Failure of the hypothalamic noradrenergic system to function in adult androgen-sterilized rats.

We have examined norepinephrine (NE) and dopamine (DA) initial concentrations, rate constants and turnover rates in microdissected regions of the hypothalamus and gonadotropin release in ovariectomized (OVX)estrogen-treated adult control and androgen-sterilized rats (ASR) (50 micrograms testosterone propionate at 5 days of age). When Silastic capsules containing estradiol (E2) were implanted one week after ovariectomy (Day 0) in control rats, afternoon luteinizing hormone (LH) surges occurred on Days 3 and 4. When 2 progesterone (P) silastic capsules were placed s.c. on Day 3 at 0900 h into E2-primed ovariectomized controls, the afternoon LH plasma surge concentrations were markedly amplified. In contrast, identical E2 or E2P treatment of adult ovariectomized ASR had no effect on plasma LH on either Days 3 or 4 after E2 capsule placement. Serum concentration differences of follicle-stimulating hormone (FSH), prolactin (Prl), E2 and P between control rats and ASR and the effects of E2 treatment on these hormone levels also were recorded. In E2-treated ASR, initial steady state concentrations of NE were significantly less than in controls in all brain regions examined. NE turnover rates increased significantly in E2-treated controls at 1500-1700 h compared to those at 1000-1200 h in median eminence (ME), medial preoptic nucleus (MPN), suprachiasmatic nucleus (SCN) but not in arcuate nucleus (AN). No increase in NE turnover rates occurred in MPN and ME and only slight increases in turnovers were observed in SCN and AN in E2-treated ASR during the afternoon. DA turnover rates declined between morning and afternoon in ME of control and ASR. In control rats, DA turnover rates increased during the afternoon in AN and MPN but remained unchanged in these same hypothalamic regions in ASR. A considerable amount of previous evidence suggests that NE may be the neural trigger which evokes the release of luteinizing hormone releasing hormone (LHRH) from ME axon terminals in normal proestrous or in E2-treated ovariectomized rats. The failure of NE to be released into the MPN and ME of ASR may account for the failure of estradiol to induce LH surges in these animals.