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Lecture 8

CNS sensory and motor (Lecture 8).docx

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PHGY 209
Erik Cook

CNS sensory and motor (Lecture 8): Sensory modalities: • Sense of taste & smell are both mediated by chemoreceptors. Taste (gustation): • Located on the tongue are papillae. • Lining these structures, around the tongue, are crevices which have taste buds. We have about 10 thousands taste buds on the tongue. • The transduction process occurs in taste cells that line the taste bud, at the top of which is a taste pour. • When you put something in your mouth, the molecules dissolves in the saliva and make their way into these taste pour and bind to chemoreceptors in the taste cells. The taste afferents then sends that information to the brain. • Chemicals that we perceive have to enter these taste pours and cells. • We only sense a few gustatory sensations despite having as much as 10 000 taste buds! Taste transduction: • Taste cells are specialized for different types of flavours. Different process for each different flavour/class. 5 different types of tastes/sensitivities. You don’t have much selectivity when it comes to sense of taste. The sensation of all the differences in food we eat come from our sense of smell. • Saltiness: Sodium (Na+) from the food we take in enters the taste cells through sodium channels. • Sour (high acid): the sense of taste associated with sour food is associated with the amount of acid in it. The highest the acid, the more sour the flavour is. Protons in acidic substances we put in our mouth tend to block ion channels or displace other ions from going through. The protons interfere or block ion channels which causes changes in the membrane potential/receptor potential and that causesAPs to be sent to the brain. • Bitter: Flavour that tells you to be careful. Many things that are harmful to you and that you wouldn’t want to ingest are bitter. Since it’s an important taste helping you figure out what you should and shouldn’t eat, “bitter” is mediated by different transduction mechanisms. o In some cases, bitter substances block potassium (K+) channels. o In other cases, bitter substances will bind to specialized receptors and activate various G-protein cascades that then open and close ion channels. (We don’t need to know the details of these cascades.) Simply remember that there are a variety of mechanisms for something that is bitter. • Sweet: Receptors bind to sugar molecules and activate G-protein cascade as well which then opens and closes ion channels. • Umami: Fifth gustatory sensation or taste. Relatively new. Chemicals that directly activate glutamate receptors in our taste cells that then are linked to opening and closing of ion channels via G-protein cascades. Umami is sort of a flavour enhancement. For instance, monosodium glutamate found in food is an umami flavour: enhancer. • Q/A: Sense of spiciness is capsasin, it’s not a flavour – capsasin is activating pain afference/heat afference/temperature afference depending on different people’s sensitivities. This enhanced the taste + how they smell (olfaction) also contributes to the spiciness. Central taste pathways: • How does taste get to the brain? • It goes from the taste cells into their axons. Then, travels via cranial nerves to the brain stem, where there are some relays. Goes through the medulla, thalamus, and then the ipsilateral gustatory cortex – ipsilateral b/c taste does not cross the midline. Olfaction: • With our sense of smell, we can discriminate 10 000 different odors compared to the 5 of the gustatory system. • Odor are molecules that enter the nasal cavity, bind into specialized receptors that are located at the top of the nasal cavity, just below the skull. This olfactory epithelium has receptors cells and a lower mucus which dissolves these odor molecules. • Alining these receptor cells which take them out in the mucus are CILIA that have all the receptors.An odor molecule thus has to bind to a receptor in one of these cilia in order to activate the olfactory receptor cell that then send their axons up across the skull lining the top of the nasal cavity and into the olfactory bulb through the olfactory nerve that is very short. • The olfactory bulb has circuitry neurons that do some processing before sending the information to the brain via the olfactory tract. • There are about 1000 different receptors in the cilia and so each olfactory receptor cell has a class of these receptors. The way we can distinguish 10 000 different odors is that for a given odor molecule it may bind to different numbers of receptors, some very strongly, some not so strongly. It’s the pattern of binding for a given odor molecule that allows 1000 odor receptors to encode 10 000 different odors that we can discriminate. Olfactory signal transduction • The binding process of all thousand receptors are linked to the transduction process the same way: G-protein cascade. • When a molecule comes down and the odor molecule binds to the receptor, it triggers a G-Protein cascade that causes the opening of ion channels. • Of these 1000 different receptors, you get a selectivity of 10 000 different odors. (STEP 3 & 4 were removed) Central olfactory pathways • How does this information get to the brain? • The receptor cells project up into the olfactory bulb, which then sends information via the olfactory tract to the brain. • Remember there are 2 sensory inputs that do not go through the brain stem via cranial nerves: vision which projects to the thalamus, but olfaction coming from the olfactory bulb and projecting to different areas is the one sensory input that doesn’t travel through the thalamus. • One of the primary targets of the olfactory bulb is the limbic system. • This system is involved in memories and emotion. It turns out, as we have experienced, certain odors can trigger emotional responses. Or they can trigger very vivid memories. • The perfume industry is totally aware of this. They try to target our olfactory system with the idea that they want to trigger some emotional response so that we