The responsiveness of the hypothalamus to electrochemical stimulation (ECS) and of the pituitary to luteinizing hormone releasing hormone (LHRH) was examined following either endogenous LH release or exogenous LH infusion on the afternoon of proestrus in rats that had received Nembutal to block the LH surge. In all animals, sequential jugular blood samples were taken and LH was determined by radioimmunoassay. Unilateral ECS of the medial preoptic area (MPOA) resulted in a peak plasma LH of 121.1±8.6 ng/ml 120 min after stimulation; ECS of the contralateral MPOA of the same animals at 200 min resulted in a peak plasma LH of 66.9±5.6 ng/ml or half that obtained following the first ECS. To eliminate a pituitary role in this phenomenon, 250 ng LHRH was given iv at 200 min following unilateral MPOA ECS. The peak in plasma LH following LHRH (510.7±60 ng/ml) was not depressed and, in fact, was significantly greater than that obtained in response to LHRH without prior ECS induced LH release (143.9±19.6 ng/ml). To compare the responses obtained following exogenous LH, purified rat LH (4 μg) was infused iv over 60 min. When plasma LH had returned to pre infusion levels, an iv pulse of 250 ng LHRH was administered; the peak in plasma LH was similar to that obtained in response to LHRH in animals without prior LH infusion. Finally, in another group of LH infused rats (4 μg/60 min), MPOA ECS was performed, resulting in a plasma LH peak half that obtained without prior exogenous LH exposure. These studies suggest decreased hypothalamic sensitivity to stimulation on proestrus due to a negative feedback of either LH or LH induced steroids.
|Original language||English (US)|
|Number of pages||6|
|State||Published - 1976|
ASJC Scopus subject areas
- Endocrinology, Diabetes and Metabolism