Hello, here's a biggie to discuss!!!
Just doing a report about the psychedelic actions of mescaline. Some things
about the research on this drug have puzzled me, however. (I'll bet
everybody else too)
Though research has shown that mescaline can selectively bind the 5-HT2
receptor (selectively?) , why does iontophoretic application to the
serotonergic raphe neurons have no behavioural effect? Do you think there
may be an artifact somewhere or are there not many 5-HT2 receptors here?
Secondly, although reduction of serotonergic cell activity may be involved
in the psychedelic experience of LSD and mescaline, I have the feeling that
5HT may not be the primary neurotransmitter effect. Mescaline has been
shown to act as an antagonist of nicotinic (not sure whether muscarinic) ACh
receptors and as a beta adrenergic blocker. Do the ARAS and locus coerulus
cells directly activate serotonergic cells? anyone have a review of the
primary basic circuit with all these 3 NT's involved? I'd like to
understand some of the basics (but I also have to restrict my paper to ~2500
words). Please feel free to email me with your opinions.
another tidbit: leu-enkephalin levels (and opioid activity?) correlate
negatively with LSD and mescaline effects. is there a "best place" to find
Do I (mr C+ in neuroanatomy) have this right yet?
Interesting topic though. In my mind so far, the primary action of 5-HT is
in the raphe nuclei, nACh at the NMJ and facial nucleus, etc, mACh- and
B-adrenergic. . .I'd better read up on their brain locations but how about
ARAS and Locus coerulus respectively? Finally mescaline has to be rewarding
so how would dopaminergic action on the nuc. accumbens get input?