Preparation for Child Psych PRITE and Boards
Revision as of 18:03, 7 August 2014 by Eugene Grudnikoff MD (Talk | contribs)
Introduction
- Selective serotonin reuptake inhibitors (SSRIs) block the serotonin transporter on the pre-synaptic neuron, increasing the serotonin available to bind to the post-synaptic 5-HT receptors.
- SSRIs have very weak affinity for other mono-amine transporters (norepinephrine and dopamine reuptake).
Delayed action
The delay in onset of action of SSRIs is the result of presynaptic and postsynaptic adaptive mechanisms.
- 5-HT1A receptor is a post-synapitc autoreceptor, which down-regulates 5-HT in response to higher 5-HT concentrations in the synapse. Blockade of 5-HT1a is hypothesized to enhance and speed up the therapeutic effect of SSRIs.
- Pindolol, a 5-HT1a antagonist, was studied in several placebo-controlled trials with promising results. [1]
- The blockade of 5-HT2A receptors (Mirtazapine, aripiprazole) also seems to improve the clinical effects of SSRIs. [1]
SSRIs and Sleep
Major Studies
STAR*D
- Non-responders to citalopram (Ci) (n=565) alone were randomized to Ci+Bupropion ER and Ci+Buspirone. Roughly 30% achieved remission in both groups. Bupropion ER group had fewer side effects and and greater reduction in symtpoms severity (NEJM 2006)
References
[1] The therapeutic role of 5-HT1A and 5-HT2A receptors in depression. J Psychiatry Neurosci. Jul 2004; 29(4): 252–265