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00:03 this is neuroscience. Midterm to review . We spend about a third of

00:11 second section of the course, focusing the neural transmission. When we talked

00:18 neuro transmission and neurons and the N. S. We discussed that

00:22 are two types of synopsis, electrical chemical have distinct features distinct anatomy.

00:27 electrical synopsis or connections that form the junctions that allow for the passage of

00:33 molecules and ions across freely. It's instantaneous activation across the gap junctions of

00:39 population that allows for neurons to synchronize large populations so they can produce a

00:45 effect downstream into the interconnected networks. then most of the rest of the

00:51 we spent talking about the chemical neural . And when we started talking about

00:56 neural transmission, we actually first focused neuro muscular junction. And we talked

01:02 how neuro muscular junction is a fairly it's a very large synapse. The

01:08 has so many different ramifications, forms templates. And when these synapses are

01:15 will contract muscle fiber that they're projecting . And so uh whenever you have

01:24 of a single clothing from neuro muscular This is a neuro muscular junction.

01:31 will cause the end plate potential. is the end plate potential is this

01:37 portion and this is the muscular action . So the in place potential is

01:44 going to be about 70 million balls size and it will always reach the

01:50 value for the action potential generation. a very powerful sin ask. It

01:57 has nicotine acetylcholine receptors because it has acetylcholine receptors and has no other signaling

02:05 inhibition then uh it's only excited for . Okay, nicotine acetylcholine receptors are

02:14 close to the synaptic flat and deeper you have all the educated sodium calcium

02:20 potassium channels. And so this is to produce a very long muscle

02:27 Very long action potential in the It's in the water of about 300

02:33 for more. Okay, these are simple synopsis they're very efficient. Synopsis

02:39 have the ability to recruit a few from the spinal nerve and move one

02:45 . A few more fibers move two for a lot of fibers. It's

02:49 recruitment but actively release these nerve vascular . You can recruit the whole arm

02:55 the whole shoulder and so on attached them. So these are systems neurotransmitter

03:01 , the seal cove, inn is of these neurotransmitter systems. So you

03:05 that there are different neurotransmitter systems. have classical amino acids which is glutamate

03:12 and glazing. We have the means we discussed and some of them we

03:17 in great detail like acetylcholine and we about peptides and the differences between synthesis

03:24 release of neural peptides versus transmitters. in addition inside these boxes we added

03:31 the cannabinoids and we added the metric oxide and monoxide and also academic

03:38 said that those are different. They're stored in the vesicles, they're not

03:42 in the Secretary Granules like peptides would rather they remember insoluble they're synthesized on

03:49 and they function and reprogrammed faction will that in a second. There are

03:55 are synthesized more when there's heightened levels activity stored in Secretary Granules and released

04:01 not as specifically as neurotransmitter vesicles would which arm mostly released and serviced at

04:08 level of the pre synaptic terminal. the pre synaptic vesicles fuse and release

04:13 . You need the action potential. deep polarization prison optically which now opens

04:19 gated calcium channels and the influx of is the second thing that is necessary

04:24 the protein protein complex to be activated the vesicles membrane to fuse with the

04:29 membrane to cause excessive doses following which will have the psychosis of the

04:34 Talk about how there was an interest understand which part of the membrane

04:40 which elements proteins and such to visualize junctions to visualize the fusion of the

04:46 . And also we mentioned an interesting . It's a die and it's imaging

04:50 the dye that is sensitive to So we talk later about different imaging

04:56 in the clinical settings such as pet and F. M. R.

04:59 . We also in the visual Talked about more experimental imaging such as

05:04 sensitive dye imaging intrinsic optical signal And this is also an experimental technique

05:10 you can image the fluctuations. The temporal dynamics. The spatial and temporal

05:16 the concentration dynamics in this particular case calcium ions. So this is calcium

05:22 dye and imaging most of the end psychosis and recycling of the neurotransmitters is

05:28 here at the pre active pre synaptic zone. Sometimes vesicles will be re

05:37 into early under some and reprocessed um acetylcholine signaling which uh acetylcholine obviously will

05:49 a bicycle. Your translator will be there in this case a meeting and

05:55 have botulinum toxins that are produced by botulinum that will target this protein protein

06:00 complex. So we talked about how are pharmaceutical drugs and there are also

06:07 of abuse and also there are chemical nature and toxins that can impede with

06:15 systems with the release of the With bio synthesis of neurotransmitter with the

06:22 of neurotransmitter with the binding of neurotransmitter optically all along this different chain of

06:28 neurotransmitter systems. We also talked about and how organophosphates cyclical industries inhibitors.

06:36 welcome back to that when we highlight in the next slide. So unlike

06:42 neuromuscular junction which just has nicotine acetylcholine just has the potential uh N.

06:50 . N. S. First of when we talk about acetylcholine, we

06:53 about nicotine IQ and Mascarenas. Acetylcholine . Okay so we know that nicotine

06:59 uh and muscular nick and the same . The cns will have a different

07:06 effect. Now when we talk about and c n s we talk about

07:13 . P. P. S. in the neuro muscular junction and plate

07:18 is not excited words and plate E. P. S.

07:23 Is excitatory post synaptic potential. And C. N. S. Apart

07:32 excitation, we also have inhibitory post potentials. Unlike the employee potentials,

07:40 E. P. S. S. A very small in size

07:42 order of a fraction of the And so in order for the membrane

07:49 to reach the threshold value for the potential in the C. N.

07:53 . You will have to have summation activation of multiple excitatory synapses in order

07:59 reach the threshold, which is not case at the neuro muscular junction.

08:04 you will have not only excitation but will also have inhibition which will be

08:09 hyper polarization in the system and potentially the deep polarization levels that would generate

08:17 action potential and the action potential is the duration of about two milliseconds.

08:23 is in contrast all to the what seeing at the level of the

08:28 So, so, an interesting For example, if I'm telling you

08:33 the fiber recruitment for the muscle one finger or move the finger versus

08:38 the whole finger or the hand, it versus one finger then in other

08:45 . For example, the cardiac muscles that doesn't typically happen because you wouldn't

08:50 to just partially open the valve or close it, that would cause a

08:55 serious cardiac problems. So E. . S. P. S.

08:59 are mediated by glutamate mediated by the of positive ions such as sodium and

09:06 to some extent. And the P. S. P.

