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00:02 This is lecture five of Neuroscience and continue our discussions on glial cells.

00:11 we already talked about radial glial cells they serve as guides for neurons and

00:18 involved in the migration and early guidance these cells and microglial cells. Wait

00:27 second. Let's move back right Rad glial cells. So we also

00:34 microglial cells, but we'll come back talk to them one more time.

00:38 little bit later. What we have oligodendrocytes. We already mentioned them oligodendrocytes

00:46 the CNS are responsible for myelination where oligodendrocyte, they have many processes and

00:53 processes will run around and axons. each one of these processes form a

01:00 myelin segment along the neuronal axons as to the peripheral nervous system where this

01:08 is produced by swan cells and Schwan . A single s swan cell is

01:15 for single segment of this mild. here it's one process of 10 liga

01:25 can insulate many processes and many Whereas the one cell is responsible for

01:33 one segment of one axon. And between these m and insulated pieces of

01:41 are what revolve loads of ground those loads of ground deer will have

01:46 expressions of voltage gated, sodium and channels. And that's how the action

01:52 will get regenerated. Once they get at the axon initial segment near the

02:00 , they will regenerate each note of VRE and travel all the way to

02:04 exon terminal. This is what myelination like. This is myelinated optic nerve

02:14 that have been cut and cross You can see that the range of

02:19 and forming around there are pretty complex direct action or at least I think

02:26 or seven, maybe even myelin basic that are important in guiding this whole

02:33 of insulation. And there's a number them involved because some of them are

02:38 in cell recognition, recognizing between the denroy and neuron that this is a

02:45 match. Uh that is not an . So others will be responsible for

02:52 the initial contact and sheets. Uh sheets of myelin other proteins will be

02:59 how compact it and control the compaction that myelin all interacting and creating these

03:07 of myelin for the installation of If there are dysfunctions in myelin,

03:16 may end up having a demyelinating And we're gonna talk about two

03:22 So we're adding two more. We talked about epilepsy and status epilepticus.

03:28 talked about Alzheimer's disease. We talked fragile x syndrome. Excellent. And

03:40 we're gonna talk about multiple sclerosis of merit tooth disease. The multiple sclerosis

03:46 a demyelination in the CNS. So affects oligodendrocytes, right. It's multiple

03:55 sides of lesion which is sclerosis, sides are multiple. So these lesions

04:03 not form in one area of the . It doesn't uh it, it's

04:08 , it's distributed and it's different in individuals. It's an autoimmune neurological

04:17 Myelin, in this case is being by a person's own immune system And

04:26 potentially also targeting myelin basic pronouns. it recognizes for one reason or

04:36 its own produced pro dance and Mylin an invader. Uh it causes a

04:47 of inflammation in the central nervous And you will see that inflammation is

04:52 a common thread here that we see in the diseases like epilepsy, Alzheimer's

05:00 , uh multiple sclerosis, it causes . And once axons lose the

05:09 there's a complete loss of axons and of axons and loss of, of

05:16 as well. There is a genetic that involves multiple genes that doesn't mean

05:25 it's inherited. But the predisposition, not an inherited disease. The predisposition

05:33 having a disease can be passed, causes uh besides this potential genetic

05:43 then you have to have something else awakens this disease. And this disease

05:51 has an onset at the age of to 30. So the onset age

05:56 important here, onset age for you see, for example,

06:01 It's really prevalent in very young It's also very prevalent in older

06:07 Onset of Alzheimer's disease is typically 55 onset of multiple sclerosis. These are

06:15 good exam questions uh at the age 20 to 30. Uh but what

06:21 that other factor? What is that event that happens that awakens either the

06:29 or if you don't have the what is the event that leads to

06:35 and demyelination? It could be infectious like viruses. And and after the

06:42 , after the infection has been the immune system still does not recognize

06:47 infected axon. Now as its it still thinks that it still needs

06:51 attack the axons. It doesn't stop attacks normal axons. It's one of

06:56 theories, environmental factors. Vitamin D also implicated, it's more prevalent than

07:05 . There's a lot of symptoms. when we talked about Alzheimer's disease,

07:09 discussed some symptoms of Alzheimer's disease. lot of symptoms here of multiple

