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      Pulsatile LH Release on Diestrus 1 in the Rat Estrous Cycle: Relation to Brain Catecholamines and Ovarian Steroid Secretion



      S. Karger AG

      Pulsatile release, LH, Diestrus 1, Catecholamines, Progesterone, Estradiol

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          This study examined (1) the possible involvement of catecholamines in the regulation of pulsatile LH release on diestrus 1 (Dl) in the rat estrous cycle, and (2) the possible importance of pulsatile LH release on Dl to ovarian estradiol and progesterone secretion on this day of the cycle. Blockade of dopamine receptors on Dl had no effect on LH secretion. However, inhibition of norepinephrine (NE) synthesis or blockade of α- but not β-adrenergic receptors decreased mean blood LH levels, and greatly suppressed pulsatile LH secretion by decreasing both LH pulse frequency and amplitude. In contrast, in the same rats, interference with brain NE function had no effect on plasma FSH levels. These data indicate that NE is an excitatory neurotransmitter in the regulation of pulsatile LH release on Dl. Acting through an α-adrenergic receptor, this neurotransmitter presumably influences both the frequency of the LHRH pulse generator and the amount of LHRH released per pulse. Moreover, the release of LH and FSH on Dl can be separated, suggesting possible differences in the mechanisms regulating secretion of these two gonadotropins. Regardless of whether pulsatile LH release had been greatly suppressed or not altered, no change occurred in plasma progesterone levels, indicating pulsatile LH release on Dl is not important for the release of progesterone that occurs on this day of the cycle. With respect to estradiol, no consistent pattern emerged between changes in pulsatile LH release induced by interference with brain NE function and plasma estradiol levels. Thus, no definitive conclusion was possible on the potential importance of pulsatile LH release to estradiol secretion on Dl.

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          Author and article information

          S. Karger AG
          27 March 2008
          : 37
          : 2
          : 91-97
          Department of Physiology, University of California School of Medicine, San Francisco, Calif.; Department of Obstetrics and Gynecology, University of Florida College of Medicine, Gainesville, Fla., USA
          123525 Neuroendocrinology 1983;37:91–97
          © 1983 S. Karger AG, Basel

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          Pages: 7
          Original Paper


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