09:08 Which are gaba mediated by the influx the an ion chloride inside the

09:15 And there are two components, the I. PSP. In the late

09:18 . PSP. Because we have here tropics signaling. In some instances mental

09:26 signaling neurotransmitters will activate. G protein receptor, G protein will immediately affect

09:35 nearby channel. So we'll talk later this as a shortcut pathway. There's

09:40 intermediaries between the decoding coupled receptor the protein channel and there's sometimes enzyme activation

09:48 downstream secondary messenger activation. And creation other intermediaries such as highnesses and hospitals

09:55 then affect the adjacent ion channels. for acetylcholine, I encourage you to

10:02 everything. The synthesis of acetylcholine, acetylcholine ester is the fact that most

10:09 the alzheimer's medications are cyclical unnecessary is . So by inhibiting the cyclical

10:16 make more civil coding available here in synopsis. There are cooling transporters that

10:23 transport molecules back to pre synaptic Re synthesize to prepare them for the

10:31 . Again, we talked about the that each one of the nicotine will

10:37 an agonist from nicotine IQ and must will be an agonist for most

10:41 So equally each one of them will their own antagonists such as curare and

10:47 for civil code in the clinic and subjects. You should know that for

10:51 exam as well. Then we talked other types of means and there were

10:56 tables that showed you how certain means precursors to other means such as

11:02 precursor of norepinephrine, norepinephrine as They slightly have, they different

11:08 They have the same type of signaling the fact that they released and they're

11:14 broken down or recycled back in the of the cattle colonies and the pre

11:18 terminals and they're broken down there by . I mean oxidizes in the prison

11:25 terminal. So regulating mono amine oxidase also another level of regulating the amount

11:32 cata column means blocking the re uptake cattle colonies, blocking the re uptake

11:38 serotonin is also a strategy for both drugs but also elicit street drugs such

11:45 cocaine. Uh Now you don't need know the synthesizing intermediaries for these molecules

11:53 you should probably focus on knowing the that we discuss on certain types of

12:00 . Again for assets. An interesting to know is glutamate gets converted into

12:05 with the help of atomic acid, box delays. And so all of

12:09 inhibitor inter neurons that release Gaba will positive for God with one of the

12:16 that we discussed um you know history for in situ hybridization, for

12:21 Uh serotonin when we had some descriptors we said wait a second. Some

12:26 these things mood appetite sleep learning. then we also have mood regulation by

12:32 cola means. Yes there's some overlapping . Their serotonin again. Uh five

12:38 . T. Will be recycled back the trend. Sport is so

12:43 Antidepressant medications that you see on the they will be referred to as serotonin

12:49 uptake inhibitors sa rise and this is re uptake. This is a re

12:57 of serotonin and you're inhibiting serotonin re of one of the classic uh depressant

13:04 brand name PROzac. There's also involvement M. A. O.

13:08 And degradation of these amine molecules. so there's also medications that controlled

13:14 A. L. S. That pretty significant antidepressant medications. It's interesting

13:19 with some of these things it takes three weeks to see an effect on

13:25 like M. A. O. . That are involved in in the

13:29 and metabolism of these elements. And cannabinoids are different. We talked about

13:35 fact that the cannabinoids produced when there very high levels of activity. Pre

13:43 lee even excited for inhibitory South will production under freely across the plasma

13:49 Retrograde fashion that will go from boston the pre synaptic size bind to g

13:54 coupled receptors close the calcium channel and the release of both excited for and

14:03 governor transmitters. The two most common in the cabinets and lander mind and

14:10 our aka donald glycerol and the most and demonized broken avenues that comes from

14:17 plant also buys the CB. One is delta line tetrahydrocannabinol delta nine

14:25 So you know the differences between and hybridization, antibodies versus strength of

14:33 R. N. A. Uh situ hybridization versus the immunity chemistry which

14:38 antibodies. Remember that another technique to neurotransmitter activity of study neurotransmitter activity on

14:46 Southeast neurotransmitter mimicry. And we also UNQ aging of the neurotransmitters. So

14:53 difference is that in this type of you're applying the fluid and then uncaged

14:59 of the neurotransmitters. They're actually cage chemical cages and your photo allies ng

15:04 light those cages and you can get lot more of the spatial and temporal

15:10 dimensional specificity using uh the caging of rather than these more classical older techniques

15:20 infusion which will lend itself to laws diffusion and will spread accordingly from higher

15:29 zones and low concentration zones. Making not as specific as an caging of

15:34 neurotransmitters. Uh in order for this to reach the action potential threshold neurons

15:43 certain responsibilities and some of these responsibilities some of these strategies are that they

15:51 spatial and temporal summation And neurons that been dirty cables of course they

15:58 And we know that the dirty cables not insulated. That means the current

16:02 going to leak out over the inverted . So we talked about the life

16:07 neurons that have a long lead That means from a maximum 100% of

16:12 current located here. It will take long distance For it to die down

16:18 37% of its maximum value which is the λ or the length constant value

16:26 this neuron. So length constance, sells a very long length constants.

16:32 great for especially temporal summation. And we talked about the fact that uh

16:41 receive excitation of addition. And if receive excitation distantly in the dendrite and

16:49 approximately there is an inhibitory input at level of the soma. You may

16:54 detect any difference at all because there be active inhibition. There will be

16:59 of the current through the shunting And so you need to really activate

17:04 lot of the excitatory synapses and then in order for the selma to see

17:11 small response because a lot of the recall. So you have to recruit

17:15 lot of synapses 40 50 60. synapses for the soma to reach the

17:21 for the action potential generation. This uh an interesting diagram which shows norepinephrine

17:28 norepinephrine through the production of a dental and cyclic GMP produces protein kind they

17:35 . And this protein kind they say really potassium channel and actually open the

17:44 channel and this is a similar mechanism we see with medical tropical acetylcholine

17:50 And so there are similarities, there's molecules that we discuss that actually can

17:55 through medical tropic cascades potassium channel such medical tropic acetylcholine norepinephrine gaba B

18:06 Okay, so there's some redundancy that talking about in targeting either the synaptic

18:12 channels or the pre synaptic. Both calcium channels for example, we'll come

18:18 and talk about that in a Okay, I think this ended this

18:27 . We moved into the next This is one more quick review for

18:33 of all of the neurotransmitter systems. that girl I seen is a major

18:41 in neurotransmitter in the spinal cord glycerine actually involved in the excitatory receptor signaling

18:48 receptor signaling in the brain. Uh is just a little bit more review

18:55 continued mascara in it. This is masculinity. Acetylcholine receptors that go through

