| 00:01 | OK. So when we started talking uh synaptic transmission, uh in the |
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| 00:08 | section of the course, I reminded about the action potential. We talked |
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| 00:14 | how the forward propagating action potential will the release of the neurotransmitter. And |
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| 00:19 | back propagating action potential is very important communication back into the cell and synaptic |
|
| 00:25 | . In particular, a type of that we call spike timing, dependent |
|
| 00:31 | . Uh For the discovery of we talked about how acetylcholine was discovered |
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| 00:37 | Odo Loi and this junction between vagus and cardiac muscle of the heart. |
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| 00:45 | the fact that the Cty Coline was slow down the heart rate. We |
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| 00:50 | distinguished between chemical and electrical synopsis and synopsis have no delay. Only a |
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| 00:56 | of signal passes through the very important synchronization of activity of uh large neuronal |
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| 01:03 | in very fast time and is subserving the structure of these gap junctions that |
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| 01:09 | hemi proteins located on two sides of of the neurons. We have chemical |
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| 01:14 | that will have vesicles that will have the release of the neurotransmitter into the |
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| 01:21 | cleft and pro synaptic densities where you receptors located, notice the differences between |
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| 01:27 | or inhibitory synopsis morphologically. And then spent some time talking about the motor |
|
| 01:34 | . In this particular instance, neuromuscular , we described the anatomy that this |
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| 01:39 | a high fidelity junction has a lot acetyl coline that gets released bonds, |
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| 01:45 | cogen receptors. The release of acetylcholine cause plate potential. It's always very |
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| 01:51 | potential of 70 millivolts or so, subsequently causing the opening of the voltage |
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| 01:56 | sodium channels in these junctional faults and influx causing the contraction of the |
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| 02:03 | So big big events there are that binds to only nicotinic acetylcholine receptors. |
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| 02:10 | need two molecules to activate one receptor that the nicotinic acetylcholine receptor will allow |
|
| 02:18 | the influx of sodium and influx of . And the influx of sodium through |
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| 02:23 | receptors will cause the initial depolarization of muscle cells, subsequently opening volt educated |
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| 02:29 | and calcium channels that will contribute to initiation of the action potential in the |
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| 02:34 | fiber. So this is excitatory and it causes a contraction and here acetyl |
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| 02:40 | , unlike in the cardiac muscle and skeletal muscle acts through nicotin acetyl poon |
|
| 02:45 | . And these synapses that are only have certain criteria for the neurotransmitter systems |
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| 02:52 | have to be synthesized, release, the fact degraded. Uh Please review |
|
| 02:57 | and we talked about major classes of , amino acid neurotransmitters where we spend |
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| 03:02 | of our time gaba glutamate signaling. is the major inhibitor neurotransmitter in the |
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| 03:08 | cord. These classes of I means we discussed aceto Cole and dopamine up |
|
| 03:14 | enough and peptides. So peptide that different and the production synthesis and transportation |
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| 03:21 | the neuropeptide was different from the uh such as a means and amino acids |
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| 03:28 | they're made upon high demand of levels activity uh processed and placed into the |
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| 03:36 | gran and like the vesicles. And not released as specifically just that the |
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| 03:43 | which rather can be released along the extent as well. In general, |
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| 03:48 | things need to happen presyn optically for neurotransmitter vesicle fusion. And that is |
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| 03:54 | in the form of the presynaptic action which will open voltage gated calcium channel |
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| 03:59 | the influx of calcium is necessary for fusion of the protein protein complex between |
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| 04:05 | vesicle and the plasma membrane and release the neurotransmitters into the synaptic clap. |
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| 04:10 | so there are some calcium sensor molecules as synaptic Tagment uh on the outside |
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| 04:15 | the vesicles set for the signaling allow the fusion of the two protein |
|
| 04:21 | Exocytosis followed by the endocytosis. We about pre fracture technique, imaging uh |
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| 04:29 | using electron microscopy. And then we discussed that these different technique of |
|
| 04:35 | . In this particular case, calcium die imaging, we imaging calcium concentrations |
|
| 04:41 | fluxes and calcium pres and the spatial dynamics of calcium. In this |
|
| 04:48 | then we talked about uh that in C N S, unlike in the |
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| 04:53 | junctions, the E P SPS are small in the order of only half |
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| 04:56 | millivolt. And sometimes you can have fusion uh instead of the full fusion |
|
| 05:02 | the C N S synopsis. And not as reliable as neuromuscular junctions. |
|
| 05:07 | then talked about the E P SPS get generated with release of glutamate and |
|
| 05:13 | . So E P SPS are much in the C N S about a |
|
| 05:17 | a mil from a single synapse, release. And IP SPS inhibitors optic |
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| 05:24 | that are mediated by influx of negatively chloride ions. They're also very small |
