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Reduced Response of the Hypothalamo-Pituitary-Adrenal Axis to ₁-Agonist Stimulation during Lactation¹

Neuroendocrine Research Group, Department of Anatomy, School of Medical Sciences (R.J.W., M.M.B., T.K., A.P.C.d.C., C.D.I.), Bristol, United Kingdom BS8 1TD; the Department of Medicine, University of Bristol, Bristol Royal Infirmary (R.J.W., A.P.C.d.C., M.H., S.L.L.), Bristol, United Kingdom BS2 8HW; and the Department of Biomedical Sciences, Ontario Veterinary College, University of Guelph (B.C.W.), Guelph, Ontario, Canada N1G 2W1

Address all correspondence and requests for reprints to: Dr. C. D. Ingram, Neuroendocrine Research Group, Department of Anatomy, School of Medical Sciences, Bristol, United Kingdom BS8 1TD. E-mail: c.ingram{at}bristol.ac.uk

To determine whether altered noradrenergic activation of the hypothalamo-pituitary-adrenal (HPA) axis contributes to the attenuated neuroendocrine response to stress observed during lactation, the effect of intracerebroventricular injection of the ₁-agonist methoxamine (100 µg) was compared between virgin and lactating rats. Virgin rats showed significant increases in plasma corticosterone after methoxamine, reaching 317 ± 44 ng/ml at 10 min and remaining significantly elevated for more than 120 min, but lactating rats showed no significant increase in corticosterone levels. Furthermore, methoxamine induced an increase in paraventricular nucleus (PVN) CRF messenger RNA expression in virgin, but not lactating, animals. Both groups of rats exhibited comparable elevations in plasma PRL after methoxamine treatment. Arginine vasopressin messenger RNA expression within the parvocellular PVN was greater in the lactating animals than in the virgin controls, but methoxamine injection was without further effect. Studies performed on ovariectomized virgin rats and ovariectomized rats receiving estradiol or progesterone replacement failed to reproduce the attenuated HPA responses seen after methoxamine treatment, although methoxamine-induced PRL levels were greatly increased by estradiol, probably arising from an effect on hormone synthesis. In vitro electrophysiological recordings of PVN neurons in hypothalamic slices from proestrous virgin and lactating rats showed that 45–52% of neurons in both groups exhibited excitatory responses to 10^-4 M methoxamine, but there was a differential response to 10^-5 M methoxamine, with PVN neurons from lactating animals failing to show a response. These data show a selective down-regulation of ₁-mediated activation of the HPA axis in lactating animals. This may contribute to the attenuated stress-induced activation of the HPA axis during lactation.

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