Expression of neuropeptide Y precursor-immunoreactivity in the hypothalamic dopaminergic tubero-infundibular system during lactation in rodents.

ABSTRACT

Evidence from physiological studies in rats shows that neuropeptide Y (NPY) has marked neuroendocrine effects on anterior pituitary function, and especially on LHRH and LH secretions. However, previous immunohistochemical studies in rats have revealed only scarce NPY-axons of medullary origin in the external zone of the hypothalamic median eminence, the common termination site of neuroendocrine adenohypophysiotropic systems. In view of this apparent contradiction, we used light microscopic immunohistochemistry to reassess the distribution of NPY in the hypothalamus of rodents of both sexes under physiological (estrous cycle in rats, pregnancy in rats, and lactation in both rats and mice) and experimental (gonadectomy in rats and adrenalectomy in both rats and mice) conditions with alterations of reproductive functions. We reasoned that such manipulations could induce changes in immunoreactivity in the NPY system involved in neuroendocrine regulation and would thus make it apparent to us. We show here that immunoreactivity for NPY and its carboxyterminal precursor-associated peptide are dramatically increased in the external median eminence of lactating female animals when compared to the other animal groups. This NYP-precursor-immunoreactivity is present, throughout lactation, in the tyrosine hydroxylase-immunoreactive (and therefore possibly dopaminergic) tubero-infundibular system. This immunoreactivity disappears rapidly from the median eminence after pup-removal. These observations suggest a role for NPY-precursor-derived peptides in the control of the suckling-induced PRL secretion and also demonstrate the chemical plasticity of the median eminence during a normal physiological event. Since in nonlactating animals and especially in normal cycling females NPY-precursor-immunoreactivity was detected in the system of medullary origin only, we conclude that, by exclusion, this system might be the one responsible for modulating gonadotropic secretion at the median eminence and/or pituitary levels.