|
| 05:29 | they're graded potentials. So, unlike potential in neuromuscular junction, the E |
|
| 05:34 | SPS and IP SPS are quite small their amplitude. Uh And when we |
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| 05:42 | about direct signaling is ionotropic signaling. when there is a binding of a |
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| 05:48 | , in this case, Gaba onto receptor, there's an influx of fluoride |
|
| 05:54 | in metabotropic signaling, there's an activation G protein complex. So there is |
|
| 06:00 | of ions through the receptor that binds that neurotransmitter molecule that there is a |
|
| 06:05 | cellular cascade activation. We spent quite bit of time in understanding the |
|
| 06:11 | So you should be responsible and knowledgeable the synthesis of acetylcholine from ace Cole |
|
| 06:18 | chat release of acetylcholine, uh binding acetyl colon in the C N S |
|
| 06:24 | both ionotropic nicotinic and metabotropic muscarinic acetylcholine degradation of acetyl colon by acetal master |
|
| 06:34 | . Again, a cot transport with of cole back into the cell and |
|
| 06:38 | through chat to acetylcholine. We also how acetyl cholinesterase inhibitors. So, |
|
| 06:47 | and pharmacological preparations that inhibit acetylcholinesterase are medications for Alzheimer's disease by inhibiting the |
|
| 06:56 | of acetyl colon is prolonging the bi of that acetyl colon in the synapse |
|
| 07:02 | therefore effect of that acetyl colon in synapse. Cylco will act as an |
|
| 07:09 | to both nicotin and muscarinic receptors. nicotine will be a natural agonist to |
|
| 07:16 | receptors and so will the ma Musca then they also have antagonists. So |
|
| 07:22 | will be inhibiting activity of nicotine or receptors and atropine respectively. We also |
|
| 07:30 | about the fact that botulinum toxins are to be interacting with this podium protein |
|
| 07:37 | fusion uh uh with uh botulinum toxins that are found from the sodium |
|
| 07:46 | And this is also the basis for and beauty usages for Botox injections, |
|
| 07:53 | well as well as uh pharmaceutical preparations treating migraines with Botox injections. And |
|
| 07:59 | there are many different substances natural as as human synthesized or gama phosphate molecules |
|
| 08:05 | act very much like acetal mester And many of these molecules will be |
|
| 08:11 | with the binding diffusion or the posy receptors for cole. And therefore the |
|
| 08:16 | function in the body or the brain on the exposure to that particular |
|
| 08:24 | Olamine. We reviewed. Also, talked about how tyrosine is precursor to |
|
| 08:29 | dopa, which is precursor to which is precursor for noa or precursor |
|
| 08:35 | uh all of these neurotransmitter systems that different uh functions. Uh and they |
|
| 08:41 | a way there are certain similarities. here, uh we talked about how |
|
| 08:46 | cocaine can block the reuptake of CTA means prolonging that they by availability of |
|
| 08:53 | . And how Cine get broken down , by monoamine oxidase. So it's |
|
| 09:02 | little bit different. You can have mono oxidase uh that are located preoptic |
|
| 09:11 | than the synaptic fla like we saw um for acetylcholine glutamate is the major |
|
| 09:20 | neurotransmitter amino acid. And then uh gets converted into the major inhibitor neurotransmitter |
|
| 09:27 | to one step reaction with the glutamic decor box list for Gad. So |
|
| 09:31 | of the cells that synthesize Gaba will gad positive and uh they will be |
|
| 09:39 | uh Ga Gaba. Uh So you stain them for both gabba and neurotransmitter |
|
| 09:44 | you're using different staining techniques or for serotonin, uh also tripp to is |
|
| 09:52 | to five hydroxy trip to which is to serotonin. Uh And here we |
|
| 09:57 | that the PROzac, a common uh name uh antidepressant medication would be blocking |
|
| 10:05 | retic prolonging availability of serotonin. Then talked about some nonconventional neurotransmitters and the |
|
| 10:14 | and also nitrous oxide, carbon monoxide AIC acid. And in particular, |
|
| 10:21 | we talked about uh anandamide and two glycerol here and the cannabinoids, we |
|
| 10:29 | how they are different from other neurotransmitters that they get produced on demand. |
|
| 10:34 | not stored in vesicles, they are soluble, they'll cross cross the membranes |
|
| 10:39 | retro retrograde target presynaptic C B one that are linked to G protein complex |
|
| 10:46 | will control or in this case, calcium channels. Therefore, there's |
|
| 10:52 | induced suppression of inhibition, depolarization, indued suppression of excitation. There's this |
|
| 10:58 | feedback loop that gets subserve by the the cannabinoid molecules. And if we |
|
| 11:05 | to label these different molecules, we use different techniques immuno as the chemistry |
|
| 11:09 | is based on the antibody and then hybridization which is based on radioactively labeled |
|
| 11:16 | with a known proper complementary sequences of acids. And then we talked about |
|
| 11:23 | of neurotransmitters, how you can apply and mimic the effect type of stimulation |
|
| 11:28 | prey. The and we said that are certain limitations to this kind of |
|
| 11:32 | application of fluids. Inevitably you have and it's nonspecific. So we discussed |
|
| 11:37 | technique of unga uncaging neurotransmitters where neurotransmitters get caged inside the chemical cages and |
|
| 11:44 | can get uncaged with photos with exposing them to very much uh more |
|
| 11:51 | spatial areas to single synopsis. And a more advantageous technique if you want |
|
| 11:57 | activate just one or two synopses in system. Then we talked about |
|
| 12:04 | So you have spatial summation. These the signals that sum made in |
|
| 12:09 | And you have temporal summation, the that sum made over time. And |
|
| 12:14 | talk about the length constant. So length constant is a distance that it |
|
| 12:19 | for this maximum current from point A point B. When it reaches 37% |
|
| 12:24 | its maximal current, it gives us is called the length constant. And |
|
| 12:29 | length constant lamb, the value, longer the lamb the value, the |
|
| 12:35 | is the length constant. The better is especially for temporal summation. If |
|
| 12:40 | cells have a longer length constant and varies across different cellular populations, the |
|
| 12:45 | constant itself. And then we talked how if you have excitation and a |
|
| 12:51 | of the exci inputs would be coming the distal dendrites of these neuronal |
|
| 12:56 | And of course, if they're unimpeded inhibition, these inhibitory synopsis uh will |
|
| 13:04 | , as you can see, there's of the dendrite here with excitation will |
|
| 13:09 | for a portion of that depolarization to perceived and felt by the of the |
|
| 13:15 | . And in the case, we about if you have excitation, but |
|
| 13:19 | also can currently have inhibition. This may cancel out the depolarization of the |
|
| 13:25 | of the SOMA. So that is this is depolarizing, this is hyper |
|
