Pindolol acts as a partial agonist at 5ht1a. It appears this translates as antagonism, effectively. Pindolol appears to have preference for blocking presynaptic receptors, meaning it theoretically disrupts the negative feedback loop without affecting postsynaptic receptors — in turn, more serotonin is available in the synaptic cleft. This is credited for the efficacy of Pindolol as an augmentation to anti-depressant therapy.
If this holds, and if presynaptic 5ht1a desensitization is a characteristic of PSSD, then we should not have any anti-depressant response to Pindolol. This could be a way of probing 5ht1a autoreceptor desensitization theory.
“ The latter drug (which is also an adrenergic beta-blocker) preferentially occupies 5-HT1A autoreceptors, thus preventing feedback inhibition of serotonin release and accelerating antidepressant response in most though not all studies (Celada et al. 2013; Portella et al. 2011). Consistent with this mechanistic interpretation, co-treatment of depressed patients with buspirone and pindolol elicited an antidepressant effect (McAllister and Massey 2003), whereas buspirone lacks antidepressant efficacy by itself, likely because its insufficient partial agonist efficacy at post-synaptic receptors (and full agonist activity at 5-HT1A autoreceptors) (Celada et al. 2013). “
https://www.ncbi.nlm.nih.gov/pmc/articl ... o=0.375940
Pindolol - Preference for pre-synaptic 5ht1a
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Re: Pindolol - Preference for pre-synaptic 5ht1a
You could also probe by taking DXM, reboxetine, or a antipsychotic which strongly agonizes 5ht1a - should give us window of emotional function
Re: Pindolol - Preference for pre-synaptic 5ht1a
So what can we do to treat it?
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