07:16 blurred or double vision, muscle weakness painful muscle spasms. Why do you

07:24 a person would have painful muscle The neurodegeneration is in the CNS,

07:33 muscles. Let's say my hand arm muscles are controlled by my spinal

07:40 , right? But the command is from where to control. We just

07:44 that with neuralink, it's coming from motor cortex. So if your neurons

07:51 missing insulation and different parts of the , including the parts of the brain

08:00 control movement to certain extent or control of normal commands, then you can

08:08 basically, it doesn't matter. You have myelin in the periphery, which

08:12 s swan cells, but your commands from the central nervous system are

08:19 So they don't get delivered properly for spinal cord to be executed. So

08:23 somebody uh takes something and contracts their , now the command is coming from

08:29 cortex, relax the fist, relax fist. And that information because of

08:35 demyelination, axons are lost. There no communication between neurons or it's

08:42 And it takes this command maybe 100 , relax the hand, relax the

08:47 until it can be, you clenching like this could be very

08:53 tingling, numbness because of the spasms the clenching or pain in the

08:58 legs, trunk or face clumsiness. it affects, it affects almost the

09:04 body. These effects in the periphery clumsiness. The effects of the pain

09:10 arms and legs again is the fact the fact that your muscles get sore

09:15 they're, when they work out, get sore. And if you don't

09:19 relax on it, that can get too or you don't relax them in

09:23 way that they need to be relaxed on the metabolism in the body,

09:29 and physical fatigue, mood changes and could be cognitive dysfunctions also. So

09:35 really kind of a varies across the because if demyelination happens in the frontal

09:41 predominantly, then it may affect more the cognitive functions. If it happens

09:47 the occipital lobe, it may affect of the vision or if it happens

09:52 the tracks of the optic nerve. example, it can start affecting the

09:57 and add it more blurry. So areas, motor closer to motor

10:03 Um Treatments for this disease are pharmaceutical other treatments or other are uh physical

10:14 . Um meditation, alternative treatments that out there apart from pharmaceuticals. And

10:21 you want to read more information and should know that whatever you add a

10:28 to, you should know that it's reliable source. It's not a popular

10:32 to visit NN BS National Institute of Neurological Miso and stroke. The National

10:41 of Health. Do you can type uh link these? You can click

10:46 these link to read all of the that is kind of a synthesized here

10:52 you. But it's always good to looking outside, especially for undergraduate students

10:57 this stage, looking outside and to links and resources that are reliable,

11:03 are peer reviewed of med that are by professional uh institutes uh like NIH

11:12 NIN BS and also professional associations. lot of times, especially for rare

11:19 . Uh before they get enough attention the bigger organizations, the myelinating disease

11:26 the PNS is Shaco Merit disease that swan cells and in particular affects myelination

11:35 the, and the limbs and legs arms. It's one of the most

11:40 inherited neurological disorders. So, this inherited, you have demyelination. Uh

11:47 onset age is typically in adolescence and adulthood. And in this case,

11:55 actually uh a mutation that causes uh of myelin protein called P MP 22

12:06 we're not looking at and it's So there's too much of this

12:09 you'll say, well, if it's much of some protein, then there's

12:12 to be a lot of myelin. this is not, you know,

12:16 things don't equate too much of one that out of seven may mean that

12:23 other six are not operating properly. the increase or decrease does not necessarily

12:29 to more or less uh myelin. this case, it's too much of

12:33 protein and too little of the myelin of weakness or paralysis, high step

12:40 with frequent tripping or falling balance Uh Individuals will have foot deformities,

12:48 deformities and their legs are referred to inverted champagne bottle or just their knees

12:57 buckled inside and they eat quite often pointing outwards. When the individuals that

13:04 the, the CMT may also the will walk sideways rather than forward.