| 13:31 | , but it is also shunting or for the currents to escape uh before |
|
| 13:37 | reach the SOMA so that they cancel completely. So we talked about that |
|
| 13:42 | you want to see an action potential neurons that you have to activate dozens |
|
| 13:48 | of the synapsis, excitatory synopsis. you have to hope that there isn't |
|
| 13:52 | of the inhibitory synopsis activation so that cell here can generate an action |
|
| 13:59 | And that is again very different and a mass from the neuromuscular junction modulation |
|
| 14:06 | neuromodulation typically is referred to the metabotropic and the intercellular signaling cascades that such |
|
| 14:13 | for example, activation of secondary messenger A and B protein kinesis. Remember |
|
| 14:20 | kinesis was will phosphate the channels and will desolate them. And in general |
|
| 14:26 | modulating. So it doesn't have a effect on the receptors and mines, |
|
| 14:30 | it's modulating downstream of potassium channels, a secondary messenger and typically metabotropic uh |
|
| 14:39 | , especially long term transcription activation by secondary messengers can have a much, |
|
| 14:45 | longer lasting cellular effect than the ionotropic through ionotropic receptors. So that was |
|
| 14:53 | first uh major lecture on neurotransmission. we moved into the second lecture. |
|
| 15:03 | we talked about a reminder about different by which this can be measured. |
|
| 15:12 | uh let me check something real No, all good. I'm gonna |
|
| 15:18 | . So not to repeat through this . OK. These are the major |
|
| 15:25 | neurotransmitter systems that we are talking Acetylcholine is something you should know |
|
| 15:31 | really well called Lagan antagonist, muscarinic colon receptor activation will open up potassium |
|
| 15:41 | . So if nicotinic will allow for of sodium and will cause depolarization, |
|
| 15:47 | on the cellular level will cause the effect will cause hyper polarization. I |
|
| 15:52 | I raise the hand and uh I uh gladly uh take a question after |
|
| 15:59 | finish the section. And if you mind to maybe write down the question |
|
| 16:04 | the chat. And then when I this section, I will look through |
|
| 16:08 | chat, uh any one of your . So I encourage anybody that has |
|
| 16:12 | is to write them down. It be easier for me to cover the |
|
| 16:16 | this way. And some of the may get answered as we review more |
|
| 16:22 | . So then we talked about glutamate and we talked about the tri part |
|
| 16:27 | . So glutamate gets released, it bind some ionotropic and metabotropic receptors will |
|
| 16:33 | transported back into neurons through glutamate neuronal transporters. But glutamate also has |
|
| 16:41 | transporters and will be retic of glutamine in glial cells. And so in |
|
| 16:48 | , glia regulates how much of glutamate available to neurons. And that's an |
|
| 16:53 | feature. OK. Catacholamines again, of some of these because we talked |
|
| 17:00 | it for 23 different lectures, but cola means would be involved mood movement |
|
| 17:06 | , visceral function. Serotonin is more mood appetite, sleep learning, uh |
|
| 17:14 | G protein cascades. We talked about isotropic and metabotropic through Aceto Cole could |
|
| 17:21 | opposing actions on the cell and metabotropic have opposing actions to each other through |
|
| 17:26 | cell. So we discussed the stimulatory beta receptor that stimulates production of cyclic |
|
| 17:33 | and inhibitory Norine alpha receptor that actually the production of cyclic K P and |
|
| 17:40 | A. So one system is pushing production of a certain molecule and a |
|
| 17:44 | physiological effect downstream in the cell. the other one is pushing it |
|
| 17:49 | but it's the same molecule. not from the both, both |
|
| 17:52 | So really the posy tic effect on cell in either an entropic or metabotropic |
|
| 17:58 | depends on the subtype of the receptor for the metabotropic receptors, the subtype |
|
| 18:03 | the G protein complex stimulatory versus inhibitory which it may be um uh bound |
|
| 18:11 | . So that uh difference when we about uh I mean neurotransmitters is that |
|
| 18:19 | are not produced everywhere in the So we talked about how the term |
|
| 18:25 | amino acid neurotransmitters will be found throughout brain and the cells would be expressing |
|
| 18:30 | . And that no, for is confined to being produced in the |
|
| 18:36 | cus and serotonin molecules are confined to nuclei. And acetyl cole will also |
|
| 18:44 | its own specific nuclei where these are cells that will produce that particular chemical |
|
| 18:51 | the whole brain. So this is different. That means that the production |
|
| 18:55 | confined to certain nucleus, but the are quite diffused and there is wide |
|
| 19:01 | into the coral subcortical spinal cord areas these nuclei that produce immune neurotransmitters. |
|
| 19:12 | So it is just a reminder of endocannabinoid signaling that it acts through C |
|
| 19:18 | one receptors and inhibits calcium channels and regulate the release of both glutamate Gaba |
|
| 19:25 | delta nine tetra hydro Komal or delta T H C is a phyto cannabinoid |
|
| 19:30 | is found in cannabis plant. And also is an agonist and it interacts |
|
| 19:35 | the C B one receptor. So mimics the activity of the endo |
|
| 19:40 | In part. Uh This is excitatory neurotransmission and inhibitory amino acid neuron |
|
| 19:48 | . So, glutamate will have its transporters. Gaba will have its own |
|
| 19:52 | , glutamate. Then we talked about APA and MD A kate receptors. |
|
| 19:58 | talked about how an E P S , the initial segment is due to |
|
| 20:03 | APA receptor activation and the late segment the E P S P is due |
|
| 20:08 | the an MD A receptor activation. that is because an MD A receptor |
|
| 20:12 | a magnesium block. So when glutamate released and it will bind to amp |
|
| 20:16 | interceptors, it will open ample receptors cause the initial depolarization through a A |
|
| 20:22 | subsequently opening an MD A receptor and the depolarization that accounts for the late |
|
| 20:29 | of the exci posy potential E P P. So an MD A receptor |
|
| 20:34 | it to be uh fully engaged. needs glutamate pre synoptic activation glycine as |
|
| 20:40 | co factor and it's a coincident So it needs to coincidentally know that |
|
| 20:46 | receptor has depolarized the posy tic which will relieve the magnesium block and |
|
| 20:52 | for the influx of sodium calcium and . So, not an MD A |
|
| 20:57 | are always permeable to sodium and potassium in some instances to calcium, but |
|
| 21:04 | an MD A receptors are permeable for influx of sodium and calcium. Because |
|
| 21:09 | MD A receptor is significant for pre by synaptic activation. It's very important |
|
| 21:15 | synaptic plasticity because it's also a significant of influx of sodium and calcium, |
|
| 21:21 | serves as a secondary messenger. Uh one of them will have their own |
|
| 21:28 | APA and an MD A and their antagonist C N Q X for non |
|
| 21:32 | MD A and A PV or A five for an MD A receptors. |
