Comment · Tue, December 2, 2014 · Ceretropic
What is Trkb down regulation and it's consequences?
Original post in this thread
[deleted] · 8 points
I read that this has been associated with Noopept but I can't make any sense of it. I'm not a scientist.
What they were answering
NellucEcon · 2 points
Isn't semax supposed to up-regulate Trkb (at the same time that it agonizes, i suppose indirectly, agonizes it)? At least that's what wikipedia says. I can read only the abstract of the the cited article, which seems unclear (it would seem that upregulated trkb mrna would increase trkb expresison, but it might not be the case):
u/MisterYouAreSoDumb · Ceretropic
Good find! I had not seen that study yet.
Interestingly, Semax treatment did not increase hippocampal BDNF levels beyond maximal BDNF levels detected in controls, suggesting that Semax modulates hippocampal BDNF expression within its physiological (possibly, circadian) range. Moreover, in contrast to the hippocampus, Semax failed to affect BDNF levels in the cerebellum, hence, pointing to a brain region-specific action of this peptide. In further support of this notion, we observed recently that Semax only induces a small (1.2-fold) and timely restricted (3 h) increase of BDNF levels in the basal forebrain (Dolotov et al., 2006). Finally, in the hippocampus, Semax resulted in the increased transcription of BDNF exon III mRNA, which is known to be CREB (cAMP-response element binding protein)-dependent (Tao et al., 1998). Our knowledge on the Semax binding sites is currently rather limited. So far, we obtained evidence that Semax binding to basal forebrain cell membranes is calcium-dependent (Dolotov et al., 2006). The pronounced effects of Semax on BDNF exon III mRNA expression now further point to the possibility that Semax acts through G-protein coupled receptors.