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BIOL 4315/6315 Neuroscience Mon Wed - NEURO MIDTERM II Review - Neurotransmission, CNS, Visual System
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00:02 this is uh midterm to review We talked about neural transmission. The
00:08 of neural transmission in the heart. the skeletal muscle. It was acetylcholine
00:15 the experiment that we described with two hearts. We discussed two types of
00:19 synopsis electrical and chemical the differences between and the fact that electrical synapses will
00:25 the high. It's a small molecules very important for synchronizing large sections of
00:31 and engaging neurons in a meaningful And they're comprised of the gap
00:37 You have a narrowing between two members 3.5 nanometers between some neurons. And
00:42 also talked about how gap junctions are present and glial cells. So this
00:47 not just neuronal specific. Then we into talking about possibilities of synaptic connectivity
00:55 accident systematic Denver Kendrick access. No. And we highlighted an
01:01 Oksana was only model a story because doesn't influence the integrative properties but rather
01:06 output properties of the cells. And this anatomy of symmetrical and excitatory cells
01:11 symmetrical in inhibitory cells at least flatted flattened vesicles that you've seen the inhibitory
01:20 neurons. We then talked about neuro junction for a long time and we
01:26 about several aspects of it how at end you have these ramifications of the
01:33 that form this massive Seongnam's that the can recruit number of fibers. You
01:38 recruit all of the fibers of the muscle because you can pick up something
01:42 one finger, you can pick up with two fingers. So you can
01:46 all of your hands and all of muscles and that will take more recruitment
01:50 the fibers to do all of So we can selectively do that.
01:55 know something that the cardiac muscle cannot . You know barely opened the valve
02:01 half open the valves are shut and . So what we have is we
02:05 a single Colin molecules we discuss that neuro muscular junction will produce an end
02:11 potential and played potential which is mediated nicotine acetylcholine receptors. It's only excitatory
02:20 . It will always produce this massive polarization about 70 million balls that will
02:26 activation of the civil coding receptors here subsequently activate called educated sodium channels,
02:33 and calcium channels. It will produce very large and long muscle action potential
02:40 of several 100 100 seconds. we'll come back and talk about
02:45 N. S. But in contrast C. N. S. We
02:48 E. P. S. S. And D. P.
02:50 . P. S. And mostly by glutamate that we talked about.
02:53 you have excitation, you have I PS. So you have inhibition which
02:58 gabar mediated and you also have acetylcholine because we have these polymer gica mean
03:06 that synthesize and project acetylcholine throughout the and they can balance the nicotine acetylcholine
03:15 the most chronic acetylcholine receptors. And also know that if nicotine it will
03:20 a little bit of excitation in the the most koranic is actually opening the
03:25 channel will cause the same effect as does in the heart and the
03:29 Silicone slows down the heart rate and neuro muscular junction that causes and potential
03:37 in the cns happening through acetylcholine receptors causes hyper polarization of the cells but
03:43 opening the potassium channel. And in C. N. S. You
03:47 E. P. S. S. That have to summit that
03:49 produce an action potential that is very on the water of a couple of
03:56 in duration. That's a good pardon me. May I ask a
04:04 or is it better to save them would you mind allowing me to get
04:09 the neural transmission session and write down questions and then I will give a
04:14 for everyone to ask their questions. thanks. Thank you. So we
04:20 about the systems the systems and some of these systems. We talked about
04:25 fact that we have amino acids, advising means little coding, dopamine,
04:33 , norepinephrine serotonin and as far as over mean molecules we discussed the civil
04:39 in great detail. We discussed norepinephrine as well as far as the cellular
04:45 signaling. We also have peptides that mentioned. We also in that separate
04:51 box have placed in the cannabinoids gasses are not stored in the vesicles remembering
05:00 and in the case of cannabinoids and oxide gasses uh they signaling the retrograde
05:10 . So, we'll review this, a difference between the expression synthesis transport
05:18 release of peptides neurotransmitters. So most the neurotransmitter reloading the synthesis is happening
05:26 in the pre synaptic terminal. For top ties, it involves other structures
05:32 the release of the peptides from the panels is not as specific and it's
05:37 as confined spatially to these special synaptic at the pre synaptic terminal action potential
05:47 not enough to cause the release of . There has to be an opening
05:52 voltage gated calcium channels influx of calcium binding to protein complex on the testicle
06:00 allowing for the vesicular member interviews with the neuronal membrane to cause exercise psychosis
06:08 following that, the release there's endo of the neurotransmitter vesicles. We talked
06:15 the freeze fracture technique briefly how to two phases of the membrane. And
06:19 also discuss these both in this case sensitive dye in images and what the
06:27 we're seeing is actually dies that are to calcium. So when there's increases
06:32 calcium concentrations, those guys will show certain fluorescence. We talked about how
06:38 is sequestered to these recent heart attack zones. And it's very clear spatial
06:45 mountains that you're seeing here in calcium during the intense stimulation you have calcium
06:51 and increases in calcium concentration that's pretty as is seen in this image in
06:58 cns you can have partial release a release most of the time. The
07:03 are handled uh directly by reloading them acidification. Sometimes they're shuttled back into
07:09 early in this zone. Uh We about how certain toxins and certain substances
07:16 affect neurotransmitter release neurotransmitter called fusion with plasma membrane uh neurotransmitter breakdown in the
07:27 left boston optic receptor channels and so . So we talked about the stadium
07:33 I know which is a toxin botulinum botulinum toxins. These toxins will target
07:42 binding complexes pretty including binding complex in co main uh Mexico and we also
07:51 organophosphates and we related organophosphates. Later we talked about alzheimer's medications and breakdown
07:58 acetylcholine in the synaptic cleft in the nervous system Instead of the E.
