1. ¹Department of Basic Sciences, Laboratory of Pharmacology, Faculty of Medicine, University of Crete, Heraklion, Crete, Greece
2. ²Neuroscience Research, Novartis Institutes for Biomedical Research, Basel, Switzerland
3. ³Department of Psychology, School of Social Sciences, University of Crete, Crete, Rethymnon, Greece

Correspondence: Professor K Thermos, Department of Basic Sciences, Laboratory of Pharmacology, Faculty of Medicine, University of Crete, Heraklion, Crete 71110, Greece. Tel: +30 2810 394533; Fax: +30 2810 394530; E-mail: thermos@med.uoc.gr

⁴Current address: Laboratory of Pharmacology, School of Medicine, University of Athens, Athens, Greece.

⁵These authors contributed equally to this work.

⁶Current address: Laboratory of Pharmacology, School of Medicine, University of Thessaly, Larissa, Greece.

We announce with great sorrow that our colleague and friend Professor Christina Spyraki passed away on 2 September 2006.

Received 20 March 2008; Revised 17 July 2008; Accepted 17 July 2008; Published online 17 September 2008.

Abstract

This study investigated how the administration (acute and chronic) of the antidepressants citalopram and desmethylimipramine (DMI) influences somatostatin (somatotropin release inhibitory factor, SRIF) levels and SRIF receptor density (sst_1–5) in rat brain. Animals received either of the following treatments: (1) saline for 21 days (control group), (2) saline for 20 days and citalopram or DMI for 1 day (citalopram or DMI acute groups), (3) citalopram or DMI for 21 days (citalopram or DMI chronic groups). Somatostatin levels were determined by radioimmunoassay. [¹²⁵I]LTT SRIF-28 binding in the absence (labeling of sst_1–5) or presence of 3 nM MK678 (labeling of sst_1/4) and [¹²⁵I]Tyr³ octreotide (labeling of sst_2/5) binding with subsequent autoradiography was performed in brains of rats treated with both antidepressants. Somatostatin levels were increased after citalopram, but not DMI administration, in the caudate-putamen, hippocampus, nucleus accumbens, and prefrontal cortex. Autoradiography studies illustrated a significant decrease in receptor density in the superficial and deep layers of frontal cortex (sst₂), as well as a significant increase in the CA1 (sst_1/4) hippocampal field in brains of chronically citalopram-treated animals. DMI administration increased sst_1/4 receptors levels in the CA1 hippocampal region. These results suggest that citalopram and to a lesser extent DMI influence the function of the somatostatin system in brain regions involved in the emotional, motivational, and cognitive aspects of behavior.