A list of puns related to "Metabotropic Glutamate Receptor"
Fasoracetam is a purported nootropic of the racetam class of drugs. It acts primarily as an agonist of all three categories of metabotropic glutamate receptors. Interesting to me, there doesn’t seem to be any mention of glutamate excess or excitotoxicity In any literature discussing the effects of fasoracetam.
However, When examining other glutamergic agonists such as ibotenic acid, terms such as brain lesioning agent and neurotoxin is commonly employed when describing it.
How is fasoracetam any different and is it a dose dependent neurotoxin or just not one at all?
Hi guys! I am not one of you, I do not have visual snow at all. The closest I experienced was the HD vision from Piracetam. I was interested in Fasoracetam which is an agonist at all metabotropic glutamate receptors. I found it too promiscuous so I went through all mGluR articles on Wikipedia to determine whether a given mGluR is positive or negative for my goals. And I found something that you might appreciate:
https://en.wikipedia.org/wiki/Metabotropic_glutamate_receptor_6
> mGluR6 is specifically expressed in the retina, in a subtype of bipolar cells that depolarize in response to light, known as ON bipolar cells. These cells form synapses with photoreceptor cells, and detect the neurotransmitter glutamate via a GPCR signal transduction cascade. The glutamate receptor mGluR6 is located post-synaptically at the tips of the bipolar cell dendrites, and is responsible for initiating a signaling cascade that ultimately controls gating of the TRPM1 channel.[7][8]
So my hypothesis is that you guys have inappropriate mGluR6 density and/or activation, and improper sensory gating by TRPM1, so it lets through background noise as signal. You have a similar sensory gating issue as found in tinnitus with audio signals and fibromyalgia with pain and other senses. Cocktail party effect, autism, and schizophrenia might also be similar.
I have searched this subreddit and /u/unknowncalicocat has already found the culprits: https://www.reddit.com/r/visualsnow/comments/hmitww/some_research_ive_done_over_the_past_few_months/
I am not familiar with the vision system and too drunk and too lazy to think about the exact events in bright and low light situations, so I let you guys figure it out. I hope I helped though. Cheers!
I´ve looked through various articles but wasnt able to find neither something thats a antagonist exept (non-reachable) research chemicals nor any mechanism of e.g. an antidepressant which decreases its function or expression.
The reason
We propose that CB1 receptor activation in the striatum decreases glutamate transporter activity and that the resulting increase in synaptic cleft glutamate concentration causes the activation of presynaptic mGluRs, which then decrease glutamate release.
Cannabinoids Decrease Corticostriatal Synaptic Transmission via an Effect on Glutamate Uptake http://www.jneurosci.org/content/23/35/11073.full.pdf
I would try this target to see whether the affective effects of MJ are reversable by this.
Edit This is on my own risk ! Playing with Glutamate can result in a brain damage and this can happen a way faster than You believe ! means Your Life and Future is fucked up or at least negatively affected ! Because mGlu are autoreceptors, thus reducing Glutamate when activated, theres a chance to get Your brain flooded with it when inhibited.
Citation: Simonyi, A et al. "The role of metabotropic glutamate receptor 5 in learning and memory processes". Drug News Perspect 2005, 18(6): 353, ISSN 0214-0934
DOI/PMID/ISBN: 10.1358/dnp.2005.18.6.927927
Hi,
I was wondering whether someone would be able to give me access to this article please?
Paper link - http://benthamscience.com/journals/current-neuropharmacology/article/131357/
Pubmed link - http://www.ncbi.nlm.nih.gov/pubmed/27296643
Any help would be greatly appreciated.
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