13:11 their motion of walking is more swaying than moving forward. Uh It reduced

13:19 to feel heat, cold and And you'll understand why when we study

13:24 somatosensory system because it's the nerves, the installation. Therefore, the perception

13:30 also reduced. It's not only the of demand, ok. Uh decreased

13:36 of proprioception, proprioception is the ability know where your body, where your

13:43 , where your joints are with respect the rest of the body parts,

13:47 well as the earth of gravity as holds you to the earth. Uh

13:54 with the spine such as scoliosis, displacement contractors, chronic shortening of muscles

14:01 tendons around joins muscle cramping and nerve treatment. The treatment is really

14:08 So for CMT the diagnosis as early possible is very important because then what

14:15 is the deformities in the uh in bones come about because the muscles are

14:21 contracting and relaxing properly because of the of the spinal nerves of the peripheral

14:30 , those muscle contractions that are again for the arm to contract it's,

14:36 instructing it, it's demanding it, not working properly. And because it's

14:41 developmental disorder, it can reshape the . And so the early it is

14:47 and the earlier these individuals are placed braces, the higher chance it is

14:53 them to keep more of the uh and more of the proper anatomical shape

15:00 their bones, which also helps with gait, the balance and walking and

15:06 and so on physical therapy, of activity and then if they have

15:13 you know, then everybody that has gets treated by different, different

15:21 OK. So two major diseases you say there's a lot of symptoms

15:25 Doctor Z, do I have to all of them? Um No,

15:31 don't. But I think that if understand what the disease is, demyelination

15:39 the CNS moans are not being that has an effect on the

15:45 And there's pain and spasms and clenching the same happens here also because now

15:50 have the myelination in the periphery. your CNS is functioning or lingo denroy

15:56 fine. But in CMT Schwann cells degenerated and now the central commands are

16:04 , you know, wave your right hand or squeeze it and relax,

16:09 and relax. But the execution on peripheral side is failing is that

16:16 So some of these things you should PNSCNS, age of onset, uh

16:24 of the major symptomologies, but I not put, you know, match

16:28 of these symptoms to one disease and to the other. And um it

16:33 be my questions will be more OK, microglia, we already looked

16:40 these really nice image. It's involved injury repair debris, clean up.

16:44 are treated as macrophages almost at the . So they will engulf the dead

16:50 and they will eat the dead cells then ostracized will come and eat the

16:56 and then who is gonna eat the ? We don't know, maybe that's

17:03 it ends actually. So far. the end of the story. It's

17:07 developing story. So they, they uh inflammatory and immune response. They

17:14 release cytokines and cytokine release is Cytokines will come up uh call upon

17:22 immune response, call upon the immune to go into the brain and start

17:28 the repair and recovery. They're sensing oxygen species. So R OS increases

17:37 nitrous oxide uh and infections. They involved in extracellular signaling. And first

17:50 all, they release cytokines and that's they communicate with other cells in the

17:55 and the immune system. And then structure that you've seen here with their

18:01 is extending out. Once they engulf dead cell, they become like a

18:06 boy like structure actually. So they their structure. But despite all of

18:10 , they're the most mobile units in brain that will actually move through the

18:14 to execute their functions. Astrocytes uh very important in neuronal signaling and also

18:25 blood brain barrier. So what is here is two neurons, you have

18:31 presynaptic terminal again on the top here green round vesicles that are filled with

18:38 transmitter. You have this yellow oyn spine and in blue, you have

18:46 process that surrounds the presynaptic terminal and postsynaptic dendritic spine. And a lot

18:54 times this kind of arrangement is referred as tripartite synapse. So, tripartite

19:03 for three tripartite synapse where the first is neuron, one presynaptic. Second

19:12 of this a synaptic neuron. And part is the astro side process.

19:18 , what it does is it regulates content around the synapse. It

19:26 In particular, if there are local and ionic concentrations in the brain

19:34 such as potassium ostracizes will very quickly and slurp up these high concentrations of

19:45 and spatially buffer through their own extensive uh processes. But also they will

19:55 interconnected with other astro sites. And prevents from potassium having very high external

20:06 , which can be detrimental to the that this is sustained instead be spatially

20:13 and dilute in a way that rise the potassium concentration. Likewise, they're

20:20 involved in neurotransmitter processing. They re neurotransmitters that get released from, from

20:29 . And they also contribute to producing , which we already discussed as the

20:35 neurotransmitter in the brain. So they not only the ions but they also

20:42 the neurotransmitters and the concentrations of this and the amount that is available for

20:50 to communicate with. So it's almost checking how many email messages to neurons

20:56 set to send to each other by giving enough uh bandwidth or megabytes.

