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| The “five senses” are normally thought of as vision, hearing, touch, smell, and taste, but a better way to think of them is as mechano-, photo-, chemo-, thermo-, and noci-ceptive. |
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| for touch (pacinian corpuscle- skin), audition (hair cell- organ of corti), and vestibular (hair cell- macula, semicircular canal) |
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| cvision- rods and cones, retina |
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| olfaction (olfactory receptors in olfactory mucosa), taste (taste bunds- tongue), arterial PO2 (carotid and oritci bodies), pH of CSF (ventrolateral medulla) |
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| temperature- cold and warm receptros on skin |
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| extremes of pain and temp- thermal nociceptors and polymodal nociceptors on skin |
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The “energy” (photons, mechanical, chemical, heat) that stimulates sensory receptors acts like neurotransmitters. In this case, we call the electrical changes “receptor potentials” instead of EPSPs.
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Mechanoreception: Touch, Hearing, Balance, Proprioception, (Pain)
-Energy detected: Mechanical
-Cell and organ of detection:
Directly stretch gated:
Skin
Muscle and tendon
Stretch gated by fluid movements:
Cochlea Semicircular canals
-Types of sensory organs in the skin; innervated by or made of DRG neurons
On–off properties and thresholds differ, giving different information about things on the skin
-Sense organs of proprioception: muscle spindles and Golgi tendon organs; innervated by DRG sensory neurons; mediate reflex responses to adjust muscle contraction
So mechanoreception is the transduction mechanism that underlies touch. But also, as I said earlier, it underlies hearing, balance, proprioception, which is the sensations that you get but you are not aware of but that you get from muscles and joints that tell you where your body is in space and how your body parts are moving in coordination.
And there's also a component of pain that's mechano sensitive. So what does that mean? So the energy that's detected in a mechanoreceptive neuron is mechanical energy. And the mechanism of transduction, as shown here, is literally ion channels that will depolarize the membrane are stretched open. So these are ion channels similar to the sodium channels and potassium channels, that we've talked about, and other neurons that respond to things like voltage.
So you may remember some of the voltage gated sodium channels of earlier neuronal videos. Those voltage gated sodium channels change their shape and open up in response to changes in the voltage of the membrane. Well, in this case, mechanoreceptive ion channels change their shape and open up in response to stretching of the cells, or mechanical deformation of the cell membrane.
And once they are opened, they begin to conduct ions into the cell usually-- positive ions into the cell-- causing depolarization. If the neuron reaches threshold, it will fire an action potential. So, in touch, we have receptors in the skin that respond to touch. We have receptors all over our bodies throughout our skin that respond to touch. And these are, again, mechanically deformed, which is what causes them to conduct ions and become depolarized.
And so we can see, there are a number of different types of receptors in the skin, some that you actually may have already heard of. The Pacinian corpuscle, it's one of the favorites. It's really beautiful and unusual looking. If you have a chance to see histology of a Pacinian corpuscle, I highly recommend it. The Meissner's corpuscles, hair follicle receptor-- so hairs in the skin. Here we go. Hairs in the skin actually have neuronal axons that wrap around. And if you have a fingernail, you can get a hold of one hair and move it. You can feel it moving. And what you're doing there is you're actually opening ion channels in the neuron that surrounds that hair follicle. And Ruffini corpuscles, Merkel corpuscles, and little tactile receptors.
And one of the things you notice about these receptors in the skin is that they have some different properties. And some of them you may even be able to predict just by looking at them. So the Pacinian corpuscle, that's down in the deeper layers of the skin. So that's probably something that takes a little more pressure to get activated because it's pretty deep. And you'll also notice that it has these layers and layers? What are these things?
These are layers and layers of connective tissue that surrounds the outside, which also helps to dampen some of the touch. So these require a fairly high intensity of touch in order to become activated. And sometimes people talk about them as being responsive to vibratory sense. They also adapt very rapidly. Some of the other sensory neurons in skin, such as the Meissner corpuscle, are also pretty rapidly adapting. But some are not. We have some that are pretty slowly adapting. And so this can explain the diversity of sensory experience that we can have on skin.
Related to the sense of touch, and usually covered with it as I'm going to do now, are the proprioceptive senses because very similar neurons are underlying this sense. So proprioceptive sense comes from sensory neurons that innervate muscle fibers or tendons. So we'll look over here, and we see sensory neurons that, for example, innervate the Golgi tendon organ.
Or we have, in this case, a sensory neuron that's wrapping around what's called an intrafusal muscle fiber, also known as a muscle spindle. The muscle spindle, when it stretches, this sensory neuron that's wrapped around it becomes activated, again, through the same mechanotransduction mechanism, stretching open an ion channel. And this sends information into the spinal cord, which creates a reflex response that causes the associated muscle fibers to contract more. So as a muscle spindle gets stretched, it's indicating to the spinal cord that there's a lot of weight on the muscle, and that causes the muscle to contract more.
