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A potential mechanism of slowed pubertal maturation after chronic administration of sodium valproic acid

From the Department of Neurology, MCP-Hahnemann Medical School, Allegheny University of the Health Sciences, Pittsburgh, PA; and the Behavioral Neurosciences Division, Department of Psychology, State University of New York at Buffalo.

Address correspondence and reprint requests to Dr. Snyder, Allegheny Neurological Associates, 420 East North Avenue, Suite 206, Pittsburgh, PA 15212.

Sodium valproic acid (VPA) occasionally delays pubertal maturation in children and gonadal and skeletal growth in juvenile, seizure-prone, inbred DBA/2J mice. Fourteen-day-old mice received either VPA or control solution, and the medial preoptic area (mPOA) of the hypothalamus was studied after 4, 7, 10, 14, or 18 days by immunocytochemically processing for gonadotropin-releasing hormone (GnRH). Significant differences were found for the proportion of bipolar to unipolar neurons in the mPOA. VPA may slow pubertal maturation by altering neurochemical systems that normally play an important role in timing maturation of the GnRH pulse generator.

Supported in part by an unrestricted educational grant from Abbott Laboratories to P.J.S. and in part by National Science Foundation grant IBN9224804 awarded to L.L.B.

Received January 31, 1997. Accepted in final form September 17, 1997.

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