21:03 , synapse formation of synaptogenesis because it's intricately involved. Both actually microglial cells

21:10 ostracizes are involved in synaptogenesis, synaptic . The ability as we talked about

21:17 the ability of the synopsis to become , larger more efficacious or smaller,

21:24 , potentially be even driven away. synopsis can be formed at synaptic

21:30 We control neuro growth and retraction and most abundant W cell. And in

21:38 to that, their feet are positioned control blood brain barrier. So with

21:46 that are in the blood, you in the beauty of cells that form

21:50 walls of the blood vessels. So have the T junctions in between

21:55 And the things that are not meant cross, they do not cross from

21:58 blood into the brain. They only if they have transporters or cot

22:04 if they're super small or if they're fat soluble or lipophilic because then they

22:10 cross through plasma membranes of the Otherwise everything, it really gets really

22:16 by the tight junctions which are further by parasites and then by ostracized.

22:24 ostroy and feet is the police check from the brain side looking to see

22:31 things can pass into the brain from blood. So you have this blood

22:37 barrier. It's a great thing because separates what is in the blood and

22:42 process into the brain. When we're . We're young, we have tight

22:50 that were uh very tightly closed and older you get or if there is

22:55 infection and inflammation, those tight junctions become loose. So blood brain barrier

23:01 become loose again, it serves a protective function at the same time it

23:07 certain difficulties for neuro pharmacological drug How, uh, how many of

23:16 have thought how drugs get into the and how drugs are usually taken?

23:20 , neurological drugs, let's say anti medications. Yes. Oh,

23:30 I thought you had a question. . Well, how do, how

23:34 you take medications? How do not ? But how do patients take

23:42 They swallow a tablet fill? What happens to that table?

23:49 Yeah. Where in the gut? yeah, it, it goes,

23:56 drops into the first of all into esophagus, it goes into your

24:04 Uh your gastric juices. There are ph 3.4 or something like that.

24:12 how, how does it get into blood absorption through the digestive system?

24:29 , digestive system? Yes. Very . Ok. Uh digestive system.

24:35 . And what else happens with the system? A lot of stuff exits

24:39 from the digestive system too. so when you take a medication,

24:48 effective medication should dissolve very quickly. longer it goes into the digestive

24:54 the longer it gets processed. There's chance that only a fraction, let's

24:59 you took something 200 mg, there's a fraction of it that will get

25:04 the blood out of those 200 Maybe it's gonna be just 2 mg

25:09 , get out. The rest of gets processed by digestive system, it

25:14 metabolized. There is liver metabolism that also. Uh now you have 2

25:23 in the blood. Now you have make sure there's 2 mg in the

25:28 cross into the brain. So you to make sure that that molecule is

25:34 is very small. Maybe it can some transporter to facilitate its entry into

25:41 , into the brain. But that's to think about when you take 200

25:47 of Advil. Uh it would be . I'd be curious to know how

25:51 of that actually gets into the If you have a headache, for

25:56 , or since the headache is not in the brain, it's in the

26:02 meninges and surrounding tissues, the So again, that's not a very

26:06 indicator. Uh because the brain feels pain, it's the tissue surrounding

26:12 the brain cells and neurons have no receptors. So there's the tissue surrounding

26:17 , the meninges that have this So it's something interesting to think

26:22 And uh neuro pharmacological drug designers always about these things, how to deliver

26:29 most effectively. What if you had nasal spray? And instead of going

26:33 digestive system, it goes directly into brain. What if you had a

26:38 preparation and you rub something on your and it goes directly into the

26:42 So it bypasses these routes, can the digestive system, sometimes can bypass

26:49 . Um uh unlike the oral All right. So this concludes our

26:57 on glia and neurons and uh nobody any questions. I'm gonna move on

27:06 the next lecture. I think I how to fool this system. I

27:29 have to disconnect from it. When gets, when it gets it,

27:33 gets frozen, it gets frozen. now we're gonna move into,

28:05 it really has a mind of its . Let me pause this recording for

28:11 second and we're talking about neuronal membrane the membrane potential. What we call

28:21 potential is voltage across the neuronal membrane any moment in time. And so

28:27 we talk about resting membrane potential, as R MP, you will find

28:34 most of the textbooks say that it minus seven to millivolts. And then

28:40 other textbooks will say minus 6560 minus millivolts. It varies but it's somewhere

28:48 minus seven to millivolts. That's, where the resting me potential is.

