Posted by Questionmark on December 1, 2003, at 18:37:02
In reply to Re: Buspar, posted by SLS on December 1, 2003, at 8:59:37
> > That is true, it is both a post synaptic and presynaptic agonist. So by activating the post synaptic receptors it has antidepressant activity, but by activating the presynaptic receptors it decreases overall serotogenic function. Presumably, is anxiolitic profile is a result of decreased activity at the 5ht2a receptor (acivation of this receptor is presumably why SSRI's can cause anxiety).
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> I did a quick search regarding the function of 5-HT1a receptors and found nothing that indicates they are excitatory upon serotonergic neurons. Maybe you can find something definitive identifying these receptors as promoting rather than inhibiting the firing of 5-HT neurons and pathways. I'll try to research it more after I ingest some caffeine. There are three areas of concentration of 5-HT1a receptors on the cell membranes of serotoninergic neurons: 1) prejunctional (terminals); 2)somatodendritic (cell body); 3) postjuntional (postsynaptic). 5-HT1a receptors at all of these locations act as inhibitory autoreceptors. At postsynaptic sites, they serve to hyperpolarize the neuron and inhibits its firing via the opening of K+ channels.
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> - Scott
Well that's bizarre. i thought that what Linkadge and others said about postsynaptic 5HT-1A receptor activation being excitatory was accurate. But if what you said is correct that it was not. And if that is the case, then it would seem like buspirone would have effects much similar to ... (dammit! damn anticholinergic memory deficit effects) .. well, the serotonin reuptake enhancer (forget what its called right now). So whats the truth?
poster:Questionmark
thread:285253
URL: http://www.dr-bob.org/babble/20031126/msgs/285653.html