https://preview.redd.it/hhqkm1fqia181.png?width=482&format=png&auto=webp&s=f9fdca0395cdb562e03590bb8ae24f94e0618733
I read that GABA made it easier for chloride ions to pass through the membrane and it was involved in both postsynaptic inhibition and presynaptic inhibition.
If I'm not mistaken, in case of presynaptic inhibition, the choride goes outside the neuron, against the concentration gradient with the help of the choride pump and this causes small depolarization which then inhibits the action potential.
In case of postsynaptic potential the chloride ions go inside the cell following the concentration gradient which then causes hyperpolarization that inhibits.
So my question is, how das GABA do it if it just opens up pathways for chloride to pass. Why is the chloride pump stronger than the concentration gradient in presynaptic inhibition and weaker in the postsynaptic potential. Does glycine actually cause this? Or does it matter what type of neuron it happens on?
When glutamate is released into the cleft from the presynaptic neuron what is causing the post synaptic neuron to depolarize? Is the glutamate binding to a postsynaptic receptor which is then opening the receptor to allow sodium ions in which then increases the internal charge of the postsynaptic neuron?
I wondered about this because the two neurons never actually touch. The synaptic cleft is very small, but if there is no connection the neurons might easily separate...
[in chemical synapses]
I have been reading literature regarding Neuronal potential measurement. Conventionally, researchers use electrode-based method to measure action potential. However, as it's of high invasiveness and low throughput several optical methods such as Genetically encoded voltage indicators (GEVIs) and chemical methods such as Voltage-sensitive dyes (VSDs) are emerging. One fundamental question I came across was GEVIs indeed can be targeted to the site of interest however, there only a few chemical methods targeting specific cell type have been developed. One such recent literature is this one: https://pubs.acs.org/doi/10.1021/jacs.0c00861. I am wondering, are neuroscience researchers really interested in measuring neuronal potential at individual synapses (which is gradient) or only at the axon hillock (as it's the one which finally matters?). I mean does measuring gradient potential at a defined area is of any interest or is it just another piece of research making no use for neuroscience researchers? (I don't know whether it's useful to synapse plasticity research and all)
Hey guys, I have to write an essay made up of a longer question which I am doing fine with, but the last part of the question( the title) Iβm a bit confused with. Does anyone have a simple way of explaining this, I will research it further but Iβm not sure where to start? Thanks
I've been looking into them and many studies such as this mention an increased presynaptic sensitivity/responsiveness and decreased postsynaptic sensitivity/responsiveness in certain mental illnesses like panic disorder and a presynaptic subsensitivity in schizophrenia.
I've read that presynaptically alpha 2 receptors have norepinephrine bind to them to prevent its own release while postsynaptically norepinephrine binds to produce stimulating effects, but the wording on some of these studies can be confusing.
This study mentions the existence of postsynaptic inhibitory alpha 2 adrenoceptors which seems to contradict what I initially thought their function.
Which leads to my next question, this study implies that in ADHD there's elevated levels of NE at the postsynaptic a2A receptors in the PFC. How exactly would people with ADHD have elevated postsynaptic a2A binding without an elevated presynaptic a2A binding to match? Most of the studies I've read almost make it seem like presynaptic a2 receptors are almost entirely responsible for binding at postsynaptic a2 receptors through their inhibition or lack thereof.
Lastly this study, along with this one seem to clarify that only the postsynaptic a2A receptors have stimulatory effects while all the the other a2 receptor subtypes, pre or postsynaptic, have inhibitory effects.
From what I learned, in the case of NMDA-dependent LTPs, if an enough amount of neurotransmitters are released, many AMPA receptors open, leading to many NMDAs opening due to depolarization. This causes Calcium ions to rush in the postsynaptic cell, leading to many changes within the synapse such as more AMPA receptors or increase in NT being released in the presynaptic cell.
So my question is this: in this process, all it takes for LTP to happen is more frequent or larger stimulations. As this is caused by the firing of pre-synaptic cells, it looks that the firing of postsynaptic cells isn't necessary. However, this NMDA-dependent LTPs are one type of Hebbian LTPs, right? Then where is the 'fire together' part of the 'cells fire together, wire together' rubric?
When serotonin passes the synaptic cleft and binds with postsynaptic proteins, what happens to them after that?
when new dendrites grow... do new postsynaptic receptors grow on/with them? if not, then where do these new dendrites get their receptors from?
apparently EEG records electrical signals originating from postsynaptic potentials and not action potentials. but what is the difference?
and then, why do only postsynaptic potentials affect EEG and not the action potentials? shouldn't the action potentials should produce signals that EEG can pick up?
I found this study on this website, quoting:
>A 2014 study looked at squirrel monkeys who had been given THC, the compound in marijuana that produces the high. The monkeys had the option to keep receiving more THC.
>
>Researchers then gave them different doses of MSX-3, which produces effects similar to those of caffeine. When given low doses of MSX-3, the monkeys gave themselves less THC. But at high doses, the monkeys gave themselves more THC.
>
>This suggests that low levels of caffeine may enhance your high so you donβt use as much. But high levels of caffeine could affect your high in the opposite way, leading you to use more marijuana.
>
>More research as needed, as this small study was conducted only on animals, not humans.
What's your opinion? Anyone knows any other study similar to this one?
I "empirically" noticed that when I'm tired and partially sleep-deprived, weed gets me higher but I thought it was a bias due to fatigue, such as need for sleep tends to make you sleepier, and being sleepy is similar to being high but not quite the same. Btw, sometimes I noticed that an evening short nap can affect high as well.
Seems like there might actually be some kind of correlation between sleep and weed high?
Friday, December 7, MG 2001, 12:30-1:20 pm, last Biology seminar. Presented by Linh Le, graduate student at Truman State University.
Can someone help me with this question
If an inhibitor of acetylcholinesterase is added to a neuromuscular junction, then the postsynaptic membrane will:
a) Be depolarized by action potentials more frequently
b) Be depolarized longer with each action potential
c) Be resistant to depolarization
d) Spontaneously depolarize
http://www.nature.com/nrn/journal/v11/n9/fig_tab/nrn2884_F1.html
I mean, is it somehow possible to get rid of that excess glutamate, or block release of it not causing any problem/health danger? Can we simply "delete" glutamate from this cycle? What if we would block AMPA and NMDA? What would happen to that glutamate which was released? What if we would use some anticonvulsant drugs like lamotrigine? Or maybe we shold increese glutamate reuptake somehow? How is it works?
Edit: So I found something https://www.youtube.com/watch?v=GMyCWup1Xqo&feature=youtu.be&t=131 That means that lamotrigine would just block the release of the glutamate like here https://imgur.com/pALdqGc , right? But without any implications?
Edit 2: related thread https://www.reddit.com/r/neuroscience/comments/4n2bo7/is_it_possible_to_eliminate_glutamate_release/