28:52 varies across different all subtypes. So not just because it's wrong actually,

28:58 somewhere around minus 70 in this diagram 65 millimoles ring me in the

29:06 But at any given time in this resting membrane potential. This is

29:16 mill measure here on this axis and is minus 65 mills. This resting

29:25 potential is going to fluctuate minus 45 is another important value. This is

29:35 threshold for action potential. So if one given moment, this ring number

29:42 potential might be 65 negative might be might be 67 might be 60.

29:50 constantly fluctuates based on the spontaneous inputs are coming into the cell. And

29:57 some of the thermodynamic changes that are locally in the different patches of the

30:03 . So if the cell moves this , this is called depolarization, the

30:11 depolarizes. And if the cell membrane happens to reach this threshold value,

30:21 will produce an action potential. So is going to be the discussion for

30:27 next few lectures is how this rusting potential comes about and how neurons is

30:35 membranes produce these action potentials. And on when the h of Oxley were

30:43 these recordings, they would place an side of the cell and the volt

30:49 or negative potential, negative 65 millivolts compared to the outside of the

30:55 which was presumed neutral in charge or millivolts. So uh now what we

31:15 to understand is the reason why we these fast potentials action potentials, which

31:21 already mentioned in the previous lecture. about one to let's say three

31:28 neuronal action potentials. So very short because we have to react to the

31:36 world and we have to react in very fast manner. So we have

31:41 have fast electrical events and fast synaptic . And so neurons are, in

31:48 the fastest cells that you have in body for processing sensor information. And

31:54 general for their activity that they can , some neurons are capable of firing

32:01 spikes per second or producing activity at Hertz, which is a lot of

32:09 potential. And one of the reasons action potentials need to be passed and

32:16 cas and action potentials need to be passed. And the uh neuromuscular ajus

32:24 is because we have to react to stimuli, We have to withdraw ouro

32:30 stimuli. This is an example of person stepping onto a nail and immediately

32:37 the leg without thinking and that happens a fraction of a second villain.

32:43 so there's a circuit, this basic and will keep coming and uh revisiting

32:49 certain extent the circuit. When we about neural transmission, we're gonna talk

32:53 neuromuscular junction. But this circuit we started discussing that you have the sensory

33:00 , which is, which is the gangland component. You have the motor

33:05 which comes out of the ventral side the spinal cord. This is the

33:08 nerve that is going to innervate this that is going to give the command

33:13 this muscle to contract. So this here and this particular uh event of

33:23 of the patellar tendon when you have stimulation of patella tendon here, sometimes

33:30 doctor's office during regular checkup or neurologist's , they may put a little mallet

33:37 your knee and they'll see how your leg bounces up, it's uh

33:43 knee jerk stretch or patella tendon also reflex. So it actually involves

33:53 these two cells. So first of the opt out of stimulus, that

33:58 is gonna be a little valid in stimulant tendon that's going to get picked

34:04 by the sensory. So, somatosensory , central axon of the pseudo unipolar

34:13 root ganglion cell that releases glutamate onto motor neurons and excites motor neurons which

34:22 multipolar cells and the exit out of ventral side and they release acetylcholine onto

34:30 muscles to cause muscular contraction. I started a table for you last

34:35 for different cell subtypes. So if have that table digitally on the

34:41 that's a, that's a good information keep adding a listed there. The

34:46 of the cells you should know for reg ganglion cell, motor neuron parameter

34:52 . You should know um whether they excitatory inhibitory what neurotransmitter they release whether

35:00 are projection cells or inhibitory interneurons. in this particular case, the sensory

35:09 is gonna send the signal to this neuron. It's going to excite this

35:13 neuron, this motor neuron is going excite this muscle. There's only one

35:19 exci synapses between motor neuron and muscle this muscle is going to contract as

35:25 muscle contracts, extensor, muscle contracts the quadriceps, extensor extends the