So, for example, if I hold out my arm, and I put something in it. Let me put this box of Kleenex in it that's sitting here. I put this box of Kleenex. This has some weight. And in order to keep my arm at the same height, I need to contract the bicep's muscle to accommodate this new weight. If I put this on my hand or somebody else, let's say, put this on my hand.
And without my knowing it, it's actually made of lead. I didn't realize. It looked like a box of Kleenex, but it's actually made of lead, so it's much heavier than I thought. So that's going to make my arm sort of fall down, and it's going to stretch the bicep's muscle. And in order to accommodate this weight that I wasn't expecting, those intrafusal muscle fibers will be stimulated. They'll stimulate their associated mechanosensory neurons, which will send information into the spinal cord-- we can see it here-- to activate motor neurons that make this muscle, or in this case, my bicep's muscle, contract more. And now, I can keep that weight up where I want it.
So muscle and tendon also have these mechanoreceptive neurons, and their activation and activity is part of the proprioceptive system. We'll talk in another video about mechanoreceptors that mediate hearing and the auditory-- the vestibular sense-- excuse me. And these are also a stretched-gated, but they're stretched by moving fluid. And we'll see it's a slightly different mechanism. But underlying the transduction is the same stretching open an ion channel to get depolarization. But for now, in this video, touch and proprioception are the two major senses that are mediated by mechanotransduction. |
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somatosensory neurons
And I want to show you one other thing about the sensory neurons that underlie touch, and actually also proprioception. But these are sometimes called the somatosensory neurons. So the somatosensory neurons are the ones that are innervating the skin and are going to eventually tell the brain what's touching the body. These neurons are a little bit unusual structurally.
And I want to just make a point about that because I know in some earlier videos, and you probably learned in other classes, neurons have this, some people use the four functional domain model where there's this cell body that gets inputs through the denigrates. And then, the cell body integrates the information that's an integration zone. And if there's enough depolarizing input the cell will reach threshold and fire an action potential, which it will conduct down its axon. And then, there'll be neuro transmitter release in the end zone. Somatosensory sensory neurons are a little funny. They're just a little bit different than the typical neuron in this way.
We can see here, here's the soma, or the cell body, of a typical somatosensory neuron. So where is this soma living in terms of gross anatomy? Well, it's living in the dorsal root ganglia. This part of the dorsal root ganglion somatosensory neuron is an axon. And that seems kind of weird, and this what confuses students a lot of times. But this part is sort of an axon but also a dendrite, and this is really the confusing part.
I'm sorry, I think I should have said, so the soma of the dorsal root ganglion somatosensory neuron has two projections. One is its axon, which goes into the spinal cord. Let me write that over here. Here, these are the nerve endings, and so neurotransmitter is released here. So this neuron will release neurotransmitter from these endings onto a spinal cord neuron. It's this side of the dorsal root ganglion cell that can be kind of confusing to students because it's myelinated. You can see that. And it is going to conduct action potentials, but those action potentials are going to the cell body.
In a typical neuron, the cell body is where you decide if there's going to be an action potential. But that's not the case in the somatosensory neurons of the dorsal root ganglion. Those decisions about whether there's going to be an action potential occur out here where the receptor potentials are generated. So if there's sufficient activation of the input zone, if you will, or the dendrite of the somatosensory neuron in the skin or in the Golgi tender organ or in the intrafusal muscle fiber, you'll get an action potential that will be propagated just right past the cell body and right on into the spinal cord. So they're a little bit different than typical neurons.
And we can see here from your book from Costanzo, the picture that they show, here's the receptor in the periphery. Here's the cell body and the dorsal root ganglia. And it's sending its axons in some place. Depending on the type of neuron it is, it will be sending axons to different regions of the spinal cord or, in some cases, even all the way up to the medulla. But that's stuff that you'll probably learn in neuroanatomy. So this is just a little description of the somatosensory neurons that serve the skin and the intrafusal muscle fibers and the Golgi tendon organs with reference to their unusual structure, which relates to their function. And just a little reminder or introduction, depending on whether you've had your neuroanatomy yet, on how this relates to the neuroanatomy of the spinal cord and the brain stem. |
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Mechanoreceptors in the Skin: Receptive Fields
-Receptive field size reflects number of neurons receiving information from an area of body surface
But the next thing to talk about when we think about the mechanoreceptors that service the skin is receptive fields. Now, all sensory neurons have some kind of receptive field, so this is a useful conversation to have right now. And I have a nice demonstration that you'll see in another video that will help you understand, I hope, mechanoreceptors and receptive fields a little bit. So let's look at what happens to sensory information once it's hit the skin, and it's gone through that dorsal root ganglion neuron and gotten into the spinal cord and is heading up towards the brain.
