Blockade of stress-induced prolactin release in monosodium glutamate-treated rats.

To elucidate the role of the medial basal hypothalamus (MBH) in stress-induced prolactin (Prl) release, adult male rats which had received monosodium glutamate (MSG 4 mg/g) on alternate days for the first 10 days of life were subjected to ether stress for 2 min. Blood samples were drawn at 0, 15, 30 and 60 min after etherization through an indwelling jugular catheter implanted 1 day before the experiment. Sixty minutes after etherization the dopamine receptor blocker spiroperidol (0.1 mg/kg) was injected intravenously and another blood sample was withdrawn 60 min later. Although there were no differences in basal levels of plasma Prl between control and MSG-treated animals, a dramatic elevation of plasma Prl was observed in control rats 15 min after etherization, whereas no significant change was seen in MSG-treated animals. Spiroperidol significantly increased plasma Prl in both groups of animals, but the magnitude of the increase in Prl levels of MSG-treated rats was roughly one-third (p less than 0.005) that of control animals. When morphine (3 mg/kg) was injected to test its capability to stimulate Prl release in MSG-treated rats, significant increases of similar magnitude of plasma Prl were observed in both groups. These results show that (1) the tuberoinfundibular dopaminergic system is functioning in MSG-treated rats to maintain Prl at low levels, (2) the stimulatory effect of morphine on Prl release is intact in MSG-treated rats, and (3) the tuberoinfundibular dopaminergic system is not responsible for stress-induced Prl release, but rather another mechanism located within the arcuate nucleus (ARC) and highly sensitive to destruction by MSG mediates stress-induced Prl release.