35:33 Ok? Kicks it up. we all know that there is this

35:40 quadriceps and the hamstring is an opposing . And we all know that if

35:46 want to, for example, contract , you can feel it. What

35:50 to your triceps, your triceps in back is relaxed. If you want

35:56 contract your triceps, what happens to biceps? Your biceps is relaxed and

36:02 . OK. So in order for circuit to fully function and just one

36:10 , one monosynaptic connection is enough to a contraction or send the command for

36:16 contraction of the muscle. But in for this to be effective extension,

36:21 have to now excite inhibitory anti neurons live in the spinal cord. And

36:30 the spinal cord, these inhibitory interneurons glycine, they also release Gava but

36:39 mostly dominated by release of glycine. this is an inhibitory neurotransmitter. And

36:48 this same axon that gets excited, sensory axon is going to excite the

36:55 neuron. But for the reflex to affected, it's going to also excite

37:00 inhibitor into neuron that inhibitor into neuron make sure that this motor neuron is

37:07 in the silent. Therefore, there's contraction. Therefore, there is relaxation

37:11 the opposing hamstring flexor muscle and you an effective reflex and the kick up

37:18 the leg. What happens if you , for example, uh having a

37:27 and there's no reaction, you bring a big m no. But

37:35 means that there's something potentially wrong in circuit and doctors or neurologists can start

37:42 certain things. There may be not sensitivity in the sensory also root

37:48 There might be too much uh uh I inhibition, for example, that

37:54 not functioning. So the opposing muscle not relaxing and the doctor can feel

38:00 the opposing muscle is not relaxing. you can start deducing some very basic

38:05 about the serpent. And of then send a patient uh follow up

38:10 if they do indeed have problems with , with this uh patella tendon

38:16 OK. So monosynaptic is enough to contract the muscles and you have to

38:25 more than one synapse. So poly is to have an effective kickup

38:33 And this is a simple reflex. a lot of uh complex reflexes that

38:38 mediated by many synopsis and many uh in in the brain or or brain

38:45 uh such as a gag reflex, example. OK. So into neurons

38:51 the spinal cord. Wow, pretty . So there is not only that

38:58 release uh glycine and Gaba, but that there are different types of the

39:05 with different dialects, tonic firing, bursting, b, light, firing

39:10 spiking or electron firing. So they different dialects, the neurons in the

39:18 cord. And they have distinct And obviously another thing that we talked

39:24 . Last lecture is their morphology that's in subtyping neurons, their dialects or

39:31 firing patterns are important and their cells markers or molecular profiles is what's going

39:39 determine what subtype of a neuron. this case, inter neuron in the

39:45 cord is being present or being recorded or studied my neuro cells.

39:56 I just did you a huge When did I start writing this last

40:03 ? Like, so here you This is a great study guide.

40:07 you notice that I wrote in the that you'll have 40 questions. Uh

40:13 they're worth about 100 points. So all of my questions are weighted the

40:18 . They're not all two points per . Uh This typically matching question is

40:27 C subtypes that I may ask you their functions, location or neurotransmitters.

40:34 so this question may be worth five . For example, other questions like

40:38 and false may be worth a point a half. Uh other questions,

40:43 choice might be worth two points, points depending on the complexity or how

40:48 information is. Is there a question matching? For example, you

40:53 what does it mean by pre um like to uh side to?

41:00 I mean, we talked about this lecture that you have cells that are

41:05 to project out of the network uh parameter cells. And you have interneurons

41:10 are local interneurons. And you also that right here, you see the

41:20 and the neuron, it stays with spinal cord, the motor neuron that

41:24 actually projection cell that grows into into the muscles. And that can

41:29 uh this is just in the spinal , but this could be between two

41:34 networks between network A and B. gonna be cells that are projection cells

41:40 then C D in Athens, local will stay locally here. And we

41:49 talked about how there's a greater variety these interneurons. And also we're seeing

41:55 not only in the hippocampus, we're seeing a great variety of morphological distinct

42:01 and functional, distinct subtypes in the cord and the interneurons. So that

42:07 , you know, not that much in the motor neurons, but more

42:11 in the inhibitor interneurons that essentially control , how much of that information is

42:18 between networks or how much of the muscles in the case of the reflexes

42:24 inhibited or in what pattern it may inhibited. So, yes, please

42:31 this. Uh And uh you'll be . The cast of chemicals.