08:03 . P. S. We have . P. S. P.
08:05 excited for possible potentials that we later and mediated through ample kini and NMDA
08:12 . And we have I. S. P. S which are
08:15 through Gaba A. And Gaba B . So you have an early component
08:19 the edition and late component. And addition we discussed the differences between Iowa
08:25 and metabolic tropics. So both are uh receptors but one of them is
08:30 receptor channel. That means when ligand to that receptor, it's a channel
08:36 nicotine acetylcholine receptor channel muscular nick. receptor channel is uh sarinic G protein
08:45 receptors are not channels but they will the G protein complexes and acetylcholine
08:53 You should know everything about the single . What are the precursor molecules?
08:58 is the synthesizing enzyme? What is enzyme that breaks it down? Uh
09:05 transport into the pre synaptic terminal to into the bicycle? And the fact
09:14 most of the alzheimer's medications targeted civil stories by blocking its local unnecessary known
09:20 colonists inhibitors or acetylcholinesterase inhibitors in the . N. S. Unlike in
09:27 neuromuscular junction, acetylcholine can act on and muscular receptors that have their distinct
09:34 . Nicotine is actually an agonist for receptors masculine is for muscular neck.
09:39 then you have a ch is the molecules that will activate both nicotine and
09:47 receptors. This theme of release of neurotransmitter and these immune systems actually
09:56 So you have equivalent kind of uh of the neurotransmitters reloading and we looked
10:03 you can also control the re update this case the cata colony re update
10:09 be controlled through uh amphetamines and illicit like cocaine. And we also look
10:16 many of these means that your style seen as a pre person till dope
10:20 dopa to dopamine and norepinephrine epinephrine and discussed that each one of these systems
10:26 their own kind of a function what responsible for a state of mind or
10:31 if you may and I asked you you don't need to know all of
10:35 intermediary enzymes here in the synthesis but should know the molecules in particular more
10:44 how it interacts with alpha data receptor the fact that you have the release
10:50 the recycling of these neurotransmitters or degradation synaptic cleft and recycling of the components
10:55 precursors mon amine oxidase. These are the molecules in this case that are
11:03 to break down the cata column And so mono amine oxidase inhibitors are
11:10 uh substances that can essentially prolong or more cata column is available in the
11:17 synaptic cluster, it could be re into the vesicles for acid amino acid
11:23 transmission. We talked about this really fact that Gaba and the major inhibitory
11:30 in the C. N. Is transformed from gloomy castle decor box
11:37 all of the inhibitory cells that release , they will be staining positive for
11:43 , serotonin Again we've listed some functions mood, appetite sleep where we talked
11:49 some precursors like trip to fan five HDP into five HD, which is
11:56 and some of the common depressant Some mood controlling medications and brand name
12:01 PROzac um quite often are interacting with re uptake of serotonin and you'll see
12:08 serotonin re uptake inhibitors. So these some of the medications again that will
12:13 through the uptake of serotonin or may it through the other intracellular components such
12:20 the M. A. S. endocannabinoid that we've discussed our anandamide too
12:27 glycerol they are synthesized on demand. when there's heightened activity between the two
12:34 and there is a lot of post activity there will be a synthesis of
12:40 . They will freely diffuse through plasma . They will function in the retrograde
12:46 . So this is an integrated release neurotransmitter from pre synaptic synaptic retrograde at
12:53 molecules will travel from boston happy to up terminal. They will buy the
12:57 . Protein coupled with South and that close and regulate the opening of the
13:02 channels. Well educated calcium channels. they will influence the release of both
13:08 and inhibit their neurotransmitters. And we'll back to this in a second and
13:13 the slides those techniques that we how we study neurotransmitters and you know
13:18 the chemistry and the hybridization. So the differences between those, we also
13:22 about neurotransmitter mimicry but we also mentioned occasion of neurotransmitters. So although I
13:29 want you to know all of the about the microscopy and the fast lasers
13:33 stuff like that. But you should a general understanding that on Cajun neurotransmitters
13:38 happens with photo license and spatially more and more specific. You can get
13:43 to single synapse level. That these of applications through electrode. They cause
13:50 lot of the dilution and spreading off substance that you're applying that you're
13:56 So just to know that we also about the fact that in cns because
14:02 E. P. S. S. Is small and so you
14:04 to activate a lot of synapses to these E. P. S.
14:08 . Summit so that they reach the for action potential, Produce the action
14:13 . And so we talked about two is the spatial summation and temporal
14:19 This concept of the length constant which if you have a maximum current,
14:24 maximum current in the cable which is insulated will actually leak out. And
14:29 distance by which this turn weeks it's 37% of its maximum value.
14:36 the length constant. So the south have a long length constant will be
14:40 good for temporal summation of integrating the information signals. We also talked about
14:47 if you activate excitation inhibition at the time. Like in this situation excitation
14:54 about active at the level of the , you're not going to be able
14:58 record much of a change because inhibition going through the central shunt or cancel
15:05 the active excitation. So the cTS . That can get produced distantly done
15:10 , may never reach the soma may mean anything. Therefore you need to
15:14 many synapses many of these dendritic spines conduct the signal into the soma to
15:20 the threshold for action potential generation. is uh uh laura binding uh and
15:30 can see that the similar uh pathway we talked later But acetylcholine receptors will
15:39 modulate potassium channels. But this is and you can see that this is
15:45 receptor actually that will modulate and that's we call it, modular for activity
15:50 there are intermediaries here. And when talk about the shortcut pathways, when
15:56 g protein goes directly and interact with potassium channel. So but it's the
16:03 kind of a similar pathways and molecules are involved in all of this.
