Behavioural and brain neurohormonal changes produced by acute heat stress in rats: influence of psychopharmacological agents.

Abstract It was observed that when animals trained for conditioned avoidance response (CAR) were kept at an environmental temperature of 40±0.5°C for 1 hr, a disruption occurred in their trained behaviour. Pretreatment of animals with antipsychotic drugs i.e. reserpine or chlorpromazine prevented this effect, whereas treatment of the animals with either LSD-25 or mescaline caused a further disruption in their performance. Analysis of the whole brain of these animals showed that while the acetylcholine content was lower in animals kept at a higher environmental temperature, the brain 5-HT and noradrenaline levels were significantly elevated. Since treatment of the animals with either reserpine or chlorpromazine prevented all these neurohormonal changes, and both mescaline and LSD-25 failed to modify these neurohormonal changes, it was difficult to identify the specific neurohormonal changes responsible for the altered behavioral responses. Further studies showed that the activities of monoamine oxidase and 5-HTP decarboxylase were unaltered while the activity of cholinesterase was significantly increased when the animals were kept at a higher environmental temperature. Thus changes in enzyme activity cannot explain the neurohormonal changes. Adrenal adrenaline estimations showed that the adrenals were partly depleted of adrenaline by the higher environmental temperature, showing that the animals were under “heat stress”. In antipsychotic treated animals, the stress-induced depletion of adrenal adrenaline was considerably reduced. Both mescaline and LSD-25 failed to counteract the stress-induced depletion of adrenal adrenaline. It was felt that the reduction in the intensity of the “alarm reaction” in the tranquillizer-treated rats kept in heat stress might be responsible for the reduction of the stress-induced neurohormonal changes. The possibility of changes in the permeability of the blood-brain barrier as a result of stress was also considered.