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In previous studies we observed that LHRH concentrations increase in the preoptic-suprachiasmatic tuberoinfundibular system (PSTS) during the morning hours of proestrus when norepinephrine (NE) and dopamine (DA) turnover rates are low. Concomitant with the preovulatory surge in gonadotropins, NE turnover rates increase, DA turnovers decrease, and LHRH declines in PSTS. The present studies examine the effects of phenobarbital (PB) on these proestrous events. PB, when given at 0900 hr proestrus, does not prevent the rise in median eminence (ME) LHRH which occurs between 0900 and 1200 hr. When the barbiturate is administered at 1200 hr, LH, FSH, and prolactin proestrous surges are blocked. While PB (given at 1200 hr) does not affect the increase in turnover rates of NE and DA which occur between 1200 and 1400 hr proestrus it markedly suppressed NE turnover rates in ME and suprachiasmatic nuclei but not in the medial preoptic nuclei between 1500 and 1700 hr. The decline in ME-DA which occurs between 1...

We have correlated catecholamine [CA; i.e. norepinephrine (NE), dopamine (DA), and epinephrine (E)] turnover rates in discrete hypothalamic nuclei and in the median eminence (ME), with concentration changes in ME LHRH and serum LH, FSH, PRL, estradiol, and progesterone levels at various times during proestrus and diestrous day 1 in 4-day cyclic rats. CA concentrations were measured with a radioenzymatic assay at 0, 60, and 120 min after ip injection of 400 mg/kg alpha-methyl-p-tyrosine, and rate constants and turnover rates were calculated. In a separate assay NE, DA, and E were separated by two-dimensional thin layer chromatography, and concentrations and turnover rates of CAs were calculated. The microdissected hypothalamic nuclei examined for NE turnover rates included the medial preoptic nucleus (MPN), suprachiasmatic nucleus (SCN), arcuate nucleus (AN), and ME. DA turnover rates also were measured in the MPN, ME, and AN. ME LHRH and serum hormone concentrations were measured by RIA. Between 0900--1200 h, proestrous serum estradiol was elevated, but other serum hormones were basal, and CA turnover rates in the brain were low. However, ME LHRH concentrations increased significantly between 0900--1200 h on proestrus. Between 1200--1500 h, serum LH, FSH, PRL, and progesterone levels increased and ME LHRH levels declined significantly; during this time interval (1200--1400 h), a significant rise in ME NE and DA turnover rates occurred. Between 1500--1700 h on proestrus, while serum gonadotropins were still rising toward peak concentrations, increased ME NE turnover rates were maintained, but increased NE turnover rates also were evident in MPN, SCN, and AN. During this same time interval (1500--1700 h), a marked decline in ME and AN DA turnover rates occurred, although such rates remained unchanged within the MPN. There were no corresponding changes in MPN E turnover rates at any of the time intervals studied. The increased turnover rates of ME NE coupled with the concomitant decline in ME LHRH levels and the rise in plasma LH and FSH levels suggest that increased NE release may be important in initiating preovulatory LH and FSH surges. These changes in brain neurotransmitters and serum hormones are not the result of a diurnal rhythm, since corresponding changes in CA turnover rates or serum gonadotropins did not occur between 0900--1100 h and 1500--1700 h diestrous day 1.