So here, we have a piece of skin. In this slide, we're going to call it a receptive field. That's better. And for today, we're going to say this is in the skin. And here's the dendrite of that cell where the receptor potential will be generated in response to stretching. This doesn't really show it, but let's say that this was a dorsal root ganglion neuron and here would be the cell body in the dorsal root ganglion. And it would be sending an axon into some part of the central nervous system in the spinal cord or the medulla.
A lot of the sensory neurons from the skin send their axons actually up to them medulla and the nucleus gracilis and nucleus cuneatus where they form a synapse release neurotransmitter and stimulate another cell, another neuron, which is going to send information further up. In the case of somatic sensory information from the skin, it would go to the thalamus where it would reach a third order neuron that would go to the cerebral cortex.
Now in the cerebral cortex in the postcentral gyrus, we have a representation of the body surface. You've probably seen pictures of this before. This is called sometimes a homunculus. And what we're seeing here is that there are neurons in these parts of the postcentral gyrus that get information from the part of the body that's shown in the homumculus.
So, for example, this part of the postcentral gyrus is receiving sensory information from the skin of the fingers and the hand and the arm. This part is getting information from the toes and the genitals. This is the face. The lips have a large area that's represented. And one thing we know right away is there's a huge representation of the fingers and the face and the hands and not such a huge representation from, for example, the feet, the legs, the arms. These actually take up relatively little space.
So what does that mean? Let's look at this. So one thing that we can say that that means is that, if we go back to this picture, we see here a sensory neuron. It has its receptive field. And that means that anything that touches this part of the skin has the potential to deform that sensory neuron and make it fire an action potential. And right nearby is another sensory neuron that's going up and sending its information up. And so the more sensory neurons that are present in the skin that make direct links all the way up to the cerebral cortex, the more conscious awareness we can have of that region of the skin.
But sometimes, a couple of different things can happen. We can have an area where there are some sensory neurons. They can all be stimulated. But when they get to their relay nucleus, let's say in the medulla or in the thalamus, one of their relay nuclei maybe further up, they converge. And so the information that goes from the relay nucleus to, let's say, the cortex is a combination of information coming from multiple sensory neurons at the periphery. In this case, the cortex can only detect one piece of information from all three of these neurons because the information is being lost at the convergent site.
So these are the larger receptive fields. These reflect the larger receptive fields that we have, for example, in the arms, in the legs, and on your back. And so to demonstrate the different sizes of receptive fields, we've developed a video that you can watch and see a demonstration using a two-point discrimination tool that will show how different parts of the skin have very different abilities to detect stimuli and have a different level of resolution. And that's in the video that accompanies this video. |
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hearing and balance.
Cell and organ of detection:
Stretch gated by fluid movements:
Cochlea
Final output: temporal lobe
As I mentioned in an earlier video, hearing and balance are both mechanically gated, but not in the same way we saw mechanical gating of the somatosensory and proprioceptive neurons that serve the skin, muscles, and tendons. The somatosensory neurons, those ion channels are literally stretched open by mechanical deformation.
That's true here, too, but it's done in a fluid environment. And so, in the cases of hearing and balance, we have closed tubes full of fluid. That fluid moves, and it's the movement of the fluid that can stretch the ion channels open. So let's look at that in terms of hearing first.
The organ of detection for hearing is the cochlea. The cochlea is here in the inner ear. We have the pinna here. Sound waves travel in. They hit the tympanic membrane, or the eardrum. They start a chain reaction of movements of the small bones of the middle ear-- the malleus, incus, and stapes. And the stapes hits a membrane on the surface of the cochlea, which starts fluid moving inside this bony structure, this curled, circular bony structure. So let's look at that.
I'm going to go down here first, and we're going to unroll the cochlea and take a look at what happens to the fluid when the stapes hits the membrane that's at the edge of the bone. So if we take the cochlea and we unroll it, we can see the structure is that it's kind of thick at one end and thin at the other.
And in the middle is another membrane, the basilar membrane. And it's on the basilar membrane, which we can also see in cross-section right here. We have the Basel membrane. All along the length of the basilar membrane is a structure called the organ of Corti. The organ of Corti-- actually, let me just take a second and show you here-- here's the basilar membrane, here's the organ of Corti sitting on top of the basilar membrane.
And we can see a couple of other membranes that are kind of separating fluid compartments in the cochlea. We have the scala vestibuli, which is sort of, if you will, above the organ of Corti; and the scala tympani, which is the region below the organ of Corti. And then, around the organ of Corti, is another area called the scala media.
So let's drill down a little further into the anatomy of this organ of Corti because, to understand the transduction mechanism, you need to understand the anatomy of the organ of Corti. So again, here's our basilar membrane. So now, we're kind of getting deeper and deeper into-- we're increasing the magnification, if you will.
So here's the basilar membrane, which again is shown here in this image here now. Scala tympani would be this region. Scala media would be up here. The scala vestibuli would be sort of over here.
Now, the organ of Corti sitting on the basilar membrane is made up of a number of cells. the Important ones are the hair cells. There are two types. The inner hair cells, these are closer to the midline. And the outer hair cells, they are sort of closer to the lateral edge.