19:02 shortcut tackling. So instead of what say through the intermediary faculty with more

19:06 an upfront with medical tropic, the is the same potassium channel. But

19:13 you don't have an intermedia is that protein subunit that's catalyzed now uh can

19:20 this potassium channel. So in academic receptor activation. CNS will cause a

19:27 polarization. Most chronic activation by opening channel positive charge. Leaving the cell

19:33 have the opposite effect will have a polarization. So we see that in

19:37 cns you can have the car and tropic versus metal tropic signaling with the

19:42 molecule cause two different effects on the cell. Um we call that with

19:51 assets and with glutamate when we talk communication between two excitatory synapses in particular

19:59 talk about tripartite synapses neuron one pre neuron to post synaptic and the third

20:05 of the synapses. We, because only neurons have intimate neuronal transporters,

20:13 release and exerts its Bhasin optic Get transported back to synaptic reloaded into

20:20 but also we ourselves have the glial transporters and they're capable of picking up

20:27 turning it into glutamine and then giving back to neurons convinced emphasize glutamate out

20:35 glutamine using contaminants. So here you a very clear demonstration of how the

20:42 of excitatory neurotransmitter glutamate is quite tightly and modulated by the astro glial cells

20:51 particular and not just by neurons and can decide it's getting more or less

20:57 decided. I mean let's say it alter the function of its transport,

21:02 may alter the function or the speed the breakdown of the molecule for it

21:07 return into neurons And so we definitely excited for neural transmission and then we

21:15 back and talked about cattle common means some of their functions. This is

21:21 some of the review and and since discussed that I am a tropic and

21:26 tropic and have opposing the actions And said well can to medical tropic have

21:31 actions and we looked at this just norepinephrine activating basically turning on the production

21:38 protein kinda say. And it's going do it if it binds the debate

21:42 receptor which is linked to G. . A. Stimulus authority protein

21:47 But if that same molecule norepinephrine binds alpha two receptor that's linked to the

21:53 . I. Division and this molecule going to basically increase the amount of

22:03 . So in this case we're talking downstream secondary messenger effects protein, chinese

22:10 , hospitals production. Remember that kinesis correlate at P. 04 group hospitalizations

22:16 defrost for a late protein channels for . And so this is referred to

22:22 push pull system. This is pushing produce more cycling and p including finance

22:27 pulling the system away from producing more the sporting finding saying So now you

22:33 an example of how to medical tropic can have an opposing different effect on

22:40 downstream signaling within the south amines are . And unlike the immune assets which

22:47 widely expressed throughout the brain the means their own specific nuclei where they have

22:54 soma the nucleus ford or local civilians going to be selma's of neurons that

23:02 these are all of the projections and arrows, external projections that will innovate

23:08 and also sub cortical regions going all way into this final cord wrapping nuclei

23:13 serotonin and then you have to see lateral fundamental nuclear magnet seller of basal

23:23 . So small populations of mirrors that these mean transmitters but they diffuse distribute

23:32 throughout the brain. Is very non innovations that are cortical and also sub

23:39 . So when we talked about when cannabinoids I had this D.

23:43 I. And then later said well S. I. Stands for equalization

23:47 compression position. And so the actions under cannabinoids and actions of THC was

23:53 discovered in in neurons by neurophysiologist and Because Canada's gets people high. So

24:00 they thought probably the receptors are not the stomach and the brain. So

24:04 gonna go look for effect there. discovered the control inhibition and then later

24:09 DsC was added because also experiments were where there was a clear example of

24:15 Canavan was also regulating levels of excitation it's regulating levels of excitation through regulating

24:23 pre synaptic, low educated calcium channel neurotransmitter release. And that's also a

24:29 story among some of the other neurotransmitters we looked at. Just like

24:34 Gaba also has its own transporters into pre synaptic terminals has transported into the

24:39 and everything along the lines of the . The synthesis their delegations transport and

24:47 synaptic receptor effects can be potentially pharmacological glutamate for anna tropic signaling functions through

24:58 and NBA incarnate receptors with their respective as soon as glutamate is released and

25:04 bind to receptors and binding of glutamate enough to open up the receptors and

25:09 the initial D. Polarization. So the E P. S.

25:14 S are produced in the C. . S. They had the early

25:31 and this early component is ample component they have the lead component. This

25:38 component of G P. S. . Is an M. D.

25:42 receptor components. So as soon as binds ample receptors it starts D

25:47 The plasma membrane magnesium is blocking an . D. A receptor. And

25:52 deep polarization from rust to more D levels will alleviate the magnesium block and

25:58 up an M. D. A that's going to be responsible for the

26:02 uh component. Late currents of the . P. S. P.

26:08 not an M. D. A . They are activated fast but once

26:13 NBA receptors are activated they will conduct lot more 50 Pecos emails of card

26:18 takin it will have their own antagonists is seeing Q. X. And

26:23 . D. A receptor will have antagonist A PV. And we discuss

26:26 when we look at the ivy plots AMP and an M. D.

26:29 receptor currents an M. D. receptor is referred to as coincident detector

26:34 it's coincidentally needs to detect glutamate binding release prison optically glutamate binding and deep

26:42 personality. So if it's just deep and M. D. A receptor

26:47 not going to open if it's just it's not going to open. But

26:51 it's glutamate and deep polarization is coincidentally detecting pre synaptic synaptic activity will bind

26:58 two and will have a significant Glycerine acts as a co factor that

27:04 the presence of YC. Glutamate binds NMDA receptor and promotes full act the

27:09 of an M. D. A . And NBA receptors are all formidable

27:13 sodium calcium and potassium and has multiple sites. So it has binding sites

27:19 the neurotransmitters. Some of the neurotransmitters also be competing with some of the

27:25 that are exogenous molecules. So when two agonists are competing for the same

27:30 on the protein to bind to the called competitive agonists antagonists are competing for

27:35 same lock. The two keys sit the same lock um They're gonna be

27:42 antagonists in that respect. And there's binding sides. PCP which is uh

27:51 a drug can cause significant effects of M. D. A receptor that

27:55 be long lasting effects. So besides accurate hallucinations or bouts of psychosis,

28:01 systems can actually buy one or two activation. But some of the list

28:05 drugs can break and you may have chronic cases of psychosis and schizophrenia that

28:12 from crystal methane use and some other hard addictive drugs and cato one we're

28:18 his antagonist in NBA receptors that once is bound to an M.

