FEED RESTRICTION IN PREPUBERTAL LAMBS - EFFECT ON PUBERTY ONSET AND ON IN-VIVO RELEASE OF LUTEINIZING-HORMONE-RELEASING HORMONE, NEUROPEPTIDE-Y AND BETA-ENDORPHIN FROM THE POSTERIOR-LATERAL MEDIAN-EMINENCE

The exact nature of the interaction between energy balance and reprodu ction is still elusive. Theoretically, nutrition-related variables mus t reach the hypothalamic luteinizing-hormone-releasing hormone (LHRH) network and/or its neuronal inputs, to alter plasma luteinizing hormon e (LH) and therefore reproductive activity. In an attempt to assess th e potential mechanism of such interaction at the median eminence (ME) level, the area of hypophysiotropic LHRH neuronal terminals and releas e, we used a decreased caloric intake lamb model which delays the onse t of puberty. Thus, we determined the in vivo release of neuropeptides , by push-pull cannula (PPC) sampling from the posterior-lateral ME, i n feed-restricted (FR) ewe lambs and in full-fed (FF), age-matched, co ntemporary control animals. Specifically, we assessed: (1) serum LH an d ME in vivo release of LHRH, beta-endorphin (beta-END) and neuropepti de Y(NPY); beta-END and NPY are two putative neuronal inputs to LHRH n euronal terminals at the ME, reported to be involved in the control of both reproduction and feed intake; (2) the effect that exogenous infu sion of beta-END through the PPC might have on the release of ME LHRH and NPY, and on plasma LH. In contrast to other works, the present res ults were obtained in lambs with intact ovaries. Furthermore, FR lambs were always compared statistically with FF contemporary paired contro ls that had attained puberty. Feed restriction decreased ME LHRH relea se, lowered plasma LH and prevented the onset of puberty. The changes induced by feed restriction in both LHRH and LH release were associate d predominantly with decreases in pulse amplitude, rather than alterat ions in pulse frequency. The decreased LHRH and LH release occurred in the presence of a decreased beta-END but unchanged NPY release from t he ME. Exogenous infusion of beta-END into the posterior-lateral ME de creased both LHRH and NPY release from this site and decreased plasma LH. In conclusion, decreased caloric intake lowers LH release and prev ents puberty onset by decreasing the amplitude of the LHRH output from the hypothalamic hypophysiotropic network. A compensatory but unsucce ssful mechanism for the FR status might be a lower beta-END-inhibitory tone on ME LHRH neuronal terminals. The unchanged release of NPY at t his site supports the specificity of the changes induced by feed restr iction on LHRH and beta-END in vivo release.