Sex-induced fos in the medial preoptic area: projections to the midbrain.

Sexual activity results in cells displaying Fos-like Immunoreactivity (FLI) in the medial preoptic area (MPOA) of male rats. This study combined retrograde tracing techniques with FLI to determine if MPOA cells displaying sex-induced FLI project to known efferent sites of the MPOA. FluoroGold was injected into the dorsal central gray, lateral central gray, ventral tegmental area, medial central tegmental field, or lateral central tegmental field of male rats that later engaged in sexual activity. Examination of FLI and FluoroGold in the MPOA revealed that the lateral region of the MPOA projected to the lateral central gray and contained smaller projections to the other regions. These findings suggest that the lateral MPOA contains secondary sex-relevant projections to the midbrain.

Quinpirole attenuates the striatal fos expression induced by escape behavior.

Several studies have shown that the D2-like dopamine receptor agonist quinpirole is able to markedly potentiate the striatal Fos expression induced by D1 agonists. The present study examined the effects of quinpirole on the striatal Fos-like immunoreactivity (FLI) induced by escape behavior. Male rats were pretreated with either saline or quinpirole (0.156, 0.625, 1.25 or 2.5 mg/kg) and 30 min later, placed in a shuttle box and required to crossover every 30 s in order to escape mild footshock. Animals were sacrificed 30 min following the completion of a 1-h block of escape trials and sections through the striatum were processed for FLI. Pretreatment with quinpirole produced a marked, dose-dependent, attenuation of escape-induced FLI in the striatum. These findings demonstrate that quinpirole affects the striatal Fos expression induced by shuttling in a very different fashion than it does that induced by D1 agonists, and further support the view that dopaminergic mechanisms play an important role in behaviorally induced striatal Fos expression.

Superovulation and embryo recovery in ewes treated with gonadotrophin-releasing hormone agonist and purified follicle-stimulating hormone.

Chronic treatment with gonadotrophin-releasing hormone (GnRH) agonist eliminates luteinizing hormone (LH) pulses and inhibits maturation of Graafian follicles in sheep. Since the presence of 'dominant' follicles may inhibit superovulatory responses, an experiment was conducted to determine whether a GnRH agonist could be used in conjunction with follicle-stimulating hormone (FSH) to induce a superovulatory response with production of normal embryos. Twenty-four Welsh Mountain ewes were chronically treated with GnRH agonist by means of a subcutaneous minipump. Twelve of the ewes were given 12 mg progesterone intramuscularly (i.m.) twice daily for four days; all ewes were then given 672 micrograms (total) of highly purified FSH continually infused intravenously for either 72 h (Group A) or 96 h (Group B) in a 2 x 2 experimental design (n = 6). Ovulation was then induced with 750 I.U. human chorionic gonadotrophin injected i.m. (Day 0) and all ewes were inseminated into the uterus with > 100 x 10(6) fresh sperm on Day 0. Embryos were flushed from the uterus, and ovaries were inspected at laparotomy on Day 5. Pretreatment with progesterone did not affect any of the parameters measured and data were pooled accordingly. There were no differences between Groups A and B in the number of ovulations or the number of embryos recovered, although there were more large unruptured follicles in Group A animals (8.8 +/- 0.8 v. 3.1 +/- 0.7, P < 0.001). The embryo recovery rate was higher in Group A ewes (52.5 v. 26.4, P < 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Site-specific effects of intracerebral injections of three neurokinins (neurokinin A, neurokinin K, and neurokinin gamma) on the expression of male rat sexual behavior.

Accumulating evidence indicates that neurokinins play a role in the neural regulation of male rat copulatory behavior. We have previously reported that injections of the neurokinin substance P into the medial preoptic nucleus facilitated male rat copulatory behavior. Recently, a number of other neurokinins, neurokinin K (neuropeptide K), neurokinin A (substance K), and neurokinin gamma (derived from the same gene as substance P), have been identified in the mammalian CNS. Therefore, in a series of experiments we examined the effects on male copulatory behavior following bilateral injections of different doses of neurokinin K (NkK), neurokinin A (NkA), or neurokinin gamma (Nk gamma) into the medial preoptic area (MPOA), bed nucleus of the stria terminalis (BnST), or the caudate/putamen. Bilateral injections of NkK into the MPOA or BnST inhibited the expression of male copulatory behavior. The most marked effect was seen following bilateral injections of 0.25 and 0.52 nmol of NkK into the MPOA and the BnST. These injections produced a dramatic suppression of copulatory behavior in previously sexually vigorous male rats when compared to control injections. In contrast, bilateral injections of three different doses of NkA into the MPOA failed to affect any parameter of male copulatory behavior. Bilateral injections of 0.431 nmol of Nk gamma into the MPOA failed to affect the expression of copulatory behavior, but significantly delayed its initiation when compared to controls. Bilateral injections of 0.251 nmol of NkK into the caudate/putamen had no significant effect on copulatory behavior in sexually vigorous male rats when compared to control injections. The results of the present study provide further support for a role of neurokinins in the regulation of copulatory behavior in male rat. Taken together, these results suggest that the effects of neurokinins upon the expression of male copulatory behavior are site specific for brain regions in the sexually dimorphic vomeronasal pathway which includes the MeA, BnST, and MPOA.

Cloning and sequencing of the sheep pituitary gonadotropin-releasing hormone receptor and changes in expression of its mRNA during the estrous cycle.

We have isolated a full length cDNA clone coding for the sheep GnRH receptor (GnRH-R). The amino acid sequence shows greater homology to the human GnRH-R sequence than the two rodent receptors published so far. We have also carried out physiological studies investigating the pattern of expression of the GnRH-R mRNA throughout the estrous cycle. GnRH receptor mRNA and GnRH binding levels were both significantly (P < 0.05) increased over luteal levels up until the time of the preovulatory LH surge, whilst post-surge, a significant (P < 0.05) decline was seen. These changes were related to increased follicle estradiol production in the follicular phase. In contrast, no changes in the abundance of LH beta mRNA were seen throughout the estrous cycle, but the pituitary content of LH significantly (P < 0.05) decreased after the preovulatory LH surge. These results suggest that there is a close relationship between the abundance of GnRH-R mRNA and translation of the GnRH-R in sheep.

GnRH-dependent and -independent components of FSH secretion after acute treatment of anoestrous ewes with ovine follicular fluid and a GnRH antagonist.

Gonadotrophin and inhibin concentrations were measured in anoestrous ewes after acute treatment with either saline, ovine follicular fluid (oFF), GnRH antagonist, or oFF and GnRH antagonist in combination. The increase in mean LH concentrations observed in ewes treated with oFF alone, was not seen in either of the groups treated with GnRH antagonist, in which LH pulsatility was completely inhibited. This result suggests that the LH rebound that follows follicular fluid treatment is GnRH dependent. Blockade of GnRH had no effect on the suppression of FSH seen after follicular fluid injection, indicating that this component of FSH secretion is independent of short-term GnRH input. After this initial suppression, a rebound release of FSH was seen in the group treated with oFF alone. The addition of GnRH antagonist appeared to decrease the rebound, suggesting that this rebound release of FSH may have a GnRH-dependent component. Inhibin concentrations in both oFF-treated groups increased after oFF injection and then declined to pretreatment values. However, a second rise in inhibin concentration, concomitant with the FSH rebound in ewes receiving oFF alone, was seen in the group treated with oFF and GnRH antagonist. As this rise in endogenous inhibin concentration could also act to suppress the rebound release of FSH, it cannot be conclusively proved from this study that GnRH input is required for the generation of the rebound release of FSH after treatment with oFF.