Different molecular forms of cholecystokinin and CCKB receptor binding in the rat brain after chronic antidepressant treatment

• Published in: Naunyn-Schmiedeberg's archives of pharmacology Vol. 355; no. 1; pp. 57 - 63
• Main Authors: Harro, J, Löfberg, C, Pähkla, R, Matto, V, Rägo, L, Oreland, L, Allikmets, L
• Format: Journal Article
• Language: English
• Published: Germany 01.01.1997
• Subjects: Animals; Antidepressive Agents - pharmacology; Brain - drug effects; Brain - metabolism; Cholecystokinin - analysis; Cholecystokinin - metabolism; Frontal Lobe - chemistry; Male; Maze Learning - drug effects; Rats; Rats, Wistar; Receptor, Cholecystokinin B; Receptors, Cholecystokinin - drug effects; Receptors, Cholecystokinin - metabolism
• ISSN: 0028-1298

Cholecystokinin (CCK) is a neuropeptide recently implicated in affective disorders. This study aimed at measuring the levels of different molecular forms of CCK and the binding characteristics of CCKB receptors in the rat brain after three weeks of treatment with four different antidepressants, imipramine, amitriptyline, desipramine, and citalopram (all at the dose of 10 mg/kg once per day i.p.). Chronic treatment with imipramine and desipramine had a significant immobility-reducing effect in the Porsolt's swim test. The effect of amitriptyline, albeit in the same direction, was not significant, and citalopram had no effect in this test. In the elevated plus-maze test of anxiety, all drugs tended to increase the number of open arm entries and the ratio open/total arm entries, but only the effects of imipramine were statistically significant. None of the treatments affected the total levels of CCK or the levels of CCK-8-sulphated, CCK-8-nonsulphated, CCK-5, or CCK-4 in the frontal cortex. There was no effect of the treatments on CCKB receptor binding in the frontal cortex, hippocampus, or striatum. Imipramine and amitriptyline, however, increased the affinity of CCKB receptor binding in the hypothalamus. Thus, no consistent effect of chronic antidepressant treatment on the CCK-ergic neurotransmission in the rats was found.