16:11 then we one more time reviewed all the neurotransmitter systems. Um We talked
16:20 acetylcholine again in great detail room, in the heart will bind to
16:25 Acetylcholine receptors slow down the heartbeat. in the skeletal muscles it will cause
16:33 and that's because essentially it's a parasympathetic . Parasympathetic control of the heart which
16:40 slowing down the heart train acetylcholinesterase acetyl choline esters inhibitors are also organic
16:48 that we discussed in the muscles We talk about nerve gasses to.
16:53 so if you block the reuptake of civil code into much of acetylcholine can
16:59 too much of the skeletal muscle contractions into tetanus lock up. And if
17:05 for example with diaphragm their breathing it can kill you by suffocating you
17:12 the nerve gasses. So this is uh an illustration of mobile tropic signaling
17:19 a civil code and masculinity receptors through shortcut and it will open up the
17:24 channel. So if nicotine acetylcholine receptor gonna allow for sodium to influx and
17:32 to reflux is gonna cause small deep . Masculinity. Acetylcholine receptor is gonna
17:38 the opening of potassium channels can cause polarization. There's no chemical intermediaries in
17:46 pathway. We have an important concept we discussed is pra glutamate regulation is
17:51 important that glial cells are viewed as third important player in neuronal synapses.
17:58 we refer to as tripartite synapse, synaptic neuron, post synaptic neuron and
18:03 because glia has glutamate transporters and it absorb glue to me and it will
18:10 into glutamine and it will share that with neurons where neuron skin. Then
18:17 synthesized illuminate and re uploaded and neurons have their own glutamate neuronal transporters
18:25 So now you can imagine that glia has a lot of control and contributes
18:31 lot to odometer jik bio synthesis and of glutamate that is that is present
18:39 neurons. Um This is just a but here we talked about if you
18:46 about for example dopamine um it can movement. It can mediate mood and
18:54 . So these cattle colony molecules they be mediating these functions the serotonin molecule
19:02 involved also in mood but appetite sleep um we talked about that you can
19:11 two opposing actions through nicotine versus most acetylcholine receptors but then we said that
19:16 tropic systems can also have opposing actions this case it's maybe not changing the
19:23 in potential but it's regulating the downstream activity. So data activation of data
19:31 by american effort will push the system produce more psychic and PM further and
19:36 and say but the same molecule norepinephrine it activates out for two receptor that
19:42 actually inhibit and pull the system away producing more of the psychology and PM
19:48 in kind and say that's why we to this push pull system, one
19:53 through one of the same molecule to receptors pushing the system and that same
19:58 to another receptor is is basically acting the opposing action in these intracellular
20:06 The unique thing about the means that discussed to sit there not like amino
20:12 that are expressed broadly throughout the cortex sub cortical structures and narrow peptides expressed
20:21 throughout different neurons. And they can co expressed with neurotransmitters but norepinephrine and
20:29 . And all the other means including locally and they have their specific nuclei
20:35 they synthesized and they have these very projections from these nuclear through the axons
20:41 they innovate broad regions of the central system and also the periphery. So
20:48 other cannabinoids we just uh just spelled by equalization of pressure. In addition
20:56 the division polarization suppression of excitation uh delta nine tetrahydrocannabinol was a fighter
21:04 So it's something that exogenous and it also interact with CB one receptors.
21:10 part of the activation of euphoria like is by Delta nine but also obviously
21:17 the endocannabinoid molecules or the bliss If you recall, ananda in Sanskrit
21:25 bliss. And that's why this molecule named anandamide glutamate to gaba glutamate.
21:35 into the pre synaptic terminal into the . Gaba has transporters into the pre
21:42 terminal into the vesicles. So there some interesting pharmacological controls and manipulations that
21:49 be pursued in the re uptake of molecules. And then transporters, let's
21:55 in glial cells for glutamine glutamate. we studied in quite a great detail
22:01 to employ an M. D. . Tiny receptors, ion a tropic
22:07 remember that the early component of P. S. P. Is
22:13 by AMFA and the late component the . P. S. P.
22:17 generated by an M. D. . So if you were to take
22:20 E. P. S. And this is a response a response
22:25 activation of many synopses in this early is gonna be our ample component in
22:33 league component of the PSP is going be mediated by the NBA receptors.
22:38 so as soon as there is release glutamate it combined two alpha receptors and
22:44 going to be deep polarization, there's to be an influence of sodium but
22:48 NBA suckers have a magnesium block and order for the sufferers to open,
22:53 has to be a post synaptic deep alpha which will alleviate the block and
22:58 for the flux of sodium and calcium ions. So we talked about the
23:06 that this is a late activating response M. D. A. But
23:11 as much stronger conductors than Tampa. have their agonists which are ample and
23:16 M. D. A. And have their respective antagonists which is
23:19 N. Q. X. And . P. D. And we
23:22 about a P. D. When looked at the I. D.
23:25 for ample in an M. A. And M. D.