|
| 21:36 | these receptor channels will also have many different binding sides. So for |
|
| 21:43 | magnesium binding site, glycine glutamate, also things like illicit street drugs, |
|
| 21:49 | P or uh angel dust that are uh and dangerous drugs that can activate |
|
| 21:57 | MD A receptor to much different degree hallucinations. And schizophrenia potentially. |
|
| 22:04 | both of these not an MD and A I ionotropic and that is different |
|
| 22:09 | metabotropic Luter signaling in this diagram. explain how in the normal physiological conditions |
|
| 22:16 | the left, the 1.2 millimoles there's very little currents of these depolarized |
|
| 22:22 | hyper polarized potentials at minus 60. some N MD A currents at minus |
|
| 22:28 | and that E P SPS E P S and MD A receptor channels and |
|
| 22:34 | receptor channels, they all have a potential with zero malt. And on |
|
| 22:39 | right side, if you remove which basically is not the case |
|
| 22:44 | if you, you have zero magnesium , you prove that an MD A |
|
| 22:48 | in the presence of liliate will be at the hyper polarized potentials. And |
|
| 22:52 | is because you're now not having that block in an MD A receptor. |
|
| 22:58 | it proves that magnesium is blocking Then we reviewed the ID curse for |
|
| 23:03 | and MD A that A A K is the peak here at the initial |
|
| 23:09 | . The peak current that is the current and then MD A current is |
|
| 23:13 | second dash line that was measured. the late current. And what we |
|
| 23:17 | is that a A K A has linear I V plot and that an |
|
| 23:22 | A receptor, the closed circles has nonlinear ad plot because they're blocked here |
|
| 23:27 | magnesium. And you need depolarization to influx of uh ions through an MD |
|
| 23:33 | receptor. Both the ample currents and MD A currents will have a reversal |
|
| 23:38 | at zero Mets. And this final here of open circles shows late |
|
| 23:46 | And this blue component here is an A component. If you put a |
|
| 23:51 | or A P five, which is an MD A receptor antagonist, uh |
|
| 23:56 | will block an MD A current. from these uh filled circles here where |
|
| 24:01 | have current and PICO apis who will nearly zero current. And of |
|
| 24:07 | a PV would not have any effect the early component, which is |
|
| 24:12 | So there's no difference between these closed and open triangles. So for the |
|
| 24:18 | of your exam, if you can the different two I V plots between |
|
| 24:24 | Kate and I V plot for an A receptor. Uh And now that |
|
| 24:28 | have reversal potentials of zero malts and A PV is a specific blocker to |
|
| 24:33 | MD A receptor. So it will an MD A receptor currents but will |
|
| 24:37 | affect APA receptor currents. You're gonna in good shape. And remember that |
|
| 24:42 | blue area under the curve here depicted uh what gets blocked by A |
|
| 24:49 | And therefore, this blue area under curve is the MD A receptor component |
|
| 24:53 | the excitatory synaptic potentials. In this slide, we discussed some interesting things |
|
| 25:00 | amper receptors that if they have a and the protein uh uh uh and |
|
| 25:07 | amino acid sequence and one substitution of amino acid can result in this protein |
|
| 25:13 | permeable to calcium versus not being permeable calcium. We also talked about the |
|
| 25:19 | or development of glutamate synopsis. And talked about how during early development, |
|
| 25:24 | are only an MD A receptor that expressed in the synopsis. The synopsis |
|
| 25:29 | then termed silence synopsis because we need receptors in order to depolarize and open |
|
| 25:36 | MD A receptors. And so there other mechanisms at play that are responsible |
|
| 25:41 | opening an MD A receptors. But lot of times glutamate release may not |
|
| 25:45 | sufficient uh to activate the synapses because will have an MD A receptor that |
|
| 25:51 | have magnesium block. And that will called silent synopsis. And later, |
|
| 25:59 | will be uh um um there will a receptors that get inserted into the |
|
| 26:07 | A and an MD A receptor is important. They are also important for |
|
| 26:11 | T P or long term potentiation or term plasticity in particular in an MD |
|
| 26:16 | receptor. So the changes, the of the synopsis, the weakening of |
|
| 26:19 | synapsis or the anatomical changes that may happening in the number of synapses that |
|
| 26:24 | expressed in different interconnected neurons, metabotropic receptor. Example, signaling is through |
|
| 26:33 | P IP two divergent cascade of IP and Bayl Glycerol uh that regulate the |
|
| 26:41 | of kinesis and phosph phos remember kinesis phosphor phospho will Deos different channels. |
|
| 26:49 | we moved into talking about the inhibitory gaba ergic activation we talked about Gabba |
|
| 26:56 | and this is Gabba A uh receptor . That's ironic binding of Gabba will |
|
| 27:02 | for influx of chloride will cause hyper or IP S P. And we |
|
| 27:06 | saw that the same receptor channel has binding sites for alcohol, ethanol, |
|
| 27:13 | , barbiturates as well as neuros. we talked about how we have Gabba |
|
| 27:19 | which is ionotropic receptor channel allows for of fluoride and causes hyper polarization. |
|
| 27:27 | and Gabba B receptors. Psyop, will open the G protein complex, |
|
| 27:33 | will open potassium channels causing more hyper . And presynaptic Gaba receptors will be |
|
| 27:42 | the through G protein complex, regulating calcium channels very similar to what we |
|
| 27:48 | with the endocannabinoid signaling. And so reviewed this really nice diagram where you |
|
| 27:54 | gag synapse, you have gala A B. So hyper polarization, more |
|
| 27:59 | polarization have auto for Gabba B which auto regulate its own release of |
|
| 28:05 | If there's spillover into the excitatory it can auto regulate the release. |
|
| 28:10 | this case, hetero regulate for the release of glutamate and also through |
|
| 28:19 | on the synaptic glutar synapses. it can regulate the uh potassium channels |
|
| 28:27 | the hyper polarization and shutting down an A receptor function. So you can |
|
| 28:32 | a direct effect on GIC synoptic transmission . You can have indirect effect through |
|
| 28:39 | of, of uh gabba view receptors you can have the control of inhibitor |
|
| 28:45 | to release through the presynaptic gaba And both will control the influx of |
|
| 28:51 | that will inhibit voltage gated calcium channel voltage gated calcium channels and the influx |
|
| 28:56 | calcium when necessary for the neurotransmitter So I also mentioned that the slide |
|
| 29:00 | be a really great slide for you write down as much information as you |
|
| 29:05 | . And if you can recall everything I just said about gag and uh |
|
| 29:12 | signaling and add more details and you're be in great shape for the |
|
| 29:17 | And that was our last slide for section. So in the meantime, |
|
| 29:22 | me check real quick for any Let's see. Is this recorded? |
|
| 29:30 | , this is recorded. Will we to recognize chemical structure where the functional |
|
