Serum concentrations of luteinizing hormone, growth hormone, and prolactin in untreated and estradiol-treated ovariectomized ewes after immunoneutralization of hypothalamic neuropeptide Y.
Malven P.V. | Haglof S.A. | Jiang H.
Ovine antiserum against a conjugate of porcine neuropeptide Y (NPY) with bovine thyroglobulin was infused repeatedly into one lateral ventricle of five ovariectomized (ovx) ewes before and after subcutaneous injection of estradiol-17 beta (E beta). Serum concentrations of LH, growth hormone (GH), and prolactin (PRL) were measured at 10-min intervals before E beta and at approximately hourly intervals 8 to 18 h after E beta injection. Control ewes were infused with ovine serum from animals immunized against bovine thyroglobulin. Basal episodic profiles (pre-E beta) of LH, GH, and PRL were similar in ovx ewes infused with control or anti-NPY serum. Injection of E beta induced a surge-like increase of serum LH, which began at 12.6 h after E beta in ewes infused with anti-NPY and at 14.4 h after E beta in ewes infused with control antiserum (P < 0.05). The magnitude of the E beta-induced surge of LH was not different between treatments. In addition to initiating a surge-like release of LH over the period 12 to 18 h after E beta, serum GH was transiently increased during the period between 10 and 15 h after E beta. In contrast, serum PRL was increased during the entire period between 8 and 18 h after E beta. Based on the effects of immunoneutralization, endogenous NPY in the brain of E beta-treated ovx ewes seems to restrain or delay the onset of the surge-like secretion of LH and probably GnRH, but endogenous NPY does not affect the episodic pulsatile releases of LH characteristic of ovx ewes. Assuming the efficacy of immunoneutralization, endogenous NPY does not seem to affect either basal or E beta-induced increases of PRL and GH. Based on the effects of exogenous E beta, the induced increases in LH, PRL, and GH in ovx ewes are temporally independent and, therefore, probably regulated by independent mechanisms.
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