MSG (4 mg/g, sc) or saline was administered to neonatal female rats on days 1, 3, 5, 7 and 9. Study 1) Prl levels were assessed at 30, 60 and 75 days after birth to monitor possible development of hyperprolactinemia. No hyperprolactinemia was observed at any time studied. Study 2) MSG and control rats were administered pentobarbital anesthesia at 2 months of age. At 20, 60 and 90 min following anesthesia, plasma was collected for assay of Prl. 20 min prior to the 90 min bleeding, BE (5 micrograms/5 ul) was stereotaxically administered, into the third ventricle. MSG-treated rats had an attenuated Prl response to the stress of anesthesia (bleeding 1). Prl levels in control and MSG-treated rats were similar at 60 min post-anesthesia (bleeding 2) which represented a return of Prl levels to baseline after stress-induced elevation of Prl. Control and MSG-treated rats exhibited an increase in plasma Prl following intracerebroventricular BE; however, the amplitude of this response was markedly attenuated in the MSG-treated animals (bleeding 3). Thus, an observed loss of TH-positive neurons in the arcuate nucleus of the hypothalamus following MSG treatment and the attenuated response of Prl to anesthesia-stress and BE administration suggests that Prl secretion in response to these agents is operative through inhibition of the TIDA system. Furthermore, these studies show that the Prl response to these agents (anesthetic and BE) is intact but sub-operational in MSG-treated rats.