| 29:35 | 00 are attached on different neurotransmitters? , you will not. Is Gamba |
|
| 29:41 | inotropic or metabotropic. Gabba A is . Gabba B is metabotropic. Uh |
|
| 29:49 | you can see Gabba B is through protein complex will control potassium channels. |
|
| 29:56 | there's no flux through Gabba B It's a G protein coupled receptor. |
|
| 30:02 | can control potassium channels posy optically and can control uh presyn optically uh calcium |
|
| 30:11 | . Uh And uh let's see, was maybe a couple more slides that |
|
| 30:16 | looked at in the activation of Gaba Gaba B, but maybe you can |
|
| 30:20 | that on your own. There's detail the actual full lecture recording for this |
|
| 30:26 | lecture. So let me pause the here for a second recording. |
|
| 30:32 | So you can review this. But briefly, we talked about how a |
|
| 30:36 | of times excitation E P S P be followed by inhibition. Gabba A |
|
| 30:41 | atropic and then Gabba B metabotropic. we discussed by Qin as a blocker |
|
| 30:47 | GAA receptor and by blocking gale A , you can increase a lot of |
|
| 30:53 | response. So basically inhibition is holding excitation. And if you block |
|
| 30:59 | you release this abnormal levels of And then we talked about briefly a |
|
| 31:04 | protein coupled uh uh structure of these , the seven transmembrane segments, they're |
|
| 31:12 | different. We talked about ionotropic. is acetyl cole two binding sides |
|
| 31:19 | M that has M one through M . These are transmembrane segments. They're |
|
| 31:26 | from when we discuss the voltage gated channels, but they will comprise a |
|
| 31:30 | . And there are some similarities between segments and there are also differences between |
|
| 31:35 | segments. That's what accounts for the and the anatomy and function of a |
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| 31:40 | of these receptors. Then I what should you know from here, |
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| 31:44 | , everything about acetylcholine nor you should that alpha and beta have the opposing |
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| 31:51 | , glutamate amp MD AC N Q and A PV. All Gabba, |
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| 31:58 | A gabba B, fluoride potassium regulation Bicuculline is an antagonist for Gabba A |
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| 32:05 | T P that acts to D and and that caffeine is an antagonist of |
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| 32:11 | demo and receptors because that's something that's popular in uh in different cultures. |
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| 32:16 | we consume that psychotropic molecule. Uh of us almost every day or several |
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| 32:21 | a day. And then we talked different uh pathways, divergence, |
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| 32:27 | redundancy, parallel streams and amplification that can create through this neurotransmitter system by |
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| 32:34 | a single receptor which will activate multiple protein complexes will increase the production or |
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| 32:39 | the production of multiple secondary messengers, protein kis and will have an extensive |
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| 32:47 | on the cells. OK. I a question. If the synoptic membrane |
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| 32:55 | a simultaneous release of blue glutamate and in the same adjacent area, what |
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| 32:59 | happen to it? What will happen it? So if you were |
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| 33:08 | I don't mean to be rude, if you were listening about 10 minutes |
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| 33:15 | , I talked about a scenario where have this kind of a situation, |
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| 33:23 | ? Um We talked about this kind a situation. Does that sound |
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| 33:29 | Does this look familiar? Yes. that sound familiar? So you have |
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| 33:37 | here of excitation and inhibition at the time and then what happens? What |
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| 33:43 | happen to it? What happens at level of the cell? There's almost |
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| 33:47 | response. So uh let's see any questions from this section. OK. |
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| 33:55 | there's any more questions from the then we're done with neurotransmission. Let's |
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| 34:00 | . I have somebody else on the . Yeah. OK, good. |
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| 34:06 | you got it. So just go some of these questions you may |
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| 34:09 | It's a lot of material. Uh please go back and you can just |
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| 34:13 | some of the slides. Video points really good because they'll allow you to |
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| 34:18 | from slide to slide. So you have to listen to all of the |
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| 34:22 | again. But if you remember visually this is a slide that talks about |
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| 34:27 | inhibition, this is a slide that about summation spatial temporal, this is |
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| 34:33 | AAA good way to remember this and whatever I I cover in this |
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| 34:41 | it doesn't mean that this is the things that are going to be on |
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| 34:44 | test. I just cannot go through of the material of seven lectures, |
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| 34:50 | is um 10.5 hours and in in hour. So I tried to do |
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| 34:59 | best to focus on some concepts to some concepts, repeat some concepts that |
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| 35:05 | maybe more complex. But uh the way to think of what is going |
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| 35:11 | be on the exam is how we the time during the actual full length |
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| 35:17 | in in our course. OK. we talked about medial dorsal, |
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| 35:26 | medial dorsal Dutra, an interior rostral coal these different directions. We talked |
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| 35:32 | different structures in the brain. We about so uh uh somatic sensations and |
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| 35:39 | outputs the three meninas, the dura , arachnoid and PM matter. The |
