Skip to main content
. Author manuscript; available in PMC: 2012 Jul 1.
Published in final edited form as: J Chem Neuroanat. 2011 Jun 6;41(4):200–218. doi: 10.1016/j.jchemneu.2011.05.010

Figure 13.

Figure 13

Schematic representation of our hypothesis regarding the neurobiology of stress sensitivity and the effect of citalopram. Based upon the current data, we speculate that even in the absence of stress, stress-sensitive animals have an overactive CRF system and an underactive serotonin system, compared to stress-resilient animals. Administration of citalopram for 15 weeks reduced CRF innervation of the DRN and increased CRF-R2 expression on serotonin neurons. Therefore, we speculate that citalopram normalized the CRF system and either directly or indirectly, upregulated CRF-R2 expression. Citalopram did not affect serotonin-related gene expression, but based upon its mechanism of action, we speculate that synaptic serotonin was increased, which in turn reduced CRF production.