Differentialin VitroStimulation by Naloxone and K+of Luteinizing Hormone-Releasing Hormone and Catecholamine Release from the Hypothalami of Intact and Castrated Rats*

Publisher Website
Google Scholar
Abstract
We compared the effects of an opiate receptor antagonist, naloxone (NAL), on in vitro LHRH and catecholamine release from the medial basal hypothalamus-preoptic area (MBH-POA) of intact and castrated adult male rats. The MBH-POA (six per chamber) were perifused in vitro for 6 h. After 1 h of preincubation, basal LHRH, dopamine (DA), norepinephrine (NE), and epinephrine (E) release were estimated in perifusates collected during the second and third hours. During the fourth hour, chambers were perifused for 30 min with medium alone or medium containing NAL; tissue viability was confirmed during the sixth hour by adding 60 mM KCl to the medium. Tissue samples were weighed at the end of the perfusion and homogenized in 0.1 N HCl for subsequent analyses of LHRH contents. The basal release rate and cumulative hourly LHRH output from the MBH-POA of intact rats was about 3 times that from castrated rats (P < 0.05). The NAL pulse stimulated LHRH release from the MBH-POA of intact and castrated rats (P< 0.05). These differential LHRH release responses reflected the differences in the MBH-POA LHRH concentrations that normally occur between intact and castrated rats and also examined at the end of the perifusion. In contrast to the LHRH response, the basal release rate and hourly output as well as NAL-induced DA release from the MBH-POA of intact and castrated rats were similar. On the other hand, as in the case of LHRH, basal NE release and hourly output from theMBH-POA of castrated rats were significantly reduced compared to those from the MBH-POa of intact rats (P < 0.05). In addition, NAL promptly stimulated NE release, and the amount released was higher from the MBH-POA of intact rats (P < 0.05). The basal amount of E released from the MBH-POA of intact and castrated rats was near or below the level of sensitivity of the assay. However, NAL increased E release from the MBH-POA of both groups of rats, and E output was apparently 2-fold higher from the MBH-POA of intact than castrates. Prior perfusion with morphine failed to block NAL-evoked stimulation of LHRH release from the MBH-POA of intact rats. These studies show that while castration produces no appreciable effect on basal and NAL-evoked DA release, basal and NAL-evoked LHRH, NE, and E release from the MBH-POA of castrated rats are drastically reduced. These observations are in line with the proposal that stimulation of LH release by NAL in male rats may be mediated by increased release of catecholamines and LHRH and that LHRH, NE, and possibly E release in vivo may be diminished after castration.