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| 35:45 | system and circulation of the spinal abnormal formation of spinal fluid and lack |
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| 35:53 | drainage can result in hydrocephalus. And we talked about the development neural tube |
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| 36:01 | or neuralation where derm is going to in nervous system and skin components uh |
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| 36:14 | the human body. And this process neural tube formation is called neuralation. |
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| 36:19 | talked about two abnormal developmental uh features this neuralation that can result in an |
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| 36:27 | or a spina bifida. And following , there is uh formation of primary |
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| 36:34 | secondary uh vesicles. And there's differentiation these brain structures into more complex |
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| 36:40 | presence on m brain and hind uh forebrain differentiating intel and diencephalon optic |
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| 36:49 | . And as we move through the , it's differentiating into the diencephalon which |
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| 36:55 | comprised of thalamus, hypothalamus of the cortex. The corpus callosum, the |
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| 37:00 | fiber bundle that interconnects the two the internal capsule, which are the |
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| 37:06 | from the thalamus into the cortex and cortex into the thalamus. Um and |
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| 37:12 | ventricular system. Now, we have further differentiation of midbrain and tectum and |
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| 37:21 | tectum will contain the corporal quadrigeminal, appear in the inferior colliculus, the |
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| 37:27 | cerebellum on the back paws on the me and then the spinal cord proper |
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| 37:35 | . So these, for example, could be great labeling questions to identify |
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| 37:41 | lobe, occipital lobe to identify lateral or the or the, the third |
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| 37:47 | the fourth ventricle. Uh And it also some similarities, major anatomical similarities |
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| 37:55 | different animal brains. And this is of such similarities where you will find |
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| 37:59 | cells and Neocortex six layered structure in . And you'll find simular subtypes of |
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| 38:08 | and simular organization a lot of times the circuits of these cells in different |
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| 38:13 | . And then we spend a little of time talking about Neocortex, described |
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| 38:18 | as a laminar structure as well as as a column of structure that can |
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| 38:22 | revealed using these three subtypes of three of dyes, the gold initial stain |
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| 38:28 | we stain and the fact that you the six layer neocortex and slightly different |
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| 38:34 | , but in very similar organization throughout cortical areas of the brain, occipital |
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| 38:40 | , temporal lobe, parietal lobe and on. And it's gonna be the |
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| 38:45 | use in this stand to describe the or architecture of these different areas of |
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| 38:51 | brain. And this is our favorite 17 after lecture uh last week which |
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| 38:59 | contains primary visual cortical area. And we spend a bit of time on |
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| 39:06 | uh on the slide. And the home message from the slide was that |
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| 39:11 | higher order species, the more advanced you are as humans, the less |
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| 39:18 | will be dedicated to the primary areas for processing primary or primal sensor |
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| 39:26 | If you may uh basic, if may and more and more space in |
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| 39:32 | brains are dedicated to association areas, information, and then association areas that |
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| 39:38 | uh capable of uh intermingling and binding sensory inputs or modalities to gather association |
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| 39:49 | that will bind visual auditory smell and sensations that are happening at the same |
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| 39:57 | . And the low water species, have a lot of the brain space |
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| 40:01 | to this primary or primal sensory information . Oh yes, this is very |
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| 40:07 | for labeling. So brain stem, plan or bell and min hemispheres and |
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| 40:13 | three nus Gang campus and Amygdala, may show up well, go ahead |
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| 40:21 | questions and we talked about diencephalon which thalamus. It's a collection of different |
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| 40:26 | and lateral geniculate nucleus is one of nucleus that we know really well. |
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| 40:30 | where the projections from the retina go the L G N and from the |
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| 40:34 | nucular nucleus and goes into the area , a primary visual cortex in the |
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| 40:40 | lobe, it also contains hypothalamus and also has super charismatic nucleus as a |
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| 40:47 | of the diencephalon. So these are good for labeling and also good for |
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| 40:53 | where the thalamus responsible for what is G N and thalamus is responsible for |
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| 40:59 | remember, thalamus is a collection of nuclei. So L G M is |
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| 41:04 | visual system M G N. Medial is for the auditory system, ventral |