28:22 A receptor that an NBA receptor is , it also changes its confirmation and

28:28 opens new holes for new keys to new laws and new keys to come

28:34 and say okay to one will bind the NMDA receptor only if it's open

28:39 means that it can be floating around it cannot bind anywhere. But an

28:43 . D. A receptor opens and a new crevice amina assets for that

28:48 to bind. It can then bind the NMDA receptors. Remember NMDA receptors

28:53 not medical traffic so meta but tropics . And we looked at very briefly

29:00 then uh glutamate inedible tropic signaling. then we came back and talked about

29:04 tropic glutamate signaling and bipolar cells in retina. All searches this diagram shows

29:09 if you use voltage clam and you the number of potential from different holding

29:14 from minus 60 plus 60. It several things. First of all this

29:19 is you have glutamate but you also the last have normal physiological concentration of

29:24 which is $1.2 million minus 60. don't see much of an NBA cars

29:29 30. You start seeing them and currents reverses zero million volts. So

29:34 ample as we saw in the So it is the holy PSP.

29:39 does the CPP they all reverse zero volts. And the I PS PS

29:45 would reverse IT chloride reversal potential which give minus 70 million volts. Now

29:50 you remove the magnesium from the extra solution. So you have this experimental

29:55 . Now you illustrate that in the of magnesium, even if the hyper

30:00 resting membrane potentials and receptor will be will still reverses zero million volts.

30:06 that proves that magnesium indeed is blocking the reception, the absence of magnesium

30:12 is enough to activate. That an . D. A receptor. When

30:15 studied the curves and we described this in which there was a stimulation and

30:21 was released and there was a post response recorded in the current. So

30:25 is voltage clamp recording and two measurements taken the early component, the early

30:30 and the late current. And we that the early current which is ample

30:34 is linear. And we voted zero balls. I say it's a vessel

30:40 because it's multiple ions flux into ample such as an M. D.

30:44 . Receptor also. And these closed open triangles is the response of this

30:50 component which is linear component, not M. D. A component measured

30:54 at the first line closed triangles and triangles in the presence or in the

31:01 of a P. V. Which an M. D. A receptor

31:04 . And this is an occurrence. says the early currents are not affected

31:08 an M. D. A receptor and they shouldn't be because a tv

31:12 and M. D. A And these circles the closed circles show

31:18 an M. D. A. is nonlinear. So you don't have

31:21 in India current at negative potentials. you have an M. D.

31:24 . Current that increases when the cells deep polarized. A number of potential

31:28 of minus 15 minus 45. You persistent in M. D.

31:33 Currents that reverse them zero miller balls and prefer to conduct in the opposite

31:38 . So an M. D. . Chart here. This I.

31:41 . Plot is taken from the second line which measures the late component of

31:45 E. P. S. And M. D. A.

31:47 is this whole blue area under the . And so if you apply to

31:52 Tv would essentially block this hole area the curve that is blue. And

31:57 are the open circles in the presence a P. V. And

32:01 D. A. Currents. Except some little residual currents. And these

32:04 circles are blocked and are staying at zero PICO ampere value. So that

32:11 that a PV does not affect the component and it's a linear component.

32:16 M. D. A. Is nonlinear component in the presence of an

32:20 . D. A. You will zero in the presence of a

32:23 D. Which is antagonist for an . D. A. You will

32:25 zero current flexing through that receptor. you recall all of the N.

32:31 . D. A receptor channels are to sodium calcium and potassium and

32:38 Some of them are permeable to Others are not. But this is

32:42 significant example that shows that within these dimensional protean channel structures, substitution of

32:50 single immuno asset and thousands of amino can now determine whether that channel is

32:57 to be permeable to calcium or So we saw that the substitution here

33:02 argentine are will now block the flux calcium for an M. B.

33:07 . Through ample receptions are early in development only an M. D.

33:12 receptor of present. So they're called synapses because there's not much of the

33:20 synaptic deep polarization that are happening ample are not there. There are other

33:25 by which in India receptors get Apart from emperor activation and the developing

33:32 and also the subunit composition that comprises different receptors. They may shift during

33:37 development. So in an M. . N. M might be a

33:41 ratio of subunits at one stage of versus later stage of development. And

33:47 is very important for L. P. Which stands for long term

33:51 for long term potentially ation because of coincident detective pre synaptic post synaptic activity

33:58 properties and M. D. A serve very well positioned for mediating and

34:04 of the calcium in mediating the plasticity the pre synaptic and post synaptic connections

34:10 therefore their effects on an M. . A receptor can be very significant

34:15 many different perspectives, ample receptors they most mobile from these glutamate receptors and

34:22 can actually enter into the synaptic space the extra synaptic spaces through this fluid

34:29 model of the plasma membrane. But a very fast fashion micrometers in

34:36 So medical tropical intimate receptors when we as we study the breakdown of

34:41 I. P two by activation of I. K. C. And

34:45 the divergence of the cascade into P. Three activation of I.

34:49 . Three recep calcium channels that are into plasma particular and the member inbound

34:57 which states and can activate another molecule remember that what what is going to

35:02 is that these timings and foster cases going to modulate the phosphor relate and

35:09 correlate different proteins and protein channels. there is a significant regulation of these

35:15 inside the cells. This is an of how metabolic tropics signaling would be

35:19 place. And that is not to confused with an M. D.

35:22 receptor which is ion tropic but it delayed activation and it has a magnesium

35:29 . When we talked about inhibition we about Gaba and Gaba a receptor in

35:36 which allows for the flux of Gaba A receptor also has multiple binding

35:41 who decides Gaba which is an endogenous in the brain, ethanol alcohol will

35:47 to Gaba receptors. Benzo dad barbiturates, no steroids will also bind

35:53 Gaba A receptor agonists. Most of substances that actually all of the substances

35:59 seeing here that agonists Gaba A So binding of gaba gaba a receptor

36:04 increase inhibition. It's a sedative. increase inhibition, its anticonvulsant, anti

36:13 , it's a sedative barbiturates, Okay, it's all increasing inhibition,

36:20 one or two glasses is sedative beyond you lose inhibition. So then it

36:25 something something different. Now Gaba You can see signaling through chloride and

36:32 B past synaptic aly signaling potassium So we talked about the two components

36:38 inhibition. Gaba A, which is by chloride and chloride is coming

36:45 And Gaba B, which is mediated metabolic tropic opening of the potassium channel

36:54 very similar to what we talked about muscular acetylcholine receptor. So now,

37:00 in this review because we're going so master stuff, you actually can connect

37:05 things and see some of the redundancy the systems and the functioning of these

37:10 in this case it's potassium is going be going out. Both of these

37:15 hyper polarizing effect. So unlike nicotine locally versus most chronic, they had

37:22 effects on the membrane. You can additive effects hyper polarization through iona tropic

37:28 A and more hyper polarization through medical Gaba B receptor and three cinematically because

37:36 talking about voltage gated calcium channels located synaptic Gaba B receptor can also block

37:42 gated calcium channels which will control neurotransmitter . I use the slide here and

37:48 said hey this is a really good . You can actually erase the figure

37:53 if you want to copy the image put all of the notes that you've

38:00 . For example this is gather be spots, synaptic potassium channel.