Above those cells is another membrane called the tectorial membrane. And the hair cells have cilia-- you can see them shown here, these black lines coming from the tops of the hair cells-- and they are embedded in the tectorial membrane. The ion channels that change the electrical potential of the membranes of the hair cells are found at the bases of the cilia that are embedded in the tectorial membrane.
So when the stapes hits the membrane of the cochlea, that mechanical energy of the stapes hitting the membrane causes the fluid that is filling this whole structure to start to flow. And you notice that the basilar membrane does not go all the way to the end of the cochlea when we unroll it. We can see that the fluid compartment is continuous.
So the fluid begins to flow around and move around the end of the basilar membrane. And as it does, depending on the frequency with which the stapes is hitting the membrane, you'll get movement of the basilar membrane because it's fluid and it's flexible. And so, as the fluid moves, it's going to push on the basilar membrane. And depending on the frequency of movement, you will get characteristic movements of the basilar membrane at certain points. So high frequencies tend to move it here, and low frequencies tend to move it here.
So the movement of the basilar membrane does something important here at the tectorial membrane. As the basilar membrane moves, when it moves up, it pushes towards the tectorial membrane. And as it moves down, it pulls away from the tectorial membrane. So this sort of oppositional movement of the tectorial membrane and the basilar membrane causes stretching of the ion channels that are located at the base of the cilia of the hair cells.
And it's that stretching that causes ion flow to change and can cause the hair cells to depolarize and release neurotransmitters, which they do here at their synapse with the auditory nerve fibers from the eighth nerve that are going to enter the brainstem and begin sending information about sound eventually up to the auditory cortex and the temporal lobe. |
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hair cells in fluid
Cell and organ of detection:
Stretch gated by fluid movements:
Semicircular canals
Final output: reflex control of posture, movements
Vestibular system is similar and located very nearby, actually, the cochlea. So actually, the bony labyrinth includes the cochlea, which is subserving hearing, and the semicircular canals, which are subserving the vestibular sense or sense of balance. So the organ of detection for balance is the semicircular canal. And similar to the cochlea, the semicircular canals are also filled with fluid. But in this case, the neurons are found just in one space at the base of the semicircular canals.
Also, they have specialized cilia. There are also hair cells similar to the ones that are in cochlea. They have cilia, and they have a special cilia called a kinocilium, and the transduction mechanism involves stretching open ion channels at the kinocilium, which can cause the cell to depolarize and release neurotransmitter onto the vestibular nerve fibers from the eighth nerve and send that information into the brain and eventually to a lot of places-- including parts of the brain stem, parts of the cerebellum, some parts of the cerebral cortex.
So what moves the fluid in the semicircular canals? It is movements of the head. So when we move our head in different directions, we move the fluid in the semicircular canals in different ways because the semicircular canals, as you can see, are oriented in three different planes. And so we can tip our head forward or back, to the side, or we can also get fluid movement in the semicircular canals by forward motion of the head-- for example, in a moving automobile or on a boat.
And depending on the direction of movement, we get movement in the canals, and that movement can move the stereocilia and kinocilium of the hair cells in one direction or the other, depending on which way the fluid is moving. And there's a hyperpolarizing direction and a depolarizing direction.
So if the fluid is moving in the right horizontal semicircular canal in response to the counter-clockwise motion of rotation of the head, we're going to get hyperpolarization and inhibition of the hair cells on that side. But on the other side, the fluid will be moving in the opposite direction, and that's going to move the cilia in a different way and cause a depolarization on that side. And the brainstem and cerebellum can interpret the information coming from the two semicircular canals in order to help us regulate our balance, posture, and not get seasick. |
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photoreception: vision
-Energy detected: Light
-Mechanism of transduction: Photon alters molecular structure of 11-cis-retinal to form all-trans retinal. This initiates a series of second- messenger activity that results in altered membrane potential.
-Cell and organ of detection: Photoreceptors in the retina of the eye
Rods: more sensitive (night vision), more abundant in periphery
Cones: less sensitive (require brighter light), color specific, high density at fovea
Retinal layers Projections to the brain
So vision is the photo receptive sense, that is the receptors that mediate our visual experience or that initiate our visual experience respond to photons of light. So the energy detected by the visual system is light.
It's a fairly complicated transduction mechanism that I think exceeds the scope of what you need to know, but we're going to just rush through it and not get too bogged down in some of the details though. But I think it's important to know the names of some of the players. So let's just quickly run through.
Photoreceptors in the eye. These are found in the retina. So, photo receptors, the organ of detection-- excuse me-- here, are the photo receptors in the retina of the eye. They are the rods and the cones. Here is a rod. Here is a cone. They look similar, but not exactly the same. And the reason-- that's how they got their name. The cone has kind of a cone shape to its outer segment and the rod is more rod-shaped.
