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DE Hendricks Jr1 , EA Meyers1 , JE Rhea1 , K-D Vo1 , H I'Anson1 *
Biology Department, Washington and Lee University, Lexington, VA 1
A single injection of monosodium glutamate (MSG) to the neonatal female rat destroys glutamate sensitive neurons in the arcuate nucleus (ARC) and subsequently induces precocious puberty (Neuroendocrinology 52:143-149; 1990). We determined if such glutamate sensitive neurons play a role in the transduction of metabolic signals to the reproductive axis of the developing female rat. In our model puberty is delayed by growth-restriction, but may be rapidly reinstated by realimentation (Am J Physiol 254:R616-R621; 1988). Our approach was to treat neonatal females with either an acute injection of MSG (4 mg/g body weight [BW]) or saline on postnatal day 2 (PD2). Each treatment group was randomly divided and either growth restricted to 80-90 g BW (MSG n=8; saline n=7), or ad libitum fed (MSG n=7; saline n=6). Although BW, Lee index (a measure of obesity), and naso-anal length were significantly different between the ad libitum and growth restricted rats (BW: ad lib 199.1 ± 4.0 g, rest 88.1 ± 0.7 g; Lee Index: ad lib 308.6 ± 2.2, rest 286.3 ± 1.4; naso-anal length: ad lib 18.92 ± 0.2 cm, rest 15.6 ± 0.1 cm), there was no effect of MSG treatment within the ad libitum or restricted groups. Day of vaginal opening was not significantly altered by MSG treatment; however, the ad libitum MSG-treated rats experienced precocious puberty (saline: PD 37 ± 0.7; MSG: PD 35 ± 0.6). No growth restricted rat reached puberty by days 56-58 (end of experiment), regardless of treatment regimen. Our findings suggest that the neurotransmitter populations within the glutamate sensitive neurons of the ARC may not transduce metabolic signals to the reproductive axis in developing female rats, and therefore may inhibit the onset puberty by a mechanism unrelated to metabolism. (Supported by Washington and Lee Univ.).
This abstract is being presented on Tuesday, August 3 at 8:00 AM to 10:15 AM at CUB 2nd Floor Ballroom.