38:07 And what else opens part synaptic fashion about perceptive. So you can put

38:14 your nose yourself a similar mechanism. here you can label yourself instead of

38:20 at the key, you can sort Gaba A. Because it's chloride Gaba

38:25 . Because it's potassium. And what talked about here, we talked about

38:29 you have an inhibitory synapses can release cause inhibition through Gaba A. Cause

38:34 inhibition through Gaba. D. But can also regulate its own release through

38:39 auto receptors. So Gaba B receptors are located on the pre synaptic inhibitory

38:45 , they will essentially shut down the through regulation of voltage gated calcium channels

38:52 they will self regulate the Gaba However there is a lot of Gaba

38:57 Gaba spills over. It also has cis optic receptors on the adjacent excitatory

39:02 and activation of the Gaba B. the pre synaptic terminal of the glutamate

39:08 can now regulate dramaturgical elements. We talked about how Gaba B can also

39:14 located post synaptic aly on these excitatory and that. Although glutamate is being

39:21 here through calcium influx and through the messenger cascades. You can actually activate

39:29 B receptor. And that Gaba B will open. potassium channels will cause

39:34 hyper polarization. That will basically start an M. D. A channel

39:42 opening by causing the hyper polarization. you can see these really nice interactions

39:48 between the inhibitor and excited synopsis. complexity that you see here that you

39:52 see in the neuromuscular junctions. Okay like I said this is a really

39:57 slide to take notes about what's happening what you've learned about. And when

40:03 talk about inhibition this is Gaba and B. So when you stimulate this

40:09 lateral nuclear itself and the relay cells the lateral nuclear nucleus. So when

40:15 stimulate an optic nerve and optic tract this case optic tract input into the

40:21 . G. M. You get followed by inhibition. If you block

40:27 A. With bike you colon, is with Gaba A. You can

40:32 excitation followed by inhibition. Small excitation you blow Gaba A. And you

40:38 the same stimulus boom, you produce abnormal excitation in these cells. So

40:44 does inhibition do? It really sculpts C. P. S.

40:47 S. It sculpts the excitation levels deep polarization levels in the south G

40:54 coupled receptors. We reviewed our seven membrane the receptors that are linked to

41:00 G protein complexes multiple different muscular We just mentioned one but there are

41:06 of masculinity and 12345 medical tropic glutamate through 12, maybe 14 since I

41:14 last time. Uh dopamine same Opioid cannabinoid CB one we talked about

41:20 one. CB two are mostly on wheel cells, will come back and

41:24 about it a teepee which buys the and receptors and we looked a little

41:28 in the ligand, trance mitigated channel and has these M one through M

41:36 trans member in segments. And there some similarities between some of the segments

41:42 some of the coding. And these are usually coming in different flavors.

41:47 alpha alpha, this is nicotine. receptor has five subunits to alpha

41:53 That's where the two molecules of acetylcholine going to buy the number, you

41:57 to buy two molecules in order for uh receptor channel to open. So

42:03 for this diagram you should know acetylcholine step dives agonists and antagonists acetylcholine

42:12 You should know the push pull system alpha and beta receptor systems for

42:20 You should know everything to an M A and an M. B,

42:23 C. And Q. X. a PV. For Gaba, you

42:27 know that there's Gaba, a laura b potassium. We only mentioned by

42:32 colon as an antagonist for Gaba A for a T. P. We

42:36 to Dennis and track prostate will also as a neurotransmitter. So that's another

42:42 that I left off of that initial were added under cannabinoids, orthodontic acid

42:48 and a denizen triphosphate. Denizen triphosphate also bind the denizen receptors. A

42:55 receptors. What they do a denison of the denizen receptors will close present

43:02 the calcium channel and excited to a . So dennison will reduce the amount

43:08 glutamate. It's an agonist but it activate the G protein and will close

43:15 channel. So it will activate G caffeine is an antagonist. So by

43:22 this pathway calcium channel. Stay open the calcium channel stay open and glutamate

43:28 getting the proper release and that's what you up in the morning when you

43:32 a cup of coffee and then we a significant amplification through neurotransmitter systems and

43:39 have the systems that can divert the that can converge systems that can work

43:43 parallel overlap and target the same effective we just saw that you can target

43:49 potassium channel through gotta be masculinity You can even target through norepinephrine but

43:55 a slightly different pathway that leads to in different defector. And uh let's

44:06 this actually concluded our neuro transmission So if there is any questions in

44:14 or on zoom, I'm running really on time but I would be happy

44:20 take a couple of questions. If I'm gonna take a couple of sips

44:26 water and continue with the C. . S. You guys missed your

44:42 couple of questions. Sleuth 400 blue fly high with an M.

44:59 . D. A. Receptor. is the neural transmitter. Glycerin is

45:04 co factor. So binding of licensing the proper binding of glutamate, proper

45:09 of an M. D. Receptor. The studies that are being

45:12 to what extent can you open an . D. A receptor and reducing

45:16 amount of glycerin or in the absence it. But for it to be

45:20 functioning it's a co factor that has co binding to a different site than

45:25 . It's not competing for the same in order for that an M.

45:29 . A. Receptor to properly Okay. C. N.

45:34 Uh We have about 10 minutes. C. N. S. So

45:40 your medical terms location? Centerior posterior, caudal dorsal, ventral,

45:46 sagittal, horizontal kurono. We talked how you have development of the brain

45:55 that. We discuss the three men said dura arachnoid and the PM.

46:00 talked about subdural hematomas that can happen maybe the brain trepidations were also used

46:05 alleviate the damage from subdural hematomas. production of cerebrospinal fluid and cord plexus

46:11 gets circulated throughout the cNS and the cord that we're talking about and some

46:19 If there's overproduction of the fluid needs be drained if it is not it

46:24 cause a bad shape of the skull the brain. This condition called

46:30 We then looked into how you have primordial tissues and the meso ecto derm

46:35 how the neural plate and the neural formation happens from the extra term.

