Low Gaba and Early Puberty

Role of GABA in the Mechanism of the Onset of Puberty in Non-Human Primates

Ei Terasawa

Department of Pediatrics and Wisconsin National Primate Research Center, University of Wisconsin, Madison, WI 53715

*Correspondence: Ei Terasawa, Ph.D., Wisconsin National Primate Research Center, University of Wisconsin, 1223 Capitol Court, Madison, WI 53715- 1299, E-mail: terasawa@primate.wisc.edu, Phone: (608) 263-3579, Fax: (608) 263-3524

Evidence indicates that GABA is an inhibitory neurotransmitter responsible for restricting luteinizing hormone-releasing hormone (LHRH) release before the onset of puberty. LHRH neurons in the hypothalamus of female rhesus monkeys are already active during the neonatal period, but subsequently enter a dormant state in the juvenile/prepubertal period because of an elevated level of GABA in the stalk-median eminence (S-ME). The developmental reduction in tonic GABA inhibition results in an increase in LHRH release in the S-ME, triggering puberty. The reduction in GABA also appears to allow an increase in glutamate release in the S-ME and this glutamate seems to further contribute to the pubertal increase in LHRH release. These observations conducted in non-human primates, as a model for humans, provide some insights into future studies of the importance of GABAergic mechanisms in the relation between onset of puberty and neurodevelopmental disorders including autism.