These are the cells that respond to photons. And the way they do so is that they are lined with-- they contain a chemical called 11-cis-retinal, which can be altered molecularly when photons hit it to become all-trans-retinal, which initiates a series of second-messenger systems within the cell that result in an altered membrane potential. You get a compound called metarhodopsin activating a G protein called transducin, which activates phosphodiesterase.
So some of these are, I'm sure, are familiar to you. Certainly phosphodiesterase, which activates a cyclic GMP. But it decreases cyclic GMP to form 5 GMP. This ultimately results in the closure of sodium channels. And if you take just a second to let that sink in-- because sometimes students skip that part and they miss an important aspect of the photoreceptor system. It closes sodium channels.
And so when light hits a rod or cone it actually hyperpolarizes the cell and turns it off. So photoreceptors are constantly active. And light actually stops them. I don't think it's worthwhile to spend a lot of time on how that information is processed in the retina. It's for, I think, a more advanced class in neuroscience and probably not important.
But I think it's useful for you to know that it's not what you expect. You think, light hits the photoreceptors and activates them and they throw higher action potentials. In fact they're releasing neurotransmitter all the time, and where there's the light-- that slows them down. And that's how we begin the process of detecting visual information. But we can talk, even without going into too much detail on that part of the mechanism, we can still get some good information about what's going on in the eye.
So let's talk about rods and cones for a minute. If we look at the-- I'm going to draw a surface of a retina here. So this is the retina. We're going to look a little deeper at the retina in another slide, but just to get you started.
And so here's the path of light, let's say. So here's our light coming into the eye, and it hits the retina. And it's actually going to go all the way through the retina to the back. And the photoreceptors, the rods and the cones are in the back of the retina. And then there are a series of neurons that move forward to the outer part of the retina, which is the retinal ganglion cell layer. And we'll see this in another slide as well. And this is where action potentials actually go to the brain. They go from the retinal ganglion cell layer. That's a G. All right?
So the rods and cones are here in the back. Rods, cones. And I'm going to try to be a little bit more-- I'll just give you a little bit more sense of things here. So we see here we have some rods and cones in the peripheral parts of the retina, and we have cones in the center. OK?
So let's talk about rods and cones. Rods are far more sensitive than cones. And what that means is they can respond to lower levels of light. It doesn't take nearly as many photons to get a rod activated as it does to get a cone activated. However, cones are the ones that we use to see colors. Rods detect photons in the blue wavelength. So we can use those at night to see well, but they're not so great for brighter colors.
The cones can detect the yellows and the blues and the reds. They're less sensitive. They require brighter light, so they're good for daytime vision, and they're color-specific. And their highest density is at the focal point of the retina. So when you focus on an object with your visual system, when you look at something, you are stimulating all cones. The rods are found at much higher densities as you move away from that center.
And one way to demonstrate this to yourself that's pretty fun is, next time you're outside on a night when there are a lot of stars, find a star in the sky that's very faint, and if you try to look at it, you try to focus your eye on that faint star, you'll see that it kind of twinkles in and out of vision. But if you look slightly away from the star so that you are putting it onto the periphery of your retina, you can actually see it much better.
That's because the rods are picking up that faint light from the star and they're more densely packed in in the periphery of the retina. But there are no rods in the focal point. So you're going have a hard time seeing the faint light at night by focusing directly on it. But look away a little bit and suddenly you'll be able to see that little faint star.
So next we're going to look at the retina and some of the layering. But before we do that let me just say-- so let me reiterate something I said earlier. There are a number of layers to the retina. We're going to see that. And then the projections, of course, of the visual system-- which are not really part of this video-- but the projections from the eye and the retina go into the brain to the lateral geniculate nucleus and then finally to the occipital lobe. And these are things that you will see in your neuroanatomy class. |
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-Focal point = fovea
• Lens directs light from the object of focus onto the fovea
-Macula-center of retina, contains the fovea; highest density of photoreceptors, highest detail vision (acuity); no rods—not as sensitive as peripheral retina
• Maculardegener}ation—wetordry
-Lens—cataracts
-Cornea—scratches
-Optic disk...
Let's look at the eye a little bit. So here's our light coming in. And it comes in through this clear outer layer of the cornea through the anterior chamber, and then it hits the lens. And you see that the lens has little muscles connecting it to the ciliary bodies. And we can change the shape of our lens in order to focus light on the fovea, the focal point. And that's what we're trying to do.
When you look at something-- when you actively identify an object that you want to look at-- what you're doing is shifting the size of the lens and moving the light that's coming from that object onto the fovea. That fovea is the cones-only region that I was just talking about.
So again, if you want to see that faint star at night what you want to do is not look directly at it. Look slightly away so that the faint star is not at your fovea, but over on the side of the retina where there are more rods. OK. All right. So that's the focal point, the fovea.
