Analysis of Pituitary Prolactin and Adrenocortical Response to Ether, Formalin or Restraint in Lactating Rats: Rise in Corticosterone, but No Increase in Plasma Prolactin Levels after Exposure to Stress

Abstract

It is well established that stress causes a rise in plasma prolactin (PRL) levels of male or cycling female rats. In lactating animals, the pituitary PRL response to stress is not well understood. Therefore, the purpose of the present study was to analyze this question in lactating rats having low or elevated prestress plasma PRL levels. The animals were exposed to ether, formalin or restraint, and plasma PRL and corticosterone levels were determined. In mothers continually together with their pups, plasma PRL levels decreased significantly after exposure to ether vapor or injection of formalin under the skin. At the same time, both agents caused a significant rise in blood corticosterone concentrations. Lactating rats isolated for 4 h had very low levels of PRL before application of stress. However, neither formalin nor restraint caused any elevation in their plasma PRL levels although both interventions increased blood corticosterone concentrations. Lactating mothers receiving formalin after a 30-min suckling stimulus preceded by 4 h isolation did not show appreciable changes in pituitary PRL secretion following the administration of formalin. For information on the mechanism of the effect of stress on PRL, lactating rats were pretreated with the dopamine receptor antagonist domperidone (injecting 80 µg/kg body weight) or were adrenalectomized 7 days prior to exposure to stress. The very high levels of PRL caused by domperidone decreased markedly in animals subjected to restraint stress. Administration of formalin to adrenalectomized lactating rats continually together with their litter caused a slight immediate decrease, followed by a transitory elevation and a subsequent small second decrease in blood PRL concentration. The depression was significantly less than in nonadrenalectomized animals receiving formalin. If formalin was administered 2 days after isolation of the mothers it caused an elevation of plasma PRL concentrations indicating that the PRL stress response pattern characteristic of nonlactating animals returns within 48 h of isolation. On the basis of the present findings we conclude that in lactating animals (a) stress causes an inhibition of PRL release from the pituitary; (b) the pituitary-adrenocortical system responds to stress, (c) the inhibition of stress-induced pituitary PRL release disappears within 48 h of separation of the mother from her litter, and (d) a dopaminergic mechanism is not involved, but the adrenocortical system may participate in the stress-induced inhibition of PRL release.