Blockade of LHRH-induced lordosis by alpha- and beta-adrenergic antagonists in ovariectomized, estrogen primed rats

Abstract

The participation of a noradrenergic mechanism in the facilitation of lordosis by luteinizing hormone-releasing hormone (LHRH) was studied in two groups of ovariectomized estrogen primed rats, with or without sexual experience. The administration of 5 micrograms estradiol benzoate (EB) alone to sexually inexperienced subjects (Ss) induced weak lordosis behavior in some of them (mean lordosis quotient, LQ = 12 +/- 19). The SC injection of 5 micrograms LHRH significantly increased this response four hours later (LQ = 38 +/- 41), though great variability was observed (59% of Ss showing LQs below 30). The systemic administration of either prazosin, an alpha-adrenergic antagonist (0.2 or 1 mg/kg), or propranolol, a beta-adrenergic antagonist (20 mg/kg), totally suppressed LHRH-induced lordosis in sexually inexperienced Ss (mean LQs = 8 +/- 11; 5 +/- 10; 18 +/- 31, respectively). In sexually experienced Ss (tested on two previous occasions with EB and LHRH) the administration of EB alone on a third test induced significant levels of lordosis (mean LQ = 51 +/- 41). The administration of 5 micrograms LHRH to sexually experienced, estrogen primed Ss induced near maximal levels of lordosis (LQ = 94 +/- 18). In these Ss, prazosin (0.2 and 1 mg/kg) and, to a lesser extent, propranolol (20 mg/kg) significantly depressed lordosis to values that were not significantly different from those obtained after EB alone (mean LQs = 59 +/- 38; 63 +/- 20; 74 +/- 32, respectively). These results indicate that blockade of noradrenergic transmission by either alpha- or beta-antagonists counteracts the stimulatory effect of LHRH on lordosis in ovariectomized estrogen primed rats with or without sexual experience.(ABSTRACT TRUNCATED AT 250 WORDS)