23:27 wrist doctors often refer to as coincident which means that they're coincidentally detecting pre
23:34 release of the transmitter glutamate and post deep polarization. And so you just
23:39 one we've made but know deep polarization . But no glutamate NMDA receptors are
23:45 going to be open. That interesting we learned is that in the spinal
23:50 licenses the major inhibitory neurotransmitter in the slicing is a co factor for binding
23:59 receptors facilitates glutamate binding to receptors many binding sites that we talked about on
24:07 M. D. A receptor including illicit drugs such as PCP and can
24:11 quite dangerous because an M. A receptor is influencing a lot of
24:17 and sometimes drugs of abuse a single for these systems can distort the system
24:23 for a long time. So we about potential schizophrenia accurate and chronic onset
24:30 some of these drugs. We also about how these different binding side some
24:35 the elements are going to compete to them the same locations. So they
24:39 be competitive agonists or competitive antagonists. want to bind to the same
24:45 Two different chemicals both will inhibit activity that channel. And so you have
24:51 binding sites and sometimes when something is to the channel and the channel is
24:57 , it also changes confirmation. So can have other molecules that will bind
25:01 to active for open channel. So 21 is something that is an antagonist
25:06 open an NBA channels. Otherwise it have an effect and cannot bind an
25:12 channels please do not confuse an D. A. Receptor channels with
25:18 tropic signaling which is G. Protein with that tropical signal. And came
25:24 when we talked about the visual system the bipolar circuit from retina. Uh
25:30 the later lectures this slide illustrated normal conditions. You won't have much of
25:36 N. D. A. Currents $1.2 million magnesium it shows you an
25:42 currents reverse at zero. So the . So there's Ep sp so there's
25:46 M. D. A. So ample were all reversed zero millet
25:50 And if you remove magnesium you can an M. D. A.
25:54 in the presence of within it. that tells you that magnesium is actually
25:59 an M. D. A receptor . Then we talked about this graph
26:02 in this graph we discussed it in case we stimulated the cell or at
26:08 glutamate and recorded post synaptic response. used voltage clamp and clamp the potential
26:13 different holding potentials. And we measured early component of the PSP and the
26:18 component of the PSP. We found the early component which is the ample
26:23 is linear component and in the presence a P. D. This linear
26:28 component is unaffected. So close they're triangles. It doesn't matter. And
26:34 presence of an M. D. receptor blocker, ample channel is unaffected
26:37 that I. D. Curve for channel is linear and M.
26:41 A. Component is these closed circles normal conditions shows you that it is
26:45 nonlinear. So it is late activating deep polarization to be activated. Also
26:51 zero mil evolves and prefers to conduct the outward directions. This is the
26:56 component here on this blue area under curve is uh is due to the
27:06 . D. A. Component. so in the presence of a
27:08 D. Would have these open circles a tv blocks in M.
27:12 A receptor. And in the presence a PV this whole blue area under
27:16 curve would collapse and you would be component but not affect the early
27:22 These are the key things that you know from this slide linear versus
27:28 And that a tv will affect only M. D. A. But
27:32 the receptor currents. All of the receptors are permissible to calcium. Only
27:39 sample receptors are permissible to calcium. is that they have this uh edited
27:47 which is substitution of the single amino . So from this side I want
27:51 to know that substituting a single amino in the really complex three dimensional structure
27:56 result in significant effect on the functions as allowing for calcium to come in
28:02 not. When we talked about her in the development are only an MD
28:06 receptors and the synapses of silent meaning in the presence of glutamate NMDA receptors
28:12 not going to open because there's no receptors to cause the post synaptic deep
28:18 . So there are other means by these post synaptic deep polarization is come
28:21 in the developmental brains. And also fact that an M. D.
28:26 receptor is they're comprised of subunits just other receptor channels that we talked
28:32 And G protein coupled receptors and there be a shift in the subunit composition
28:37 the ratio shift that the subunit. uh an M. D. A
28:42 are very much involved in LTP which long term potentially ation or long term
28:48 that we talked about when we discuss period of development and these plastic events
28:53 are happening in our brains. And there are changes of activity in these
29:00 with age and ample sufferers are very . So they will move through these
29:06 synaptic spaces into the synaptic spaces through membrane within milliseconds. So there's considerable
29:14 of these proteins, trans membrane proteins the plasma membrane, medical tropical
29:20 We just very briefly looked at the uh breakdown of P. I.
29:27 . Tuning to I. P. and release of the I.
29:29 Three dependent calcium release from the smooth plasma particular and Israel which remains membrane
29:37 and activates another molecule protein kinesis. kindness as a prospera waiting molecules and
29:44 defense for alisO kinda says channels and a lot of times can help the
29:50 keep open and conducting and defense for them can cause the opposite effect,
29:55 closing those channels. There's a fine between these molecules inside the south.
30:01 we moved on to Gaba and we about how Gaba also just like an
30:05 . D. A receptor is an . Glutamate receptor. Gaba also has
30:10 lot of different binding sides. Gavel bind to this is Gaba a receptor
30:14 particular ethanol or alcohol, benzodiazepine barbiturates. Uh no steroids that will
30:22 all affecting Gaba receptor. Gaba A will allow for the flux of chloride
30:30 Gaba B activation will open up potassium of possum optically the I.
30:37 S. B. Components, the a component, this chloride mediator followed
30:43 Gaba B component which is uh potassium and that's potassium leaving the south and
30:53 hyper polarization. So you can see gather B. Is a metal nonprofit
30:58 that's links automatically potassium channels organization. synaptic lee. It's linked to calcium
31:06 that can cause the closure of voltage calcium channels prison optical and therefore influence
31:11 pre synaptic vesicles release, which is of what endocrine avenues do also.
