Posted by Joe Schmoe on November 14, 2010, at 11:49:14
In reply to Re: Vilazodone vs Nefazodone - 5-HT receptors » bearfan, posted by linkadge on November 14, 2010, at 8:05:10
> Some argue that the clinical efficacy of SSRI's is primarily due to 5-ht1a agonism. If this is the case, than agents more selective to this receptor could be more effective/selective.
>
> From the profile, I would believe claims that the drug is potentially better for anxiety and/or reduced sexual dysfunction and/or insomnia.
>
> Linkadge
Here is something interesting I ran across on another forum:"To clarify for those that don't really understand (as I didn't fully up until just a few days ago), these 5-HT1A partial agonists aren't actually enhancing 5-HT1A receptor activity at all, they're decreasing it by blocking/competing with serotonin -- a full agonist --, exclusvely at inhibitory 5-HT1A somatodendritic autoreceptors. This results in increased serotonin release and enhanced activity at 5-HT1A postsynaptic receptors. Note that these drugs have significantly higher affinity for somatodendritic autoreceptors over postsynaptic receptors, as receptors on the cell body and dendrites are much more accessible than those in synapses. Hence, at the low doses in which they're used, they inhibit autoreceptors with little actual action on postsynaptic receptors at all, resulting in therapeutic benefits."
http://www.socialanxietysupport.com/forum/f30/vilazodone-82779/#post1256448
I believe the drug company researching Vilazodone is claiming that this H-5T1a blockade of the somatic autoreceptors is what (somehow) leads to greater dopamine activity elsewhere.
poster:Joe Schmoe
thread:970074
URL: http://www.dr-bob.org/babble/20101107/msgs/970202.html