And the lens, again, directs light from the object of focus onto the fovea. There is also something called the macula. And you've probably heard of macular degeneration. And this is the center of the retina. It contains the fovea, but it's larger than the fovea, and it's called the macula. "Macula" is the Latin word for "spot." I always wanted to have a dog named Macula. I always thought that would be a great name for a dog. [LAUGHS] Because it means "spot." And when you learn how to do your eye examination you'll be able to see the spot, or the macula, which is the center of the retina.
It has the highest density of photoreceptors. But again, not rods. This is the area where you get the best visual acuity, and this is why we focus things in the center of our retina. But it's not as sensitive as the peripheral retina. And of course we can get macular degeneration, which you'll be learning about in your clinical classes.
Other clinical issues that can come up with the eye, of course, are cataracts. A lot of people get cataracts, which are accumulations of protein in the lens. And so when you have cataracts the light hits them and it scatters. And what you get is a perceptual image of scattered light. So sometimes people will report that they're looking at a-- if they see a car coming towards them on the road, if they have cataracts it might look like the car has many headlights instead of one. Or streetlights will look like sort of starbursts instead of just a light.
Another thing that can happen with the eye itself is the cornea can get scratched. So the cornea needs to be very clear for light to come through. And, again, if you have scratches in the cornea you're going to get some diffraction of light, which can distort the image that you're trying to look at.
And then finally my favorite part of the eye is the optic disk. So let's look at what the optic disk is. I'm going to show you where it is. It's sort of off just to the side, at the edge of the macula. And this is a really important part of the eye. And if you can understand the optic disk, I think you'll have a good understanding of how vision works. |
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The optic disk is sometimes also known as the blind spot. So let's see why that's true. All right. So here I told you we were going to see the layers of the retina in a little bit more detail. So here is our map of the layers of the retina. This is from your Costanzo book. This is light coming in. It's coming in from this direction. So just to make sure that we understand what's going on-- the cornea would be here. The lens would be here. And then the light comes in and hits the retina.
And it goes through the layers of the ganglion cells, and some other layers called the inner plexiform layer, the inner nuclear layer, outer plexiform, outer nuclear. So these layers all contain neurons, different types of neurons, bipolar cells and amacrine cells and different types of neurons that are going to process the visual information from the rods and cones. We're seeing only rods here, but there might also be a cone. We can draw a cone in here.
So the photoreceptor layer at the back, where the photons from the light are actually stimulating the transduction mechanism, are going to send information forward. When these cells are active they're sending information forward and that information is being processed very heavily by the cells in the layers-- the inner and outer and nuclear and plexiform layers.
The final output of the retina is the retinal ganglion cell. And the retinal ganglion cells have axons that go to the brain. They are going to go to the lateral geniculate nucleus. So these are the retinal geniculate axons. They go through the optic nerve. OK?
Now, what's neat is that as that retinal ganglion cells are sending their axons out into the optic nerve they sort of coalesce along the surface of the retina. And they sort of all move towards the optic disk. And the optic disk is where the optic nerve-- all these axons from all the retinal ganglion cells coming together-- the optic nerve forms that cable that then penetrates through the back of the retina and enters the brain.
So at this point, where the optic nerve is leaving the retina, there are no photo receptors. The retina is perforated there. There are no photoreceptors. There are no inner and outer plexiform and nuclear layers. It's a blind spot. When light comes in-- when you're looking at images and light comes in and it hits different parts of the retina depending on where it's coming from, any light that goes to this part of the retina is not detected because there are no photoreceptors there to detect it. |
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So I'd like to demonstrate that. I want you to demonstrate that on yourselves, actually, and prove to yourselves that you have a blind spot. And so this demonstration should be available to you somewhere online. My recommendation is that you print it out on a piece of paper. But you can try it on-- if you have an iPad you might be able to do this with your iPad. But if you can't, then you might want to just print it out on a piece of paper.
So basically what we're going to do is we're going to do two demonstrations. First of all I want you to prove to yourselves that you have a blind spot in your retina. Because it doesn't feel like you have one. Right? Nobody has a conscious experience of having, like, a hole in their visual field. But if you take this piece of paper and hold it-- we're going to look at the top part first. We're going to do this part first.
OK. So this is to demo the blind spot. All right. And what you do is you close your left eye and focus your right eye on the circle. Not on the x. On the circle. OK? And you hold the paper-- or, if you try it on your iPad, again, it might work. You hold it out at arm's length. While you're focusing that right eye on the circle, move the paper towards you and see what happens to the X. OK.
What should happen is that it should disappear. If it doesn't disappear, my experience has been that students are not looking at the circle. So if trying it and you're like, the X never disappears, you get the paper all the way up to your nose and the X is still there, make sure that you're focusing that right eye on the circle and that your left eye is closed. That's been my experience with where students have a problem.
The second demonstration down here is going to demonstrate something different. Once you've proven to yourself that you have a blind spot the next question is, why don't you notice it when you're just going through your day? Why don't you always have this hole in your visual field?