31:17 there's multiple ways in which you can this voltage gated calcium channels under an
31:21 of molecules through Gaba B. Pre receptors to reach the same end
31:29 And we finally talked about this diagram we discuss the inhibitory synapse that will
31:36 Gaba and Gaba B. Cause hyper . Gaba synapses will also have order
31:42 that are gathered B. And they self regulate the release by blocking the
31:47 educated calcium channel. Excitatory synapse can influenced by Gaba receptors to review the
31:54 signaling or through the spillover of Gaba to the hetero synaptic pre synaptic gaba
32:01 that are also located from excitatory synaptic and can really regulate the release of
32:09 pre synaptic glutamate in that matter So I always said that the slide
32:14 really great if you want to review you learned about Gaba and glutamate and
32:20 tropic versus on the tropic and opening the potassium channel. For example here
32:25 can put Gaba B. But here can also put colon receptor by circling
32:31 meaning receptor is also notable, tropic the potassium channel, that's why the
32:39 is really good for you to take and a lot of things that you've
32:43 in the previous lectures. So we about gaba and gaba B. We
32:49 about how you can see that if have excitation that's checked by inhibition you
32:55 a small excited response but by queue as a blocker for gaba A.
33:00 if you block inhibition, gaba it's number to trace that same stimulus
33:05 causes a massive deep polarization, a response pasta map quickly so you can
33:10 how inhibition shapes and controls excitatory post potentials and ultimately the post synaptic response
33:19 the action potentials. G protein coupled . We discussed the seven trance member
33:24 structures in many different G protein coupled . We've highlighted a few. We've
33:31 about um alpha data. We talked uh mascara, nick versus nicotine
33:38 We talked about CB one and and we didn't talk about CB two.
33:44 a cannabinoid receptor to which is primarily neuron on glial cells and 80 P
33:51 binds the denison reception will review that little bit more. This is transmitter
33:57 ion channel structure. And we again about the receptor sucked out the agonist
34:04 antagonist and I said that you should acetylcholine everything on the single calling.
34:10 should know norepinephrine alpha beta push pull glutamate opera and NBA candidate and metadata
34:20 system to a lesser extent Gabba Gabba that we just mentioned by cooking island
34:27 gotta be antagonists blocker A. P. Because we mentioned that dennison
34:34 an agonist for a type or dennison and caffeine is an antagonist for dentists
34:40 suffering. And when a dentist in is active in blocks glutamate release a
34:45 in blocks glutamate release and caffeine promotes release. Okay. And we have
34:54 through this chemical system and you have . You have several uh neurotransmitters converging
35:03 the on the same effective system inside cell or the same channel. You
35:09 redundancy activating the same receptor or getting the same channel or the same cellular
35:16 downstream. These are all of the things that we talked about. I
35:21 take a quick but he had ons if anybody else has any questions.
35:31 I had two questions I'd like to first when you talk about in plate
35:37 reversal potential along with I. S. P and G P.
35:41 P reversal potentials that's still referring to the iona tropic channel. Like the
35:48 the ions flow changes reverses. Is what you mean? Yes. Except
35:55 when we talked about equilibrium potentials in first section, equilibrium potentials were calculated
36:03 just one single lion. So for the end plate potential it's looking at
36:09 A. C. H receptor and looking at the sodium and the potassium
36:14 of together, correct? Okay. the second question I have is that
36:23 the lecture and textbook we kind of about the Gaba proton anti porter for
36:28 particular pump and that proton gradient in practice exam you mentioned dopamine packing with
36:37 protein proton gradient. Is the proton used for every neurotransmitter type. There
36:45 an acidification in the vesicles. That is influencing the loading and the
36:53 . We didn't go in that great a detail on that. Um So
36:58 surprised if I'm related to dopamine and so that would be applicable to
37:09 serotonin norepinephrine and whatever else we've talked . They're re uploading. Yes.
37:16 they will they will have the transporters well into the vesicles with the proton
37:24 and their certification. Can you repeat question with the same like proton gradient
37:33 driving it? If you can answer question that neurotransmitter loading is influenced by
37:42 gradient and acidification. You're all Okay thanks any more questions. Anybody
37:51 zoom online or in person. All . Yes. So on these section
38:03 you talk about the types of neurotransmitters end up phenomenal weights be under what
38:11 of neurotransmitter would be any of those or? No because they're not.
38:27 You mean can you co express some these molecules together with other cannabinoids.
38:33 and cannabinoid g protein coupled receptors are most ubiquitously express prison ethically? So
38:40 of the present terminals will have them . And it would be considered under
38:46 of those types. No, they're because they are not stored in
38:52 Remember it's valuable and they function in fashion. No, it's somewhat similar
39:00 gasses because gasses are also not stored vesicles and also function and retrograde
39:08 Alright, so let's continue with this let's start talking about the brain.
