| First Author | Diaz SL | Year | 2012 |
| Journal | Mol Psychiatry | Volume | 17 |
| Issue | 2 | Pages | 154-63 |
| PubMed ID | 22158014 | Mgi Jnum | J:278413 |
| Mgi Id | MGI:6331048 | Doi | 10.1038/mp.2011.159 |
| Citation | Diaz SL, et al. (2012) 5-HT(2B) receptors are required for serotonin-selective antidepressant actions. Mol Psychiatry 17(2):154-63 |
| abstractText | The therapeutic effects induced by serotonin-selective reuptake inhibitor (SSRI) antidepressants are initially triggered by blocking the serotonin transporter and rely on long-term adaptations of pre- and post-synaptic receptors. We show here that long-term behavioral and neurogenic SSRI effects are abolished after either genetic or pharmacological inactivation of 5-HT(2B) receptors. Conversely, direct agonist stimulation of 5-HT(2B) receptors induces an SSRI-like response in behavioral and neurogenic assays. Moreover, the observation that (i) this receptor is expressed by raphe serotonergic neurons, (ii) the SSRI-induced increase in hippocampal extracellular serotonin concentration is strongly reduced in the absence of functional 5-HT(2B) receptors and (iii) a selective 5-HT(2B) agonist mimics SSRI responses, supports a positive regulation of serotonergic neurons by 5-HT(2B) receptors. The 5-HT(2B) receptor appears, therefore, to positively modulate serotonergic activity and to be required for the therapeutic actions of SSRIs. Consequently, the 5-HT(2B) receptor should be considered as a new tractable target in the combat against depression. |
