Lordosis In Estrogen-primed Rats Research Articles

GABAergic drugs alter hypothalamic serotonin release and lordosis in estrogen-primed rats

The effects of muscimol, a GABA A agonist, and phaclofen, a GABA B antagonist, on serotonin (5HT) release in the mediobasal hypothalamus and lordosis behavior were studied in freely moving rats using in vivo microdialysis. Two days after implantation of bilateral guide cannulae directed towards the ventromedial nucleus of the hypothalamus (VMH), ovariectomized rats were primed with estradiol (E 2). The rats were implanted with microdialysis probes 24 h later. Following a pretest for lordosis, perfusate 5HT was measured at 20-min intervals until the baseline was stable. The rats were treated with 10, 30 or 100 μM muscimol or 30 and 100 μM phaclofen in artificial CSF delivered via reverse dialysis for 40 min. Control animals were continuously perfused with artificial CSF. Behavior was tested 20, 60 and 180 min after introduction of the drug. Decreased hypothalamic 5HT (40–60% of baseline) and marked facilitation of lordosis were present 20 min after administration of either drug. The effects of 10 and 30 μM muscimol and 30 μM phaclofen on both 5HT and lordosis were reversed after 180 min. Reversal of the behavioral and neurochemical effects were not evident in either the 100 μM muscimol or 100 μM phaclofen groups at the time-points tested. Proceptive responses were observed in phaclofen-treated rats but not in rats treated with muscimol. Levels of hypothalamic 5HT and lordosis quotients in control rats did not significantly differ from initial values. These results suggest that GABAergic effects on lordosis may be mediated through an interaction with 5HT in the mediobasal hypothalamus.

Nitric oxide mediates sexual behavior in female rats.

Nitric oxide (NO), an active free radical formed during the conversion of arginine to citrulline by the enzyme NO synthase (NOS), mediates vasorelaxation, cytotoxicity, and neurotransmission. Neurons containing NOS (NOergic) are located in the hypothalamus. These NOergic neurons control the release of several hypothalamic peptides. Release of NO from these NOergic neurons stimulates pulsatile release of luteinizing hormone-releasing hormone (LHRH) in vivo and LHRH release in vitro. LHRH not only induces LH release, which induces ovulation, but also facilitates female sexual behavior. Sexual behavior can be induced reliably in estrogen-primed ovariectomized female rats by progesterone (P). This behavior consists of proceptive behavior to attract the male and the assumption of a clear characteristic posture, lordosis, when mounted by the male. To ascertain the role of NO in the control of sexual behavior in female rats, an inhibitor of NOS, NG-monomethyl-L-arginine was microinjected into the third cerebral ventricle (3V) of conscious, ovariectomized, estrogen-primed rats with indwelling cannulae. NG-Monomethyl-L-arginine (10-1000 micrograms) prevented P-facilitated lordosis when administered intracerebroventricularly into the 3V, 20 min prior to the 3V injection of P. NG-Monomethyl-D-arginine, which does not inhibit NOS, did not inhibit lordosis under the same experimental conditions. Microinjection into the 3V of sodium nitroprusside (SNP), which spontaneously releases NO, facilitated lordosis in estrogen-primed rats in the absence of P. The facilitation of lordosis induced by either P or SNP was prevented by intracerebroventricular injection of hemoglobin, which binds NO. Lordosis facilitated by P or SNP was blocked by injection of LHRH antiserum into the 3V. The results are interpreted to mean that the P-facilitated lordosis response is mediated by LHRH release. Furthermore, since NO release from SNP also facilitates lordosis in the absence of P and this response could be blocked by LHRH antiserum, we conclude that P brings about the release of NO, which stimulates LHRH release that facilitates lordosis. Thus, the results indicate that NO induces LHRH release and that LHRH then plays a crucial role in mediation of sexual behavior in the female rats.

Persistence of dihydrotestosterone inhibition of lordosis in estrogen-primed rats fed a tryptophan-deficient diet

Administering increasing dosages of 5α-dihydrotestosterone propionate (DHTP) (0, 40, or 80 μ/100 g in oil daily) to ovariectomized female rats treated concurrently with estradiol benzoate (EB) (1 μg/100 g in oil daily) caused significant, equivalent reductions in lordotic responsiveness in rats maintained either on a tryptophan-deficient corn diet or on a corn diet to which L-tryptophan was added. Whole brain concentrations of 5-hydroxytryptamine (5-HT) and of 5-hydroxyindoleacetic acid were approximately two times higher in rats fed corn+tryptophan versus corn alone. These findings suggest that the ability of DHTP to inhibit lordosis probably depends upon some mechanism other than a facilitation of 5-HT release from serotonergic neurons.

Alpha-methyltryptamine blocks facilitation of lordosis by progesterone in spayed, estrogen-primed rats

Alpha-methyltryptamine, a drug which stimulates serotonergic receptors in the central nervous system, inhibited the induction of sexual receptivity in spayed female rats by estradiol benzoate and progesterone. The drug had no effect on the sexual receptivity induced by estradiol benzoate alone. These data are consistent with the hypothesis that progesterone facilitates lordosis in estrogen-primed rats by inhibiting a serotonergic system in the brain. The data also suggest that estradiol and progesterone act on separate neurochemical systems to induced estrous behavior in rats.

Potassium Chloride-Induced Lordosis Behavior in Rats Is Mediated by the Adrenal Glands

Potassium chloride applied topically to the neocortex facilitates lordosis behavior in estrogen-primed ovariectomized rats. This effect is absent in rats that are also adrenalectomized. Potassium chloride fails to facilitate lordosis in estrogen-primed rats, with intact adrenals, which are pretreated with dexamethasone, an inhibitor of the release of adrenocorticotropic hormone. Adrenalectomized rats that have been treated with dexamethasone are capable of responding to progesterone with the display of lordosis. The results suggest that application of potassium chloride to the neocortex acts as a stressor that causes the release of adrenal progestin.