39:19 the good things we learned about the . Remember? The interior austral,
39:24 quartile, dorsal and ventral, mid , horizontal kurono some terminology. We
39:33 cerebro cerebellum. It means it starts cerebellum cerebrum goes to cerebellum. Cerebellum
39:40 means it starts in cerebellum goes the and we talked about major parts of
39:48 major parts of the brain and we about the three men injuries, the
39:54 mater, the arachnoid and the dura to uh and the features the ventricular
40:02 and production of the CSF and the plexus. We talked about abnormal accumulations
40:12 cerebrospinal fluid that can lead to hydrocephalus that we need to be drained Otherwise
40:18 can influence the shape of the skull then we discuss new relation. The
40:24 of neural tube from the neural plate the formation of the nervous system from
40:33 essentially After no relation went through a of conditions that can be related to
40:42 folding of the neural tube if it's is an especially if it's called which
40:48 be the latter one that can be surgically and then after that and your
40:55 process you have differentiation process. We processes and suffering. The forebrain measure
41:01 brain and hind brain and the poor differentiates into telling metallic Mexico's because cerebrum
41:09 cephalon Stalin's hypothalamus, you also have vesicles in hind brain, mid
41:16 You have further differentiation into the hemispheres the corpus callosum is the major fiber
41:23 that interconnected two hemispheres. Diane cephalon is thalamus and hypothalamus internal capsule which
41:30 the lama cortical connections that are going following us into the cortex. And
41:36 are the different parts of uh more brain um in the color code
41:45 So I think the best way to best lies to talk about here.
41:52 then we talked about later individual system we introduced this concept, neocortex is
41:57 six layer structure. It's a laminar and it's also columnist structure that has
42:02 and a and that here we added addition to missile stain and golgi stain
42:07 we already knew, we added the stain which is specifically for accents and
42:12 you stay in the accidents, we clearly see this article movement up through
42:17 column and inter connectivity in this column like fashion that came up remember as
42:23 processing networks such as orientation columns and connected into the ocular dominance columns and
42:29 connected into hyper columns for both But you see this beautiful anatomy throughout
42:36 parts of the cortex where they're in parietal occipital lobes. We also talked
42:42 the fact that a lot of the in our brains is dedicated to
42:47 tertiary co ordinary and association areas. these are more sophisticated levels of sensor
42:53 processing that we have over the other that dedicate a lot of their brain
42:59 to just the primary sensor information which I always say related division.
43:04 like what do I see? But really. How do I feel about
43:08 I see and what am I going do about what I see. Uh
43:12 the best slide again is here you the division of spinal cord into the
43:18 lumbar, thoracic, cervical division of into medulla, oblon, gata,
43:23 and midbrain. You have sort of attacks on the back of the
43:27 You have diane cephalon, you have nuclei that we've discussed our basil
43:34 so initiates motor commands. Uh complex of the motor commands. We talked
43:41 hippocampus, part of the brain is for semantic memory, spatial memory as
43:48 . Some memory encoding and memory recall it relates to storytelling which is semantic
43:54 and amygdala which is essentially fear nucleus fear center and also a center that
44:01 um recognition of emotions on another person's . So sort of specialized there in
44:09 amygdala that recognizes if a person is at you angry or they're happy.
44:16 different parts of the brain are involved simple functions and all of these images
44:22 not necessarily these images. They're all labeling images. So for labeling questions
44:27 can expect to see the exact same are completely different images or they're in
44:33 angles and different rotation. You should able to tell them quite easily just
44:38 looking at them. When we talked don cephalon we talked about thalamus,
44:45 is a collection of distinct nuclei. nucleus processes its own specific functions a
44:51 nucleus processes visual information, medial nucleus auditor information, mental posterior lateral nuclear
44:58 , sensor information. This is all the information and routes to cerebral cortex
45:03 it gets processed into the court As you saw with the visual signals
45:09 the retina into L. G. . And then it went into the
45:13 visual cortex. So auditory signal will into M. G. N.
45:17 then it will go into the auditory And we'll look at it when we
45:21 the auditory system. We also talked this uh very special nucleus particular economic
45:28 which is like a sheet of cells covers these nuclear within these nucleus that
45:34 all gM. You have relay cells you have inhibitor and exam natori
45:39 They modulate the activity. They tune sensor activity and they also receive a
45:44 of inputs back from the cortex. cortex can very much influence the activity
45:49 the thalamus. The hypothalamus we talk is involved in the neuro endocrine system
45:54 under green system it's controlling several important . And for the super charismatic nucleus
46:01 mentioned that it is the master body regulator which controls our circadian or diurnal
46:08 . There's more images of the optic . As um and there's a corpus
46:17 here. Okay. Uh there's the , there's the hippocampus. These are
46:24 very good labeling questions. This is back and you can see the
46:29 you move the cerebellum, you have cerebellum peed on calls and above you
46:35 have superior curriculum, interior curriculum. of the corporate quadra gemini. Superior
46:40 is already came up and we studied visual system, a portion of the
46:44 fibers. About 10% of retinal outputs into the superior curriculum for psychotic eye
46:50 and fast kind of a jump like movements that we discussed. Inferior curriculum
46:56 be concerned with the auditor information And when it came to these cranial
47:02 we had a different slide that we and uh we used this slide here
47:13 you're welcome to use any pneumonic you or you don't have to use
47:18 you can just memorize everything without any monix. Um But this pneumonic works
47:25 me and I pointed out that you know the following cranial nerves. For
47:29 exam one which is a factory to is optic three which is ocular motor
47:38 it's just inevitable that you should know because it's three. It's ocular it's
47:44 that moves the eyeball. And we looked at these muscles connected to the
47:49 when we studied the anatomy. So would be muscles that would move the
47:54 . Then you have trigeminal which is five. Trigeminal is also the largest
48:00 located that there are the bonds here the three components. Okay, number
48:07 which is this is the cochlear nerve we will study that component of that
48:14 when we study the auditory system. number 10 which is the vagus nerve
48:21 the vagus nerve. Because auto low stimulated vagus nerve to discover acetylcholine.