46:41 you have this process of no relation during this process of no relation.

46:46 there is a dysfunction in roster, may end up with anencephaly dysfunction with

46:52 folding of the neural tube may lead spin bifida bifida be surgically corrected.

46:59 then from this neural tube you have process formation of forebrain, midbrain,

47:05 brain and further differentiation of forebrain into talent cephalon phallic vesicles and diane cephalon

47:12 is thalamus and hypothalamus optic vesicles. we traced the differentiation of midbrain for

47:20 into corporate quadra gemini, this superior and Nero caligula pointed out the major

47:26 in the in cephalon thalamus hypothalamus, connectivity here through corpus callosum of the

47:32 hemispheres. The projections from the thalamus, cortical and cortical thalamic through

47:36 internal capsule. And here is the large lateral ventricles for the cerebrospinal fluids

47:44 there will be a lot of labeling . Uh Mostly I think labeling questions

47:49 come from C. N. From this portion and some from the

47:55 system. But when you're learning something labeling you should learn it in

48:01 So not for that specific image but a different image also. And you

48:06 quiz yourself online if you can label different parts of the brain here,

48:10 introduce the cortical organization in the cortex we said it's a laminar structure but

48:15 also a columnist structure. Okay. we introduce the new die here.

48:21 wider stain that is axon specific and clearly shows these vertical projections that are

48:26 within the cortex across the lamb in in a vertical fashion. And then

48:31 also touched upon the fact that in brains the primary sensory areas are very

48:37 compared to the rest of the size the brain and the lower order

48:40 including cats and some other animals like . They're all concerned about the primary

48:45 processing which I also see what I for the visual cortex but not necessarily

48:51 you interpret what I see or how I feel about what I see?

48:54 really about what I see rather than it and making a bigger picture overall

48:59 other senses which happens in the association . Look at the division's major divisions

49:06 the spinal cord, signal number, , cervical brainstem and midbrain attached cerebellum

49:14 the back we talked about different functions these structures. We talked about service

49:20 example, force and range of learning motor skills which is procedural

49:24 We talked about basal ganglia as motor initiation and some of the complex motor

49:32 patterns that are being stored and initiated basal ganglia, zebra hemispheres and

49:39 in addition to basal ganglia. We talked about hippocampus and amygdala. So

49:45 we talked about hippocampus and amygdala I there was an image maybe somewhere

49:51 This is amygdala, this is the . We talked about the hippocampus is

49:55 for semantic memory, places, spatial memory and spatial navigation, encoding

50:02 that memory and recall of that So that's different from procedural memory that

50:07 just discussed with cerebellum. Amygdala is fear center. Also Magdala will have

50:13 very special area that recognizes emotions in faces. So it can tell you

50:18 digital cortex can tell you're looking at face, this is what it looks

50:23 amygdala eventually through complex communications will say an angry face, stayed away or

50:30 they're happy you know, don't go them. So complex activities in the

50:37 we don't think about them but many parts of the brain are involved.

50:41 we're doing simple tasks. We talked dan cycle and talentless different nuclear and

50:47 processing different sensory functions for L. . N. S. Provisions.

50:51 media is for auditory GPL ventral posterior is for the summer to censor information

50:57 it goes into cortex and surrounding these which have their own circus society and

51:02 circuits within these nuclei surrounding these nuclear the radical Islamic sheet economic nucleus which

51:10 another layer of inhibition that controls activity the Islamic nuclei and they're not

51:17 So they have their own functions and gating the incoming sensor information hypothalamus we

51:24 is involved in the neuro endocrine system super charismatic nucleus which is a part

51:29 the cephalon is the control of the rhythms and a small portion of our

51:35 . Gay, angry and sell outputs the retina, innovative, super cosmetic

51:40 , a few percentages of all of original fibers and innovate here is the

51:45 callosum that we discussed in a different . That's what I said. Don't

51:49 where corpus callosum is. Um One , because I may ask you about

51:52 callosum in another slide that that is the one that you learned in.

51:58 it's better just to learn where the are. Talked about the cerebellum.

52:02 if you remove the cerebellum you expose corporate corporate Germania, superior curricula here

52:08 we discussed in the visual system and psychotic eye movements so they will get

52:12 small portion of the retinal ganglion cells into the superior caligula to inform them

52:17 there's light outside. This is the ventricle going into the spinal canal for

52:22 ventricle system and then we talked about cranial nerves and I said that with

52:28 cranial nerves I use the pneumonic you have to use the pneumonic. I

52:33 that pneumonic but what I asked you I asked you to know six of

52:38 nerves. One which is all factory which is optic three which is ocular

52:44 . We saw these beautiful muscles that attached to the eyeball. Popular

52:49 So this is the control of the movement of the eye. Trigeminal,

52:55 largest nerve you should be able to its stock optic nerves that should recognize

53:00 often track should be pretty easily for . So five trigeminal than eight vestibular

53:06 because we'll come back and talk about especially the cochlear to component of the

53:11 cochlear nerve when we talk about the system and 10 is the vagus nerve

53:17 runs very extensively through this. So of the cranial nerves will be controlling

53:21 lot of the census and motion around face, head and neck. And

53:25 of the cranial nerves will have broad throughout the body. Vagus nerve is

53:29 example of that Vegas nervous, innovating heart. That's where auto low we

53:35 between the nerve and the cardiac muscle the acetylcholine is a neurotransmitter and there

53:43 is an inhibitor neurotransmitter because most of receptors in the heart are masculine IQ

53:51 receptors and it's really very sympathetic control your body sympathetic. Everything is up

53:58 rate up higher sympathetic down. So is through vagus nerve and settle Colin

54:03 the heart. That's the mechanism that civil coding that we really discovered.

