the basket because of repetition, but remember it’s not muscle memory because the thoughts are not stored in our muscles, our plan is in our brain. So that’s why we call this motor memory, which improves our performance accuracy for actions we’ve done before.

An AP can originate from many different places meaning information can be sensed and then travel through the CNS to be processed and form a response. The AP can originate in the periphery through external sensors and internal sensors, which we learned last unit, or in the cerebral cortex. In the cerebral cortex, once again, is where we see conscious thought, actions are voluntary. They can also originate in the brainstem, this is involuntary, and happens through effectors.

Flow between these sections depends on the type of response or process the AP needs to go through first. For example if it’s a reflex, it travels from sensors straight to effectors. If it’s conscious thought, it travels from sensors to cortex, if there is an override taking place, it will travel from cortex to brainstem. So try to piece all of that together but just remember that this is an extremely complex system, there’s a lot more going on than what we’ve described, a lot more than just simple reflexes, and a lot of locations where APs can originate.

Make sure you also look at the control of our internal environment. This is a huge topic in the next course, physiology II or 3810, so make sure you know that it consists of the sensors which sense any change in homeostasis, which is where the body wants to stay so like under 38 degrees celsius, pH of 7.4, pressure of oxygen in the blood, all of those regulatory elements of the body, if they change, the body senses this and sends it to the coordination centre which is the brain stem which will send a signal to the effectors to change it. So the effectors are just the systems that will make the change in the body that will fix whatever element is off right now.

There is also the override centre which is in the cerebral cortex. That’s another thing you can remember with letters because you would think cerebral cortex, double c, would go with coordinating center, double c, but remember it’s actually the not case. The two double C names don’t go together, so you can remember that the override centre is in the cerebral cortex. Anyways, so the override centre can be responsible for telling your regulated variables to stop or work differently, so when you’re holding your breath, that’s your override centre overriding your coordinating centre which wants you to breathe.

We’re going to talk briefly about the autonomic nervous system, which has two separate efferent branches. The two branches are the parasympathetic nervous system, which we call the PNS, and the sympathetic nervous system, which is the SNS, which you may have heard about in different courses before. SNS and PNS work together to control cardiac muscle fibres, which are the fibres that work to make the heart contract. SNS increases force of heart contraction, and PNS decreases the rate of force contraction.

A difficult concept to understand when thinking about the SNS and PNS is lateral inhibition. The lateral inhibition is communication between the two systems to lessen the amount of activity of the other. If we think about it, this makes sense because they have opposing actions, so they would communicate to inhibit each other.

Okay that brings us to the end of our content for this podcast. Once again, we want to encourage you guys to continue thinking about the concepts in this subunit in terms of segregation and integration. There are many examples of this so see if you can explain segregation of information from left and right visual fields in each eye, different conducting speeds of ganglion cell types, integration and pooling of information from multiple neurons for receptive fields, and any other examples you guys find on your own. See you next time!