42:43 OK. No, I started you finish it. So it's

42:51 it's a powerpoint. So you can uh you know, insert more uh

42:57 uh as we study more information. , the cast of chemicals that creates

43:04 potential across number. And then we about this resting memory potential minus 65

43:11 , we have ions, we have that surrounds or these ions are dissolved

43:16 water, it's uh polar. So both inside the so and extracellular fluid

43:22 it's oxygen that attracts extra electrons and negative charge. Hydrogen has positive

43:29 You have h2o other polar molecules dissolve water. Very basic stuff. Ions

43:36 atoms of molecules that have a net charge. They form ionic bonds such

43:42 sodium fluoride salt difference in the number protons or electrons is what we call

43:49 valence or charge. So you can N A plus which is monovalent versus

43:56 two plus, which is divalent CS positive charge and A plus versus anions

44:04 negative charge like chloride minus, for . And that's just a little type

44:11 the. So some basic stuff for . So uh sodium chloride here,

44:18 example, is dissolved in water and dominating in that extracellular fluid. Um

44:26 is just the repetition, CS and . The CS and anions will be

44:32 by water molecules. And we refer these spheres of hydration or sometimes cloud

44:38 hydration because depending on the size and charge, the spheres of hydration will

44:45 have a different size, depending on size and the charge of the ions

44:51 bilayer in the membrane. We already about the hydrophobic versus hydrophilic components.

45:00 hydrophilic is dissolved in water due to electrical charge. Uh but these stay

45:08 , they don't dissolve. So, are hydrophobic and they contribute to rusting

45:12 action potentials. So you have this . This membrane is what separates the

45:19 and ions cannot cross through this phospholipid . They need channels in order to

45:27 the plasma membrane, they cannot they cannot squeeze themselves in between the

45:34 hydrophilic and hydrophobic compounds there. Uh we have amino assets which are the

45:43 blocks for proteins and building blocks for of interest for us which are channels

45:49 in this case, ion channels. for the next three lectures, we

45:53 talk about voltage gated or voltage dependent channels, especially when we get to

45:59 action potentials. Next lecture. But acids are you building blocks, they

46:06 peptide bonds in between them. You essential and non essential amino acids.

46:13 amino acids are the ones that you to ingest. So they do

46:18 you do not synthesize them. They from your food dietary intake. Quinoa

46:25 one of the best grains that has of the most diverse composition of the

46:32 amino acids um which is really cool if you don't use quinoa and in

46:39 diet, I don't use enough of , but I just used it the

46:42 day. So I talk about Uh it's a pretty cool grain,

46:47 know, because sometimes when you're cooking or especially if you're preparing food

46:54 Uh It's difficult to think of like is gonna be my carb, what

46:58 gonna be my protein? What is be my veggie you know. Uh

47:04 and when you start thinking about it's like rice, pasta, uh

47:10 , rice, pasta, potatoes, , fries, pasta. No,

47:18 you know, so it's important to all of these different grains like you

47:22 , on your diet. So these acids, they serve as building blocks

47:28 proteins. They have these primary structures become secondary structures and as they wind

47:36 into that al he don't exist or in the south and native sheets as

47:42 secondary ter structures, the co sun . So the secondary structures is a

47:52 . These transmembrane segments come together and ordinary structure, uh tertiary structure of

48:00 subunit. These subunits come together and form the whole channel and the composition

48:07 these channels could be from several different of sub units. So they will

48:13 different designations such as alpha beta gamma some other protein channels like NR one

48:20 two. So you have proteins, have polar R groups, nonpolar R

48:28 . These proteins are selected for they're selected for specific ions. That

48:34 that an ion channel selected for sodium going to conduct sodium. A channel

48:41 for potassium is going to allow for to flux through it. Calcium is

48:47 to allow for calcium to flux through lot of these channels are voltage gated

48:52 we'll talk about. When we talk neurotransmission, we'll talk about Ln gated

48:57 channels, talk about auditory system and we'll talk about mechanically gated uh hair

49:04 or mechanically gated potassium channel. So is gonna be more information coming your

49:10 . So, thank you very much your patience and I hope everyone has

49:14 good weekend. Uh, the rest the week, you know, I'll

49:17 everyone here on Monday.

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