54:10 then we moved into the spinal We walked through the anatomy and said

54:14 you have seven cervical vertebra you have thoracic five lumber. And you have

54:21 which within each one of these Within vertebral column you have a spinal

54:25 that's associated. But for cervical you'll eight cervical nerves. Uh and then

54:31 have 12 thoracic nerves coming in a lens. The proper spinal cord is

54:35 start with number 23 and number 23 becomes caught a quien and surprise into

54:41 fibers and innovate the lower portions of body. If somebody has a brain

54:46 for example such as meningitis, they undergo spinal tap and the spinal tap

54:51 is typically going to be between Two and three, inserting a needle

54:56 the meninges and trying to sample the spinal fluid without damaging the spinal cord

55:01 . And if you sample the cerebral fluid here that seems to the spinal

55:06 is bathing your brain. So if detect infection here, bacterial or

55:10 it is in in the in the the severe room as well. So

55:15 way of looking at it. Epidural anesthesia that is done to anesthetize the

55:21 portion of the body. Epidural is typical anesthesia that some women choose to

55:26 during the birthing process to alleviate the from the contractions in the lower body

55:34 . So now in uterus. Now spinal nerves are comprised of the sensory

55:40 motor component. You have the ventral dorsal horns. The dorsal horns with

55:46 sensory component is going to come Ventral horns is where you have motor

55:51 that are located there that will send axons out. Okay. And then

55:55 have these major ascending sensory pathways. as you can know the dorsal column

56:00 the major sending sensory pathway and also you to remember that ascending sensory descending

56:07 not sensory, descending his motor because is descending is descending down into the

56:13 cord ultimately the output of the spinal is not to think about stuff but

56:19 execute the contraction of the muscle and motor movement. Okay. And then

56:24 course you know the cranial nerves are now that I'm speaking you know moving

56:28 tongue and speech areas and communication with of that and waving my hands through

56:35 cortical spinal and the llamas spinal outputs so on. So I didn't ask

56:41 to remember the descending but I asked to remember the descending of motor but

56:45 ask you to know that dorsal calling major sending sensory pathways to innovation through

56:52 peripheral nervous system. We mentioned briefly talked about imaging techniques that we said

56:56 our static imaging techniques, X ray scan. And then there is a

57:01 imaging techniques and these are clinical functional techniques and we compared pet positive emission

57:08 which tracks the oxy glucose neurons that active from consume a lot of glucose

57:15 neurons that are active also consume a of oxygen FmR. I functional magnetic

57:21 imagery will be tracking the levels of oxygenation. So you can actually produce

57:26 measurements of these brain maps and these maps. These hotspots will show you

57:32 active areas of the brain as a who's performing certain tasks. Just like

57:37 looked at at the very first two of this course and also mentioned that

57:42 procedure can be quite difficult to young or to elderly patients or patients that

57:47 claustrophobia especially for head and neck And I also mentioned that Patton Fmr

57:53 also be used outside head and neck diagnosing different things such as cancerous activities

57:58 cancer cells in different parts of the . Okay so this concluded the pretty

58:07 the um C. N. And I would recommend for you to

58:13 major parts and functions of the N. S. Again maybe I

58:18 take that diagram that I was just you with different divisions of spinal

58:24 brain stem and C. N. . And I would use that maybe

58:28 a as a note taking I would like cervical, 12 cervical Uh sorry

58:37 cervical nerves, 12 thoracic nerves. we put c. seven which means

58:44 are seven cervical vertebra. But then would put C nerve eight has eight

58:51 . So you can take notes on . Then for example brainstem when it's

58:55 down the duo of long gotta write the function and then you're gonna be

58:59 really good shape for this section to visual system will discuss the properties of

59:06 anatomy of the eye. In general walked all the way from the

59:11 from the eye into the primary visual and we ended there in the primary

59:16 courthouse. So we did talk about there are streams that are going to

59:21 into the parietal areas and the temporal that will process different parts of this

59:26 information. But when we stop you the primary visual cortex we actually have

59:31 primal sketch what we call that the world. So please review the anatomy

59:37 the eye. That phone is a security region located very centrally. This

59:43 circuit of photoreceptors, bipolar cells, ganglion cells, the processing of

59:49 And when attempts to that, we about how photo receptors are responsible for

59:55 transaction ganglion cells will be the only from the retina. You have these

60:01 layers. There's major differences in the segments of the photo receptors where the

60:06 are very sensitive and they have free discs that are loaded with photo pigments

60:11 different systems, rises from night Very high sensitivity combs is for chromatic

60:16 three types of cloners and for direct of light and high acuity. So

60:23 are expressed in the central areas of phobia of the retina laws are concentrated

60:28 the periphery and because you have these types of cones, you can undergo

60:33 we call color mixing and producing a of different colors and use that we're

60:40 . So uh if you recall in dark, the photo receptors actually d

60:46 because there's influx of sodium in the of cycling GMP in the light.

60:51 photo transaction is such that this retinol from trance turns into cysts in the

60:57 and actually activates the G protein which decreases the presence of cyclic

61:03 And in the absence of cyclic the sodium channels closed. Therefore

61:08 they're actually hyper polarized in the When we talked about the receptive field

61:13 of the south. And we said if you were to connect to the

61:16 ganglion cell newer to stimulate retina. is this retinal ganglion cell is going

61:21 be most responsive to and we found it's most responsive to these circles of

61:26 that have center and surround light center lights around dark center or dark

61:32 That's what Britain is most responsible This is the anatomy. It is

61:36 to groups of photo receptors. This what retinas processing. We later saw

61:41 L. G. M. Is seeing the same point by point representation

61:44 these concentric centers surround receptive field properties only in the primary court actually had

61:50 convergence of these receptive field properties in different shapes that allowed us to produce

61:55 primal sketch of the outside world. looked at the circuit and a lot

62:00 people are confused about the circuit but are several things that I wanted you

62:03 know about the circuit despite the fact there's light or dark. Just remember

62:09 in the dark, neurons are d in the light are hyper polarized.

