Abstract Dr. S. J. Legan

Sandra Legan, PhD

S. J. Legan, Ph.D.; Dept. of Physiology, Univ. of Kentucky, Lexington, KY.

Title: Circadian control of the luteinizing hormone (LH) surge: Role of multiple oscillators. 

Synopsis:

In rodents, the preovulatory LH surge is timed by a circadian rhythm that is entrained by the photoperiod.  Under normal photoperiodic conditions, daily barbiturate treatment during the ~ 2 h “critical period” on proestrous afternoon for 1-3 days delays the preovulatory LH surge and ovulation, which occur at the same time, but 1-3 days later, respectively, indicating that a daily neural signal is required during this critical period for the LH surge.  When animals are exposed to constant dim light, subsequent LH surges are delayed, and the longer the exposure to constant photoperiod, the longer the delay, indicating circadian control of the LH surge.  Paradoxically, a non-photic phase advance of 2 hours or more in the circadian activity rhythm delays occurrence of estrus by one day, suggesting that phase advancing the circadian clock causes a delay in the LH surge.  Based on the foregoing observations, we hypothesized that barbiturate administration phase advances the circadian pacemaker.  Further, if the phase advance is longer than about 2 hours, the duration of the critical period for the neural signal for the LH surge, it will cause a delay in the LH surge.  Our results supported this hypothesis and based on reports that mutations in circadian clock genes prolong estrous cycles and disrupt LH surges, we have begun to investigate the role of clock genes in the neurons of the hypothalamic suprachiasmatic nuclei (SCN), site of the circadian pacemaker, and the gonadotropin-releasing hormone (GnRH) neurons, which control LH release and their interactions in control of the LH surge.      

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Updated 04/12/2007

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