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.

This article provides an overview of the increasing number of observations indicating that excitatory amino acids are involved in the control of prolactin secretion. The information available suggests that these amino acids exert a stimulatory action on hypophysial prolactin. Administration of a glutamate receptor agonist induces significant increase in prolactin release in rats, monkeys, and rams. In contrast, noncompetitive antagonists of N-methyl-D-aspartate receptors decrease plasma levels and attenuate the preovulatory surge of prolactin. It appears that the endogenous glutamatergic system participates not only in the regulation of basal secretion of prolactin, but also in the control of physiological prolactin responses induced by the suckling stimulus or by stress. Recent findings suggest that the glutamatergic innervation of the hypothalamic paraventricular nucleus is involved in the mediation of the neural signal of the suckling stimulus-induced prolactin release as well as in the mediation of the stress-induced release of prolactin.

Suckling‐induced prolactin release is a widely studied neuroendocrine reflex, comprising a neural afferent and a humoral efferent component. The information on the brain structures involved in this reflex is fairly limited. The present studies focused on this question. The following hypothalamic interventions were made in lactating rats and the dams were tested for the suckling‐induced prolactin response: (i) unilateral or (ii) bilateral frontal cuts at the level of the anterior and posterior hypothalamus; (iii) administration of 5,7‐dihydroxytryptamine or (iv) 6‐hydroxydopamine into the hypothalamic paraventricular nucleus (PVN) to destroy serotonergic and catecholaminergic innervation of the cell group, respectively; (v) lesion of the medial subdivision of the PVN; and (vi) horizontal knife cuts below the PVN. Bilateral posterior and bilateral or unilateral anterior frontal cuts caused blockade of the suckling‐induced release of prolactin. Likewise, most dams receiving 5,7‐dihydroxytryptamine in the PVN did not respond to the suckling stimulus. Immunocytochemistry revealed that, in those rats which did not show a rise in plasma prolactin, there were almost no serotonergic fibres and terminals in the PVN, while in dams which exhibited a response, numerous serotonergic elements were evident. 6‐Hydroxydopamine treatment did not cause significant alteration in the prolactin response. Lesion of the medial, largely parvocellular subdivision of the PVN, or horizontal knife cuts below this cell group, blocked the hormone response. The findings demonstrate for the first time that: (i) interruption of the connections between the brain stem and the hypothalamus interferes with the prolactin response to the suckling stimulus; (ii) serotonergic fibres terminating in the hypothalamic PVN are involved in the mediation of the suckling stimulus; and (iii) within the PVN, neurones in the medial, largely parvocellular subdivision of the cell group take part in the transfer of the neural signal, eventually inducing prolactin release.

No abstract