62:14 these photoreceptors can be enacted to either is going to be excited. So

62:22 the cell is excited this cell is to be excited because it's acting through

62:28 a tropic receptors glutamate acting through medical receptors and some bipolar cells will express

62:34 tropical receptors eliminate these metal tropic receptors gonna be inhibitory. So this is

62:40 inverting it doesn't mean that inhibition is . This is the same neurotransmitter

62:45 But if it goes here deep polarization in the light, it's what hyper

62:52 sign, conserving hyper polarization Simon servant polarization. That means this cell is

62:59 reacting to the cell in the likely reacting to the cell is going

63:03 be this around. That's why it's center. It's not reacting to the

63:08 in the light. This is hyper . If there is no blue to

63:12 this is hyper polarized. Inverting is do what D polarizing. This is

63:17 polarization. So this polarized, the is on center game. Okay so

63:23 this details that there's sign conserving sign . So I'm conserving island tropic

63:29 inverting is metabolic tropic signaling. the light in the dark. I

63:33 ask you questions like the light was off set yourself. It's connected to

63:39 medical tropic bipolar cell you know. I want you to know that this

63:44 tropic on the tropic that you can essentially to the same which has been

63:49 to cells can have a different effect of the ganglion cells. And also

63:55 you to know that Gaba or inhibition produced by horizontal cells. So there's

64:01 when we talk about negative feedback if excite, the cell is assigned conserving

64:06 going to excite this horizontal cells but horizontal cell is inhibitory Gaba and it's

64:12 to project back from the same cells excited and what projects Gaba onto this

64:17 receptive and hit the suspect. And there's this horizontal lot of control basically

64:24 is inhibitory control. Otherwise the entire here is just glutamate. I'm not

64:31 it's all excitatory because we have signed burden but it's all glued dramaturgical signaling

64:35 this direction going down to the horizontal . So the ones that introduced this

64:40 allergic or inhibitory levels of signaling. but you having fun yet can we

64:50 this in three minutes. Sign inverting in conserving. This was an interesting

64:57 . We talked about critical period of . Critical period of plasticity. We

65:01 in animals like rodents is the first of life in humans depends for what

65:06 we learn different things at different stages life, it is typically into the

65:11 when we are most susceptible to learning best and recovery from injury the best

65:16 well because of the chemistry and because the connectivity and plasticity that is still

65:22 . And so we saw an example how short term deprivation, sensory deprivation

65:26 vision in one eye. And these during the critical period of development can

65:32 the projections into the cortex. Most them will come into layer form

65:38 This will change the function so the will not be as responsive to images

65:43 the eye that was closed. And you prolong this deprivations to longer period

65:48 time you can forever change the anatomy the functionality of the cortex where it's

65:54 ignoring all of the stimulation coming in the side doesn't mean that the circuit

65:58 the eye is destroyed but the cortex not responsive to the activity coming from

66:02 . I kind of forgot that it important during this critical period of development

66:08 now there is no regain or recovery function. So when we talk about

66:15 visual field deficits is a great exam too. When you talk about damage

66:19 one nerve on one side and equivalent that is closed you online, that's

66:26 damage that you will see on the field. When you talk about damage

66:31 the optic tract. You're talking about that crossover contra and it's a lateral

66:37 that stay on the same side. that retina collect cups. They're not

66:44 . If your retina was flat and portion would be looking here. This

66:49 will be looking here and this portion be looking here. This will be

66:53 here. Retina is not flat. this portion is looking here. This

67:00 is looking here. This portion is at So put your two hands like

67:06 and verte and tell me where your retinas are looking in the periphery.

67:12 we're looking at the periphery nasal retinas the ones that cross over you cause

67:19 to nasal retinas to the chi as over. You lose peripheral vision.

67:25 tunnel vision. So do this exercise you're having difficulty and of course you

67:30 memorize what it does to the optic but now if you know which one

67:33 it in concert is going to be to do this exercise. Close one

67:37 for one nerve damage and remember that writing these kinds of cops. This

67:42 looking over there and now flat the is not flat like this. Okay

67:49 is the damage. We have six . We have this written the

67:53 Point by point representation from the retina the L. G. M.

67:57 have the magna and the powerful We have very small primary visual cortex

68:02 17. This point by point representation all the way to the visual

68:07 We have very specialized anatomy and layer where the projections come from the

68:12 We have the stride cortex which are dominance columns. Australia belongs to activation

68:18 only one eye. So the signal mine. Ocular that signal starts becoming

68:23 . In layers 23 there's salama cortical that come in mostly to layer

68:28 Except for the intermediary that bypass layer directly into layers 23. There is

68:34 inter cortical loop that communicates information from to 3 passes it along laterally through

68:40 to three communicates it back to deep and outside from cortex and the thalamus

68:45 also completes this loop layer. Force llama cortical inputs of inter cortical loop

68:51 the cortex have cortical thalamic outputs. so most of the L.

68:55 M. What it receives is cortical and therefore L. G.

69:00 Is really listening and following with cortex to say the blobs which is cytochrome

69:08 increased metabolic activity found in letters to . The south. We asked that

69:13 question we ask the question how can maximally activate right now ganglion cells relay

69:19 and it turned out with the circular Concentric patterns. And then we ask

69:24 can we maximally activate primary visual cortical and it was no longer circles it

69:29 now bars of light and it was activated when it was in a specific

69:35 , specific angle or in a specific of movement, left to right,

69:41 to left up and down diagonally all the 360°. And then we comprised these

69:48 receptive fields and these receptive fields gave different shapes to work with. And

69:53 convergence of simple cells and complex styles us even more shapes to work with

69:58 comprising out of these shapes, what call the primal sketch, which is

70:04 and motion and color that you would on the outside world. We talked

70:09 voltage sensitive dye imaging technique and we in this case that die sensitive to

70:13 in voltage and that was a great to use to delineate these orientation

70:19 These are the smallest units, orientation 31 50 let's say 100 micrometers in

70:25 . And we said, how do fit? These are micro processing units

70:29 south located adjacent to each other, similar orientation to go around this

70:34 You will process orientation all the way 360 degrees. And then we

70:40 let's put this all together, we the blogs and layer 23. We

70:44 the boundaries of the ocular dominance We have these hyper columns. These

70:50 columns, we have the ocular dominance . The blobs within each ocular dominance

70:56 will have multiple of these orientations column . And we finally discussed elastic

71:01 which is the intrinsic optical signal. said that there's no die here.

71:05 no eye on down the drain will reflect its properties and the cell will

71:10 reflecting properties as a function of So this light wide that you're sitting

71:16 in faith represents this zone here, is this contra lateral zone, Oculus

71:24 zone. You can actually visualize on surface of the brand. So this

71:27 more of an experimental technique again about sensitive dyes both and the intrinsic optical

71:33 rather than the clinical application. But is something you should know that active

71:38 will not only consume glucose oxygen, will swell and they will change the

71:44 properties because their membranes are becoming thinner least neurons well. And we ended

71:51 . So for the sake of saving lecture and uploading it, I'm gonna

71:57 the recording here and happy to take few questions for about five minutes until

72:04 have to clear out of this I'm wishing everyone good luck on

72:09 I'm hoping everyone is registered. I'll this review session now. It was

72:14 better than yesterday's and I didn't have interruptions. So thank you, thank

72:19 . That was being on zoom and will see everyone in person next week

72:25 the

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