Investigations in to the effects of exogenous corticosterone on responses to stress , addiction and cognition in rat models

Abstract

Glucocorticoids, the major stress hormones play a regulatory role in responses to stress. Evidence suggests that smaller increase of glucocorticoids is adaptive and help to cope with the stress. On the other hand, higher increase of glucocorticoids impairs adaptation to stress. The present study was initially designed to understand the role of corticosterone, the principal glucocorticoids in rats; in stress responses. In view of a role of stress in the modulation of cognitive functions and facilitation of reinforcing effects of drugs of abuse, effects of corticosterone on learning and memory and reinforcing effects of drugs of abuse were also monitored. Important findings of the present study are as follow: 1. Corticosterone facilitates memory retention at doses of 10, 25 &50 mg/kg but impairs learning acquisition at 10mg/kg. Food intake is decreased at 25 & 50 mg/kg of corticosterone. Higher dose (50 mg/kg) increases locomotor activity that is associated with an increase in the concentration of dopamine in the striatum. 2. Exposure to daily 2hr immobilization stress decreases food intakes and growth rates but adaption occurs after 5 days. While administration of corticosterone (10 mg/kg) impairs this adaptation. Exposure to 2h Immobilization stress impairs acquisition and facilitates memory extinction but stress effects on learning and memory are attenuated in corticosterone treated animals. 3. Repeated administration of apomorphine produces sensitization in the motor behavior. Sensitization effects of apomorphine are attenuated in rats repeatedly injected with corticosterone. Although both apomorphine and corticosterone impair memory extinction but administration of corticosterone in apomorphine treated animals does not potentiate this effect. 4. Administration of ethanol impairs learning acquisition and retention of memory. Administration of corticosterone (50mg/kg; daily for 1 week) produces impairment of memory reconsolidation in ethanol treated rats. At this dose, corticosterone also potentiates ethanol intake. It is suggested that glucocorticoids can cause memory impairments in alcoholics. We conclude that corticosterone improves cognitive functions and attenuates stressinduced memory impairments. Moreover, the administration of corticosterone can potentiate the reinforcing effects of drugs of abuse and memory impairments in abusers. Findings suggest an important role of glucocorticoids in cognition, addiction and adaptation to stress.