buy their product. • Olfaction is a strong trigger of these types of memories. Strong projection to the neuro- circuits in the brain that are involved in emotions and memories. (End of sensory systems) Consciousness We know little about it from a physiological point of view. What is the neurophysiological basis of you and your mental life? Neuroscientists have a hard time measuring and defining consciousness. State of consciousness: level of arousal (awake, asleep, etc.) – we can measure this not only from behaviour (more about it later) Conscious experience: thoughts, feelings, desires, ideas, etc => rich mental life! – what is the neural basis for our conscious experiences? We wish we knew more about this. Hard to pin down. We assume we all share this rich mental life, but do we know? The electroencephalograph (EEG) • State of consciousness can be measured in 2 ways: behaviour (awake/asleep) and measuring of brain activity through EEG. • What brain structure is located closest to the scalp? The gray matter of the cerebral cortex (2-3 mm of neuron cell bodies). The white matter below it are all the axons connecting different areas of cortex and cortex to different nuclei and ganglia located in the brain. • EEG consists of 64, 32 or 16 electrodes put on the scalp. They are measuring the activity of neurons located near the scalp, in the gray matter of the cerebral cortex. • These electrodes measure a population activity of tens of millions of these neurons. o Airplane view of city lights -> we can’t tell what each person is doing based on the pattern of light.All we can say is the difference between a city and a town. • Each one of these electrodes measures voltage over time in microvolts. There are two aspects of what is being measured by EEG. o The frequency which is related to levels of responsiveness: whether alert, relaxed, or asleep. o Amplitude which is related to synchronous neural activity: if all neurons are being activated independently, the amplitude will be small, but if they start firing APs all the same time, the amplitude starts to grow bigger.  Synchronous neural activity: “flashes” if all people would turn on and off their lights at the same time in the city. If all do it independently, then from an airplane, we would just see a bunch of lights.  Example of synchronous neural activity: In epilepsy (1% of population), circuitries in the brain, oftentimes in temporal areas of the cortex, become highly synchronized – start firing all together at the same time. This pathological state causes seizures, which you can measure in the EEG. The amplitude is small and then starts getting bigger – too much synchronous neural activity. EEGs reflect mental states • Frequencies reflect whether subject is relaxed or alert. • If we are relaxed with eyes closed but not sleeping, you get these alpha rhythms with lower frequencies and bigger amplitudes. • Beta rhythms are more when you’re alert, thinking. Alterness is associated with smaller amplitude and faster frequencies. • Q/A:Amplitude is bigger when we’re relaxed and/or sleeping because mental activity requires asynchronous activity. With all your neurons doing the same thing, your brain is not working very well and is not processing anything. When the brain is working is when all the neurons and different circuits are going out independently. Stages of sleep: • Differenciating between awake and sleep (level of alertness) is done through the EEG. Different stages of sleep can also be evaluated through the EEG. • As we progress through sleep, certain typical changes occur in the EEG. • We start off with low amplitudes, but over the course of 30-45 minutes the amplitude get bigger and frequencies start to slow down. • NREM (slow-wave) sleep => Non-rapid-eye-movements sleep • Classified with 4 stages. • After reaching stage 4, we start going back up to stage 3,2,1.And that’s when we pop into REM sleep (rapid-eye-movement). Paradoxical because the EEG during REM sleep look almost the same as when awake.Also low amplitude and fast frequencies. REM is the deep sleep, when we’re dreaming. We’ll stay in REM sleep for a while and then we go back to stage 1,2,3,4 over the course of an hour or and go back again 3,2,1.And you do that all night long. • When young, we spend more time in REM sleep and less as we get older. Physiological changes during sleep: • Progression of the sleep pattern during the night: 1,2,3,4,3,2,1 + (REM) + 2,3,4,3,2,1 + (REM) + … • As we progress through the night, the REM sleep may last a bit longer. • The physiological signatures of REM sleep are of course increased eye movements (pops up when there is REM sleep). • There is also increased inhibition of skeletal muscle (we’re sort of floppy). But twitching can occur. • Heart rate jumps up during REM sleep and goes back down. Same for respiration rate. • One problem in sleeping is SLEEPAPNEA– sudden reduction in respiration.As we get older, some people have floppy tongue at the back of their throat and as they go into sleep and approach REM sleep where they have an increased inhibition of skeletal muscle the tongue and other parts of the throat fall off and block respiration for just a bit and wakes you up. Prevents these patients from experiencing a lot of REM sleep which then triggers health problems along the way. Q/A: Sleep apnea might be linked to certain obesity problems. • Q/A: why is REM sleep so important? Why is sleep important? Hypothesis – there are chemical structural changes that go in your brain during these different stages of sleep including REM sleep. Consolidation of memories. It’s been shown that if you learn something and then you have a good night sleep, you remember the material better the next day than staying up all night studying. • Sleep is tied to these kinds of changes and people who have sleep apnea have other health problems too. States of consciousness: • What is regulating our sleep/awake cycle? It’s called the circadian rhythm. • Circadian rhythm:Aroughly 16 hour awake and 8 hour sleep cycle. Can vary between individuals => natural sleep/awake cycle.
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