And the reason is because your brain gets used to it and fills it in. And this demonstration, where we have what looks like an x but actually is not an x, it's actually just four lines, lined up in a way that if they were connected they would be an X. Do the same exercise.
Close your right eye. Focus your left eye-- I'm sorry. Close your left eye and focus your right eye on the circle. So close your left eye and focus your right eye on the circle and move the paper towards you. And what you should see is you should see this X fill in. And when you see that, you are having an hallucination. [CHUCKLES] Right? Because your brain is putting visual information where there is none. So this is the brain filling in. |
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Definition
Thermoreception: Temperature, (Pain), Taste*
-Energy detected: Temperature
-Mechanism of transduction:
Temperature change above or below a set value activates an ion channel conductance of a TRP family of channels
Many of the TRP channels have chemical gating mechanisms as well
-Cell and organ of detection:
Skin receptors
Oral epithelium/tongue
Thermoreception is just like a voltage gated channel, except in this case, temperature gates the channel. In chemoreception, some chemical gates a channel.
So let's look at some examples of thermoreception and chemoreception. We'll start with thermoreception or temperature sense. Thermoreceptors are our temperature sensors, which are in the skin. They can also mediate pain. This shouldn't be any surprise. We know that, for example, temperatures over 45 degrees Celsius are usually perceived as painful.
And interestingly, they can also be part of our taste system. So the energy detected here is temperature. However, thermoreceptors also have chemoreceptive capability. The mechanism of transduction is that a temperature change above or below some value, depending on the channel, activates the channel. And so the channels in thermoreception are the TRP channels, that TRP family of ion channels.
These channels conduct ions that can depolarize membranes, just like a voltage gated sodium channel does. And we can see here that there are a number of TRP channels. These are some of the important members of the TRP channel family.
And we have them lined up under a temperature scale. And what we can see is that each one of the channels has some unique temperature that initiates the firing action potentials and releasing neurotransmitter, or initiates depolarization, I should say, in these channels. So for example, TRPA1 is a cooler channel, whereas TRP V2 has a pretty high temperature. So its going to be detecting high temperature.
And so, depending on which channel is being activated, the brain learns this is hot. These are cooler. These tend to be cooler.
And so the thing that's kind of neat about the TRP channels is, as I said, they're also chemoreceptive. And so we have these foods, the compounds, that are in some of our foods that can also activate some of the TRP channels. For example, mint can activate TRP M8. And chili peppers, the capsaicin in chili peppers, can activate some of the TRP V channels, TRP V1 and so forth.
And so where when you eat a chili pepper, we have a sensation of heat because our brain associates the activation of cells by TRP V1 with thermoreception or with heat sensation. But when you activate that channel with capsaicin, which is a chemical, you get a perceptual experience that's similar to heat. So that's kind of neat, I think, about the TRP channels.
We find these kinds of channels in the skin because, obviously, our skin is pretty sensitive to temperature, as it should be. That's very adaptive. And we find them, of course, in the mouth and on the tongue. |
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Chemoreception: Taste, Smell, (Pain*)
-Energy detected: Chemical
-Mechanism of transduction:
Chemical agents activate or travel through an ion channel
-Cell and organ of detection:
Tongue
Nasal epithelia Skin
Chemoreception is something we think about with smell and taste. The energy detected is chemical. And the mechanism of transduction is chemical agents simply bind to a channel that has a binding site for them. And that causes them to open.
So this is just like a muscarinic channel or the nicotinic acetylcholine receptor being activated by acetylcholine. It's the same idea. These are chemicals that act like neurotransmitters.
But again, they're not coming from another neuron. They're now coming from the environment. So for example, in taste, where we have all chemoreceptors. We have different kinds of molecules that have different properties. So for example, bitter molecules or sweet molecules, like sugar, the umami taste is something that comes from amino acids generally. Sourness comes from hydrogen ions, from acids. And the salty taste comes, not surprisingly, from sodium and salts.
And they can activate in different ways, channels causing depolarization of the cells. So in the case of bittersweet and umami, there's actually some other TRP channels that are activated on the tongue by molecules coming from bittersweet or savory foods binding to G-protein coupled receptors and activating IP3 and calcium. These are second messenger systems that you're probably familiar with.
In the case of sour and salty, we actually have channels that directly enable sodium entry in response to high sodium or high hydrogen ion or proton concentrations at the tongue, again, causing depolarization of the receptor cells. And then those cells are going to release neurotransmitter and activate other neurons sending information in to the brain eventually where it will reach consciousness.
And we find these chemoreceptive cells in the tongue. We find them in the nasal epithelia. And we also will see some chemoreceptors in the skin. But they serve a slightly different function, as we'll see.
