title: Forced swim test-induced endocrine and immune changes in the rat: effect of subacute desipramine treatment.
abstract: Previously it has been reported that forced swim test (FST) exposure activates the HPA-axis and produces alterations in both cellular and noncellular immunity in rats. Furthermore, there is evidence to suggest that pretreatment with antidepressants has a protective effect against FST-induced immune changes. The purpose of the present study was to examine the effect of subacute treatment with the tricyclic antidepressant desipramine (DMI, 5 and 10 mg/kg; I.P.) on immobility in the FST, and on FST-induced changes in endocrine and immune parameters in the rat. DMI treatment at a dose of 10 mg/kg produced a significant reduction in immobility time in the FST, while the 5 mg/kg dose was ineffective. FST exposure produced a significant increase in serum corticosterone and a decrease in adrenal ascorbic acid concentrations, neither of which were significantly attenuated by DMI pretreatment. There was a slight but nonsignificant suppression of PHA-induced lymphocyte proliferation 15 min post-FST exposure. However, DMI treatment produced a significant increase in lymphocyte proliferation at this time point. FST exposure caused a reduction in the percentage of lymphocytes and an increase in the percentage of neutrophils in the peripheral blood; DMI treatment failed to significantly alter these stress-induced changes. There was a profound reduction in relative spleen weight observed in DMI-treated animals 120 min post-FST exposure and this was accompanied by an increase in circulating RBC concentrations. In conclusion, although the FST-induced behavioral changes were normalized by DMI treatment the peripheral aberrations induced by FST exposure (with the exception of lymphocyte proliferation) were not. In addition, DMI pretreatment induced stress-like changes in corticosterone, adrenal ascorbic acid and leucocyte subpopulations in the control animals.
authors.affiliation: Department of Pharmacology, University College, Galway, Ireland.
authors.forename: T J
authors.initials: TJ
authors.lastname: Connor
authors.forename: J P
authors.initials: JP
authors.lastname: Kelly
authors.forename: B E
authors.initials: BE
authors.lastname: Leonard
mesh_terms: D000311:Adrenal Glands / Q000378:metabolism; D000818:Animals; D000929:Antidepressive Agents, Tricyclic / Q000627:therapeutic use*; D001205:Ascorbic Acid / Q000378:metabolism; D003345:Corticosterone / Q000097:blood; D003863:Depression / Q000188:drug therapy* / Q000276:immunology / Q000503:physiopathology; D003891:Desipramine / Q000627:therapeutic use*; D004195:Disease Models, Animal; D004353:Drug Evaluation, Preclinical; D004703:Endocrine System / Q000187:drug effects*; D007107:Immune System / Q000187:drug effects*; D007962:Leukocytes / Q000187:drug effects; D008297:Male; D009929:Organ Size / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D013550:Swimming
chemical_list: D000929:Antidepressive Agents, Tricyclic; D001205:Ascorbic Acid; D003891:Desipramine; D003345:Corticosterone