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| 41:10 | lateral here V P L is for SOMA sensory information. And this is |
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| 41:14 | station before all of the sensory inputs proceeded, gets sent to the |
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| 41:21 | the vis visual visual cortex, auditor auditory cortex, the matter sensor to |
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| 41:26 | matter sensory cortex where all of that eventually becomes at the uh highest order |
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| 41:33 | and cognition and perceptions of the sensor as well as motor output. This |
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| 41:40 | uh singular gyrus. We talked about and great structure that we all know |
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| 41:45 | hippocampus and the Amygdala. So all these uh that I've mentioned, this |
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| 41:50 | the cerebellum. And if you peel cerebellum, you expose the p where |
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| 41:56 | cerebellum is attached on. And in midbrain, you expose the superior coli |
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| 42:01 | are responsible for psychic eye movement. we learned in the visual system and |
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| 42:05 | colli that you learn in the auditory are responsible for hearing information processing. |
|
| 42:12 | then we talked about the cranial nurse I asked you to know the following |
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| 42:17 | nerves. Number one olfactory and you label it here because it's not shown |
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| 42:21 | this diagram. That's the first cranial olfactory. OK. Optic nerve I |
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| 42:28 | to know for you to know there's and right optic nerve. Then there |
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| 42:31 | an optics. And after the you have optic tract. If you |
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| 42:36 | nasal fibers are the ones that are cross over contralateral and temporal fibers from |
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| 42:42 | optic nerve are gonna stay ipsilateral on same side. Uh This is in |
|
| 42:47 | visual system, you can review So I would like for you to |
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| 42:50 | the optic nerve, I would like you to know the third nerve, |
|
| 42:54 | motor nerve because it implies uh what particular nerve does. It's a ocular |
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| 43:00 | nerve. So it moves the it controls the muscles of the |
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| 43:05 | Then I asked you to know number , which is trigeminal nerve. And |
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| 43:11 | because it's the largest nerve. And should be very easily uh able to |
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| 43:15 | optic nerves in the Kias. And two uh trigeminal nerve stalks that are |
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| 43:21 | in different area of the brain and ponds and they're very easily recognizable. |
|
| 43:27 | coal nerve I wanted you to know vestibular cochlea because it's the nerve that |
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| 43:32 | study when we study uh cochlea apparatus um auditory system. And finally, |
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| 43:41 | 10, which is vagus nerve. I want you to remember vagus nerve |
|
| 43:45 | we started by describing how neural transmission discovered. And that was by stimulation |
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| 43:51 | the vagus nerve. And also because nerve is not only innervating the heart |
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| 43:57 | and releasing acetal code in there. one of the most extensive cranial nerves |
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| 44:02 | runs throughout the extent of the human and innervating uh viscera. Um unlike |
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| 44:09 | nerves that are not as extensive and pretty targeted anatomically. Then we discussed |
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| 44:15 | major divisions in the spinal cord and vertebra of the spinal cord and also |
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| 44:20 | nerves of the spinal cord. So had c one through seven cervical |
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| 44:27 | each associated with the cervical nerve, through eight thoractic T one through |
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| 44:32 | 12 lumbra, L one to L . And here one that is |
|
| 44:37 | OK. So we talked about how proper uh spinal cord proper structures. |
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| 44:44 | number two, number three. And that, you have called it iguana |
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| 44:49 | clinically significant because you do spinal taps you do epidural anesthesia typically below L |
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| 44:58 | L three. So that you don't the nerve or in the cases of |
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| 45:04 | spinal tap, you sample through the fluid. In the case of the |
|
| 45:08 | anesthesia, you want to anesthetize the portion of the body which is done |
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| 45:13 | the birthing process. So it's gonna very painful uh for contractions of the |
|
| 45:19 | . And that's where this type of will be used. So each spinal |
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| 45:24 | is comprised of the sensory component, is dorsal root component and it goes |
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| 45:29 | the dorsal horn here. And from ventral horn, you have the output |
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| 45:34 | the motor neurons. Ascending information is be carried through the dorsal columns. |
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| 45:39 | is major sending sensor information here. then the other one here is a |
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| 45:45 | phyla ascending track that is located right on the ventral side and the |
|
| 45:52 | And then you have multiple descending mode pathways. And I asked you not |
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| 45:56 | to memorize those pathways, but I you to know and easily identify the |
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| 46:02 | column as the major ascending. Because you know that this is major sending |
|
| 46:07 | in the future, you study anything in the health professions. So you'll |
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| 46:11 | that in other tracks that may be on your exams or in some questions |