48:28 we know that it's one of the viscerally extensive cardiac innovation, extensive nerves
48:35 you see coming off the brain So now let's go back to the
48:44 here following the review of the cranial , we reviewed the spinal nerves and
48:51 saw how spinal nerves have their own areas where the exit. Ags,
48:59 Uh thoracic lumbar and sacral and you eight pairs of cervical nerves, 12
49:08 of thoracic, five pairs of And they each correspond to the vertebra
49:16 you have and the British column And we talked about the fact that
49:20 spinal cord proper becomes caught a a horse's tail and about L.
49:27 , L. Three which is no proper one structure. And this is
49:32 the place where if you have an in the brain. In some medical
49:37 you may get a spinal tap Where a small needle is inserted through the
49:45 to sample some of the fluid down around L. two,
49:50 3 or below. So as not download the spinal cord proper tissue but
49:56 go in the middle in between these to suck up a little bit liberal
50:00 fluid. And if there was a infection then you would know that that
50:06 is there by looking at the cerebrospinal . Um In some instances uh it
50:12 be also done for anesthesia purposes like anesthesia which is quite often done during
50:20 birthing process which can numb the bottom lower extremities and the bottom part of
50:28 body essentially. Okay for the spinal and the nerves, we discuss how
50:34 spinal nerves, the collection of the component, Taking that information, the
50:39 and the motor component, which is difference that the Africans come into.
50:45 central axon comes into this butterfly shapes dorsal horn and the ventral horn.
50:51 And you have the ascending sensory And I asked you to know the
50:56 college major sending pathways and then I that there's a lot of descending pathways
51:03 I don't want you to know the pathways. I don't want you to
51:05 able to label them or recognize Please do if you want to.
51:10 you should know that there are motor . Everything that's ascending is sensory,
51:16 is that's descending his motor it's not to help A light stimulus come in
51:26 or touch stimulus is descending signals that going down through the through the spinal
51:33 . So again and I said light just misspoke because everything from the neck
51:38 this process and the spinal cord, spinal nerves, everything that we just
51:42 at the brains talent all of these nerves is was going to process everything
51:47 the face that had a neck but have nerves that run extensively throughout the
51:53 such as the vagus nerve. Then talked about imaging, we said that
51:59 are static imaging techniques, X ray scans static. Then there is functional
52:05 which is pet scans F. R. I. And what you
52:11 is in pet scans you're looking at consumption of glucose and F.
52:16 R. I. You're looking at consumption of oxygen and that's a common
52:21 . Active neurons consume energy. They polarize, they consume oxygen. And
52:29 we talked in the last lecture I there's voltage sensitive dyes as experimental technique
52:36 will record the deep polarization. So neurons will de polarize and then I
52:41 mentioned intrinsic optical signal. I said can actually visualize the cells because when
52:46 cells are active they consume a lot glucose and a lot of oxygen,
52:51 also swell. So but these are typical clinical techniques that we've discussed the
52:57 scans and then from our eyes that used to essentially track brain activity and
53:05 what we call these brain maps that you different parts of the brain is
53:10 different during different tasks. And of these techniques we also mentioned can be
53:17 for many different purposes that can be in different parts of the body to
53:22 abnormal activity to detect cancer cells in in the whole body actually. But
53:29 the head and neck scans they're pretty procedures. And we even mentioned that
53:34 everybody can even go through this procedure going under general anesthesia potentially because it
53:42 uh it is quite quite significant not like a regular dental scan. Okay
53:49 with this we finished the C. . S. And we moved into
53:53 visual system and I'm almost out of . So first of all gonna leave
53:59 questions about C. N. But I think it is pretty straightforward
54:03 you review the slides and if you the images and a good way to
54:10 it is uh I was looking for online earlier today and I saw some
54:17 and don't quote me but it is about quiz Zealand or quiz Land or
54:22 like that. And then I was for some information on your muscular junction
54:27 I don't like the images in the . I was thinking maybe I need
54:30 have a different image. And it pretty cool because it had empty boxes
54:37 label everything in this neurotransmitter release. so this is what you may want
54:43 do also is you may want to everything you may want to practice especially
54:51 these images, Find a different image and see if you can still recognize
54:57 occipital, oh see if you can recognize hippocampus, this is the basil
55:04 or something like that or the corpus and that's a good way to prepare
55:09 that. Uh And as far as system goes, we did talk about
55:15 anatomy of the eye and in general talked through the entire system, We
55:21 the entire visual system when I say , we stopped at V.
55:26 which is the primary visual cortex and we said oh there's this beautiful Catholics
55:30 this stuff gap was over here and this motion and this color and it
55:35 blended with sound. So we couldn't all the way through even the secondary
55:40 where things get even more complex. the visual processing gets more complex uh
55:46 the anatomy of the eye. It's basic things I think that almost everybody
55:52 the anatomy of the eye but you want to review it. When we
55:56 about the circuit, you should know retinal circuit the processing of information because
56:03 photo receptors to bipolar cells to retinal cells um You should know that photo
56:10 is the photo transaction and ganglion cells the only output after retina. Uh
56:18 there are differences especially in the outer of the photo receptors where you have
56:23 floating discs and rods. And that two systems. Rod system vs.
