Comment · Thu, January 21, 2016 · Ceretropic & Nootropics Depot
Long-lasting downregulation of GABAergic synapses after repeated administration of anxiogenic drugs - possible implication for Fasoracetam?
Original post in this thread
I_Strahd · 5 points
Hello there,
I've been experimenting with a bevy of noots over the past couple years - and over that time, have remained consistently interested in fasoracetam for it's apparent potential in up-regulating the gaba system.
However, the use of gaba antagonists, for which this compound is considered, is still - in general - a mystery to me in terms of their long-term effect on an otherwise healthy brain.
Then today I happened upon this old study, which seems to make the case that:
"a long-lasting down regulation of GABAergic synapses can be obtained after repeated administration of anxiogenic, proconvulsant and convulsant negative modulators of GABAergic transmission. The latter finding further suggests that GABAergic synapses undergo rapid and persistent plastic changes when the GABAergic transmission is persistently inhibited."
http://www.ncbi.nlm.nih.gov/pubmed/1981393
and I'm left wondering...if fasoracetam's primary method of action is to antagonize gaba(b) receptors, will this, in actuality, have a negative impact on the functioning of the gaba system?
Similarly, will this mechanism hold,. in general, for all gaba antagonists?
And lastly, what is to be made of this c…
What they were answering
DeltruS · 1 points
I personally haven't noticed anything worse than my baseline coming off of lavender but is hard to tell, I need more time to experiment.
Also I believe that α2δ subunit can be attached to every vdcc.
https://en.m.wikipedia.org/wiki/Voltage-dependent_calcium_channel
If I understand it right, activation of the auxilary subunits would alter the pattern/intensity of activation of the main pore(the α1 Subunit). And different combinations of subunits make p/q, n, etc channel types.
An interesting theory would be if nerves use a sort of morse code to send data to the brain, and the vdcc can send several types of data. Ie touch vs painful touch. I read somehere that α2δ Subunit were upregulated in chronic pain.
https://en.m.wikipedia.org/wiki/Neural_coding
I've read here and somewhere else a long time ago that nerves can send different data along their path, and that the brain uses certain variables to interpret.
It is just a theory, but it makes sense if a few syndromes would be due to a problem with the difficult task of sending and deciphering different data along one nerve. Ie complex regional pain syndrome, autism (who often have sensory problems and describe sitting still as "painful"), etc.
u/MisterYouAreSoDumb · Ceretropic & Nootropics Depot
That could very well be. It might also be more complex than just subunit activation. There could be gene expression changes that are downstream of the receptor activation that get altered. We know that immediate early gene expression is altered by calcium transmission. Look at ARC (activity-regulated cytoskeleton-associated protein). It's expressed at NMDA sites, and reduces AMPA currents. It has been implicated in Autism and Alzheimer's.