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| 46:16 | things like that, they're most likely to be descending if they're located outside |
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| 46:21 | the dorsal column. So that's an feature to know, you know, |
|
| 46:27 | then we talked about autonomic nervous system we don't spend enough time studying the |
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| 46:33 | nervous system. And with this uh slide, we then moved to talk |
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| 46:40 | imaging. OK. And we talked imaging techniques and we said that there's |
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| 46:46 | imaging. So you can have x-ray C T imaging, you can also |
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| 46:51 | static imaging of MRI. And then you're looking for neuronal activity or activated |
|
| 47:00 | areas, you have to use pat emission tomography or F MRI. Uh |
|
| 47:07 | in the most basic cases, and , pet will measure consumption of |
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| 47:12 | F MRI will measure oxygenation levels of . As we discussed that active neurons |
|
| 47:18 | be drawing a lot more blood, more oxygen and consuming more of the |
|
| 47:24 | and glucose is sort of like a the, the fuel and the food |
|
| 47:29 | for neurons. And in general, discussed that these procedures pet scans and |
|
| 47:34 | MRI S that are quite challenging for individual. In the case of pet |
|
| 47:38 | , you have to actually have a labeled solution that's injected inside of you |
|
| 47:44 | order to expose uh the areas of brain in our case that you're most |
|
| 47:50 | in. And we talked about how fact that in experimental imaging, you |
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| 47:54 | have this calcium sensitive imaging, you have both of sensitive di imaging. |
|
| 47:59 | talked about intrinsic optical signal and we about the visual system. These are |
|
| 48:04 | experimental techniques. And in many experimental techniques, you can actually get a |
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| 48:10 | of a single cell and sometimes even synapse and also different levels. You |
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| 48:15 | image a number of cells or circuits larger areas of the brain called macroscopic |
|
| 48:21 | of the brain. But in the , you don't have that ability and |
|
| 48:26 | of these techniques that they are Um that means that the skull is |
|
| 48:31 | being cut up. Nothing is being at like in many experimental neuroscience |
|
| 48:36 | But there are limitations in resolution, resolution where you cannot have a resolution |
|
| 48:41 | a single cell using these techniques. rather you're looking at the complexes of |
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| 48:46 | of neurons or nuclei that are involved uh revealing a specific function of a |
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| 48:53 | part of the brain during a specific , auditory or visual and so |
|
| 49:01 | OK, let's see questions. Questions A T P primarily function as an |
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| 49:09 | or inhibitor, neurotransmitter. Hm. a great question. And you cannot |
|
| 49:15 | talk about this as exci inhibitor. when we talk about excitation and |
|
| 49:19 | we're typically referring to glutamate Gaba. you talk about E P and these |
|
| 49:25 | , then you're really looking at the control and what A T P |
|
| 49:31 | it actually controls in large part uh glial function. And you cannot really |
|
| 49:39 | that A T P is uh primary , although it can exci although it |
|
| 49:44 | stimulate cells and uh caffeine can actually that same receptor denison receptor. So |
|
| 49:53 | just kind of it depends on the really of the receptor that binds to |
|
| 49:59 | acts through in the subtype of the . Do we have to remember the |
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| 50:04 | of the cranial nerves? So, you can remember this six nerves that |
|
| 50:08 | just mentioned, I think it's pretty to say that olfactory nerve is responsible |
|
| 50:14 | all faction optic nerve is responsible for , ocular motor for the movement of |
|
| 50:18 | eye, trigeminal, the largest sensor motor nerve of your, of your |
|
| 50:24 | vestibular cochlea sensory nerve that processes information and cochlea and vagus nerve uh runs |
|
| 50:33 | and was discovered uh where neurotransmission was . Do we need to know the |
|
| 50:39 | of vertebra nerves on precise location like six? Where is C 67 |
|
| 50:46 | Is it between 67 or is it ? Now? But the precise |
|
| 50:50 | You should know of the vertebra and subdivisions, major subdivisions of the cervical |
|
| 50:57 | Lumb and sacral for the spinal Uh The parameter cells in the Neocortex |
|
| 51:02 | and excitatory, they're excitatory. So cells release glutamate, they're excitatory cells |
|
| 51:08 | the inhibitory cells will be producing and Gaba is the second midterm not cumulative |
|
| 51:15 | only cover these seven lectures including content in the quiz. Yes, that's |
|
| 51:20 | . The midterm two will cover seven including content covered in the quiz, |
|
| 51:26 | is really just a repeating information that will be tested on. May even |
|
| 51:31 | the same question or two. Uh never know that you had on the |
|
| 51:36 | . So if you prepare for the , a lot of it might be |
|
| 51:39 | review for you and you can just up with more of the new information |
|
| 51:43 | information that you think is more Which part of the thalamus did we |
|
| 51:48 | to know? OK. That's a question for now. I think you |
|
| 51:52 | know later nu nucleus which is labeled that diagram and ventral posterior lateral nucleus |
|
| 51:59 | shows it has some matter, sensory in general, you should know that |
|
| 52:04 | is a collection of different nuclei responsible different functions. But in as far |
|
| 52:09 | having precise locations of the nu their apart from the lateral geniculate nucleus, |
|
| 52:15 | we already studied in the visual And for now, you don't have |
|
| 52:18 | know anything much more than that? . Are there any more questions on |
|
| 52:28 | C N S and imaging of neuronal in the brain? If not, |
|
| 52:36 | I'm actually going to uh think about this review session. Um because as |
|
| 52:44 | mentioned, the other information that we on the visual system is very new |
|
| 52:53 | I would like for you to review fresh. Uh We covered it in |
|
| 52:58 | lectures and the second lecture I had lot of information I would really recommend |
|
| 53:03 | review it, but I'm happy to any questions on the visual system. |
|
| 53:11 | . Well, if there are no questions, I thank you all for |
|
| 53:14 | here and putting your time into reviewing material. Please study hard and I |
|
| 53:20 | everyone to ace the test later this . Thank you and take care |
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