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This thesis investigates the role of central 5-hydroxytryptamine (5-HT) in the process of adaptation to chronic stress. Central 5-HT of male rats was depleted by bilateral intraventricular (i.c.v.) infusion of the neurotoxin 5,7-dihydroxytryptamine (5,7-DHT) with the use of specific re-uptake blockers to protect the dopamine (DA) and noradrenaline (NA) system. They were then exposed to different chronic stress paradigms. The effect of 5-HT depletion on social defeat was studied. Lesioned or sham-operated rats were either exposed daily for 10 days to a second larger aggressive male in the latter's home cage, or simply transferred to an empty cage (control procedure). Lesioned rats failed to show the increased freezing behaviour during the pre-defeat phase of the social interaction test characteristics of sham-operated animals. Core temperature increased during aggressive interaction in sham-operated rats, and this did not adapt with repeated stress. By contrast, stress-induced hyperthermia was accentuated in 5-HT-reduced rats as the number of defeat sessions increased. Basal core temperature was unaffected by 5-HT depletion. Heart rate increased during social defeat, but this did not adapt with repeated stress: 5-HT depletion had no effect on this cardiovascular response. Basal corticosterone was increased in lesioned rats, but the progressive reduction in stress response over days was not altered. C-fos expression patterns in lateral preoptic area (LPOA) and medial amygdala (Me-AMY) in rats with repeated defeat were altered by 5-HT depletion. These results suggest that 5-HT is important in the modulation of overall adaptation process in exposure to chronic stress. |