We studied the influence of orchiectomy (GDX) and steroid administration on the level of cytosolic androgen receptor in rat levator ani muscle and rat skeletal muscles (tibialis anterior and extensor digitorum longus). Androgen receptor binding to muscle cytosol was measured using [3H]methyltrienolone (R1881) as ligand, a 100-fold molar excess of unlabeled R1881 to assess nonspecific binding, and a 500-fold molar excess of triamcinolone acetonide to prevent binding to glucocorticoid and progestin receptors. Bound and free ligand were separated by column chromatography with Sephadex G-75. In levator ani muscles from intact animals (controls), maximum R1881 binding (Bmax), determined by Scatchard analysis, was 2.5 fmol/mg protein (Kd = 0.68 nM). Thirty days after GDX, Bmax increased to 500% of the control value, with no significant change in Kd (0.96 nM). Using saturating levels of R1881, Bmax was increased to 280% of the control value 12 h post-GDX, 600% at 14 days, 478% at 30 days, and 133% at 44 days. The increase in receptor binding was blocked by cycloheximide. Administration of Silastic capsules containing testosterone propionate 30 days post-GDX resulted in R1881 binding at the control level at 44 days. Surprisingly, administration of 17 beta-estradiol (E2) 30 days post-GDX resulted in increased (480%) R1881 binding. Thus, E2 may cause induction of the cytosolic androgen receptor in levator ani muscle from GDX rats; alternatively, the rate of receptor degradation may be altered. R1881 binding by skeletal muscle cytosol was increased 139% at 12 h, 212% on day 14, 220% on day 30, and 158% on day 44 with respect to the control value. Administration of testosterone propionate at 30 days caused R1881 binding to return to the control value by day 44, whereas E2 was without influence. The differences in response of levator ani and skeletal muscle receptors may account for the differential effects of sex steroids on these muscle types.

Progesterone (P) amplifies and advances gonadotropin surges when administered to estradiol (E2)-treated ovariectomized rats. While daily rhythmic LH surges continue to occur in E2-treated rats, they are extinguished in E2- and P (E2P)-treated animals 24 h after P treatment. We examined whether this negative feedback effect on P affect catecholamine activity within the median eminence, medial preoptic nucleus, arcuate nucleus, and suprachiasmatic nucleus and also the changes which occur in median eminence LHRH concentrations. Twenty-four hours after P exposure, LH and FSH surges in E2P-treated rats are extinguished, and the magnitude of the PRL surge is reduced. In E2-treated rats, there is an increase in medial preoptic nucleus, suprachiasmatic nucleus, and median eminence NE turnover rates from 1000--1200 to 1500--1700 h, but these changed in NE activity do not occur in E2-treated rats which received P 24 h earlier. Rather, such E2P-treated animals have markedly elevated medial preoptic nucleus, arcuate nucleus, and median eminence DA turnover rates during the period that plasma gonadotropin levels are suppressed. No differences in median eminence LHRH concentrations in E2- or E2P-treated rats were detected. P may exert its negative feedback action in suppressing LH, FSH, and PRL release by blocking activation of the hypothalamic noradrenergic system and by increasing dopaminergic activity within the tuberoinfundibular system.

Specific areas of the preoptico-suprachiasmatictuberoinfundibular system (PSTS) were microdissected at various hours on proestrus and diestrous day 1 in rats. LHRH concentrations were measured by RIA to determine if the patterns of change observed in the median eminence (ME) were paralleled by similar LHRH patterns in the remainder of the PSTS. Another group of proestrous rats received phenobarbital to block preovulatory gonadotropin surges, and LHRH concentrations in the PSTS were measured throughout the afternoon hours. Plasma concentrations of LH, FSH, estradiol, and progesterone were determined in all animals. Rats were decapitated on proestrus and diestrous day 1 at 0900, 1200,1500, and 1800 h. Proestrous animals that received phenobarbital at noon were sacrificed at 1500 and 1800 h. The following brain areas were microdissected: the suprachiasmatic preoptic nucleus, medial preoptic nucleus, suprachiasmatic nucleus, anterior hypothalamic nucleus retrochiasmatic area, arcuate nucleus, and ME. On the d...

While LHRH evokes the release of both LH and FSH under a wide spectrum of experimental conditions, this hormone has not been shown to induce the discharge of FSH unaccompanied by LH release. As a consequence, the possibility that a separate FSHRH exists has not been discounted. These experiments were designed to demonstrate that LHRH is capable of promoting marked increases in plasma FSH concomitant with physiologically insignificant changes in plasma LH and, thus, that LHRH is also FSHRH. Seven groups of cyclic female rats received phenobarbital at 1200 h proestrus to block spontaneous preovulatory LH and FSH surges. These various groups then were subdivided according to whether phosphate-buffered saline (PBS), LHRH, or both was infused (iv). The experimental protocol consisted of infusing material for an initial 30 min (priming period), stopping the infusion for 30 min (rest interval), and again infusing material for an additional 210 min (maintenance period). When PBS was infused during the priming and...