56:28 system rod is no colors. Night cones. You have three types of
56:33 . This chromatic vision but it also a lot of direct access rays of
56:38 . You have very high levels of and density of cone photoreceptors and a
56:44 which is this central region responsible for security vision. And you have three
56:49 of cones, the blue, the and the red ones. And so
56:54 activating different counts to different extent you produce this what we call color mixing
57:07 for photo trans duck shin. Just that this photo transaction happens when you
57:14 have activation by light and the change the retinol from transcend to assist and
57:22 activation of the G. Protium and of cyclic GMP into GMP. And
57:29 fact is in the dark. The receptors leave D polarized in the
57:36 The photo receptors hyper polarized and the polarized because there's no cycle of GMP
57:43 the sodium channel is no longer So now they're hyper polarized. When
57:50 talked about receptive field properties. We said that the best way to get
57:56 activation from the retina or from the sauces by shining these pots of light
58:02 the retina and either have the center the surround that led or the center
58:08 dark and the surround that's dark. this is what retina processes these centers
58:13 things that are drawing on the board this is probably one of the most
58:21 slides. But what I want you know about this is already mentioned in
58:26 that I'll do it again. So the fact that whether it's d polarized
58:30 hyper polarized in the dark and the know that fact that in the dark
58:35 d polarized and the light is Then the questions that I may have
58:41 the only one that type of bipolar that express psychotropic receptors. So that
58:47 medical tropic is that is to say tropic receptors. Glutamate will hyper polarized
58:56 . Although this does d polarized because said eliminate will hyper polarized because it's
59:01 inverted so no glutamate, the cell be polarized because it's it's in the
59:08 there is no no. So you that there is time conservative versus
59:12 And so the level of the bipolar you have final topic and medical problems
59:17 the tropics. I'm conservative medical traffic and then you have the signaling system
59:24 into ganglion cells which is an Okay, so pretty pretty straightforward.
59:32 isn't gonna be two questions. The was shown on the photo receptor that's
59:36 in the surrounding region, the cell with the Natoma. Tropically glutamate
59:43 But knowing these things this is a interesting level of of of of divergence
59:49 of how how this path click can the light and inhibit other cells.
59:54 if this photo receptor was connected, these cells were connected to another will
60:00 the opposite effect because they were under and they were in the dark at
60:03 moment. And then the other thing recall is that you have the inhibition
60:10 you have a particular horizontal sounds. this is a conservative estimate will be
60:15 itself and this is signed and verdict deep polarization of horizontal cell will cause
60:22 of the we call this negative feedback the negative feedback. Because you polarize
60:28 cell and you get fed inhibition and get hyper polarized. So this is
60:34 I remember about um these slides here uh finally I'm pretty much out of
60:44 but in the central processing when we about this we talked about plasticity.
60:50 review the critical period of development and and how even a short term deprivation
60:56 cause significant restructuring of the inputs and function of the cortex recall all of
61:05 outputs. These are great questions for exam. So again damaged the nerve
61:11 your eye and you have the damage nerve on one side damage to optic
61:17 . That's not gonna work because optic will contain both components from from both
61:23 . Okay. Uh Super cosmetic. Sorry a damage of the eye.
61:31 tunnel vision. You lose the periphery you lose the fibers that are crossing
61:40 . Number always retina it's like the . So this looking there in the
61:46 , this is looking ahead and temporal looking right here in this bipolar in
61:52 binocular zone that we have and all good stuff. The magna power vallee
62:00 123456 neocortex projections into neocortex. You ocular dominance columns where the projections come
62:09 on binoculars at the latter form. They start blending information of layers to
62:14 . So you have kilometer cortical You have inter cortical loop and you
62:18 cortical thalamic output. Also you have and layers 23. Mostly the process
62:24 activity. The cells are now in cortex reacting to bars of life instead
62:29 circles like they did in retina and on they have direction selectivity. They
62:35 orientation selectivity. There's convergence where you build sophisticated receptive fields now and you
62:44 produce a primal sketch and you can these unitary basic units or orientation columns
62:50 more complex hyper columns and image this using intrinsic Alaa optic signal or voltage
62:58 dyes. So there that was. , easy. Okay. Alright so
63:04 am out of time. I won't any questions that anybody may have.
63:15 , this line this slide is if look at the orientation columns, it
63:22 about 100 micrometers in size and it's single orientation column. Now you're trying
63:28 see how does this orientation column, microprocessing unit? How does that fit
63:33 the bigger picture? How does that with the ocular dominance columns that you
63:37 in Australia cortex? Right, so life puts it all together into what
63:43 call a hyper column which will have dominance extended throughout the entire six
63:50 Although you only see the layer Right? So you have contacted C
63:55 these ocular dominance columns will actually have of these orientation columns with their pinwheels
64:03 . That interesting thing is after you the boundaries between ocular dominance policy looking
64:09 two above. Because ocular dominance is you see that the center will contain
64:15 blobs. So somehow the center and to three that are concerned with color
64:21 are also demanding more metabolic energy which cited from oxides staying here. And
64:27 this shows that this y that you here in light right here. You
64:34 this in light also a response to Y here. But what you're seeing
64:38 is the intrinsic optical signal when you one. I actually can see a
64:44 in reflective properties in the brain. these hyper columns. Again, you'll
64:49 many of these hyper columns. Now talking about one millimeter size much
64:56 Okay. And you have multiple of hyper columns in your primary visual
65:04 Because you have the contra contra contra you have multiple of these orientation columns
65:10 blobs that are extending within this So does that help? Okay.
65:20 you everyone. I'm sorry if I the very last section it's just because
65:25 got interrupted at the very beginning. gonna stop the recording so I can
65:30 it and I will see how tomorrow's goes. But I may upload the
65:36 from tomorrow because of the interruptions
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