I'm sorry. Let me go back for a second. So this is taste. We saw here, our taste transduction mechanism. And here, we have our other big chemoreceptive sense, which is smell. |
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Definition
Chemoreception: Taste, Smell, (Pain)
-Energy detected: Mechanical
-Mechanism of transduction:
Chemical agents activate or travel through an ion channel
-Cell and organ of detection:
Tongue, Nasal epithelia, Skin
And odorant molecules, which can be lots of different things, enter the olfactory epithelia through the nose or through the mouth. They can enter in both ways where there are olfactory receptor cells that have receptors for odorant chemicals on their cilia.
And those odorant chemicals can bind to the olfactory receptors. And they activate at G proteins. And utilizing a cyclic AMP mediated second messenger system, they cause the opening of ion channels, which causes the olfactory cells to depolarize. And then information enters olfactory nerve and gets into the brain where it can eventually reach consciousness. Then these are found primarily in the nasal epithelia for smell.
So we've seen, briefly, that chemoreceptors serve our taste and smell senses. And again, these are just receptors for chemicals from the environment, either odorant molecules or the molecules from food that we taste. But the other chemoreception that we'll talk about in the next video observes the sense of pain or nociception. |
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Definition
- Mechanical stabbing of skin stimulates free nerve endings of nociceptors
- Thermal temperatures above 45°C, extreme cold
-Chemical compounds released by tissue damage
• Histamine
• K+
• H+
• Substance P
• Lactic acid
• ACh, serotonin
• Arachidonic acid (prostaglandin) |
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Term
| Properties of nociceptors |
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Definition
-Sensitization-hyperalgesia-nociceptors become more sensitive after activation. It hurts to touch a swollen area
• Gate control-light touch around a painful area can block action potentials in nociceptors from reaching the spinal cord (rubbing makes it feel better)
• Two-step pain: A-delta fibers fire first and inform the brain of a location where something is causing pain. C-fibers fire later and create the ache |
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Term
| nociception energy detected, cell and organ of detection, mechanism of transduction |
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Definition
-Energy detected: Mechanical, thermal, or chemical or polymodal
- Cell and organ of detection:
Nociceptors, free nerve endings
- Mechanism of transduction:
Mechanical, thermal, or chemical
Mediate spinal flexor reflexes (withdrawal)
Project to cerebral cortex, where pain is experienced
Project to limbic system, where emotional salience is added to pain |
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| three main pathways for pain: |
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Definition
1. Neospinothalamic
• Transmits sharp, immediate pain, myelinated A-delta
• Small receptive fields
• Takes pain information to post-central gyrus via thalamus
• Decussates in spinal cord
• Brown–Sequard syndrome*
2. Paleospinothalamic
• Transmits slow, aching pain, unmyelinated C fibers
• Large receptive fields
• Takes pain to thalamus on both sides, also to cortex
• Complex pathway branches in several places
3. Archispinothalamic
• Polymodal nocineurons in spinal cord stimulated by nociceptors
• Carry information to the limbic system of the brain
• Anterior cingulate cortex, if cut or damaged, removes affective components of pain and is a form of pain relief |
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Definition
Archispinothalamic and paleospinothalamic pathways project to regions of the brainstem called periaqueductal gray (PAG), where opiates synthesizing neurons reside.
These neurons release opiates, beta-endorphin (mu receptors), enkephalin (delta receptors), and dynorphin (kappa receptors), onto the ascending pain neurons in the spinal cord to reduce their activity.
Opiate drugs are opiate receptor agonists. Anti-prostaglandins relieve pain locally.
Emotional stress can inhibit pain pathways—hero syndrome.
Cingulotomy—old treatment for intractable pain was to cut the connections of the cingulate cortex to the rest of the cerebral cortex. Pain was still perceived but was not considered “painful.” |
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Definition
Acute
• Pain that occurs at the time of injury and subsides with healing
• Treatment based on pain level
Chronic
• Pain that persists after injury has healed or exceeds observable injury
• May be due to scarring, adhesions
• Fibromyalgia
• May be due to neural plasticity and development of improperly activated cerebral cortex neurons (similar to phantom pain) |
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Definition
• The International Association for the Study of Pain defines pain as an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.
• Standard categories of pain include: nociceptive pain, inflammatory pain, dysfunctional pain, neuropathic pain |
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Term
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Definition
pain that arises from actual or threatened damage to nonneural tissue and is due to the activation of nociceptors (high threshold sensory receptors of the peripheral somatosensory nervous system that can transduce and encode noxious stimuli). This term, designed to contrast with neuropathic pain, is used to describe pain occurring with a normally functioning somatosensory nervous system as opposed to the abnormal function seen
in neuropathic pain |
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Definition
| pain in the presence of inflammation that is increased by pressure |
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Definition
| maladaptive pain, typically triggered without an external stimulus, which does not serve a known protective function (e.g., pain associated with fibromyalgia, irritable bowel syndrome, and some types of headache) |
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Definition
| pain caused by a lesion or disease of the somatosensory nervous system. Neuropathic pain is a clinical description (and not a diagnosis) that requires a demonstrable lesion or a disease that satisfies established neurological diagnostic criteria. |
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