Biomedical subjects

L Caligaris

Publications and source records attributed to L Caligaris.

At least 19 recordsLinked to original sources

PubMed1992

Daily variations in the sensitivity of proestrous LH surge in the inhibitory effect of intraventricular injection of 5-HT or GABA in rats.

Intraventricular injection of 5-hydroxytryptamine (5-HT) into female rats at 11:00 h on the day of proestrus inhibited the preovulatory surge of luteinizing hormone (LH) and ovulation. A similar response was observed after the activation of the serotonergic system by stimulation of the median raphe nucleus. A diurnal rhythm of these responses was observed. In rats acclimated to a 14-h:10-h light:dark cycle the potency of 5-HT to inhibit the LH surge and ovulation was 2.06 and 2.3 times greater, respectively, when injected at 11:00 h than at 13:00 h. Also stimulation of the median raphe nucleus at 11:00 h was significantly more effective in inhibiting these parameters than stimulation at 13:00 h. Similarly, the ability of gamma-amino-butyric acid (GABA) to inhibit the preovulatory LH surge and ovulation was greater in rats injected in the morning than in the afternoon. The results of this study indicate that during proestrus the sensitivity of 5-HT and GABA to induce inhibition of preovulatory LH release and ovulation shows daily variations with maximal effect before the critical period.

Animals↗

PubMed1990

Further evidence of an opposite effect of dorsal and median raphe nuclei on the proestrous surge of LH.

The effect of stimulation or lesions of either the dorsal or the median raphe nucleus on the proestrous surge of LH and on ovulation was studied in rats kept under constant illumination. Electrochemical stimulation (anodic DC of 100 microA during 30 sec) was applied at noon on the day of proestrus through chronically implanted electrodes. Lesions of the raphe nuclei were made by passing a cathodic current of 1 mA for 20 sec through nichrome electrodes stereotaxically implanted. Blood samples from freely behaving rats were obtained hourly through cannulae inserted into the jugular vein. Rats under constant light from diestrous day 1 or diestrous day 2 showed a delay in the onset of the LH surge of the next proestrus. Stimulation applied into the median raphe nucleus inhibited proestrous LH release and blocked ovulation, whereas stimulation of the dorsal raphe nucleus resulted in enhanced LH release in rats under constant light from diestrous day 2 but not from diestrous day 1. In turn, in rats bearing lesions in the dorsal raphe nucleus LH surges were decreased and ovulation was blocked, but rats with lesions in the median raphe nucleus exhibited enhanced LH release. It is concluded that the dorsal and the median raphe nuclei exert opposite effects on the proestrous surge of LH and on ovulation.

Animals↗

PubMed1989

Inhibition of proestrous LH surge and ovulation in rats evoked by stimulation of the medial raphe nucleus involves a GABA-mediated mechanism.

The neurotransmitters involved in the inhibition of luteinizing hormone (LH) release induced by electrochemical stimulation (anodic d.c., 100 microA/30 s) of the medial raphe nucleus (MRn) were studied. Stimulation applied at noon on the day of proestrus blocked the preovulatory surge of LH and ovulation. This effect was prevented by pretreating the animals (15 min before stimulation) with the 5-HT antagonist, methysergide (3.5 mg/kg, i.p.). The inhibition of LH release induced by stimulation of the MRn was also suppressed by the injection of the gamma-aminobutyric acid (GABA) antagonists, picrotoxin (0.8 mg/kg, i.p.) and bicuculline (6 mg/kg, i.p.). Injection of 5-HT (15 micrograms) into the third ventricle on the day of proestrus mimicked the effect of MRn stimulation, a response which was prevented by methysergide, picrotoxin or bicuculline. An intraventricular injection of GABA (10 micrograms) also inhibited the preovulatory surge of LH and ovulation, but whereas the administration of bicuculline prevented the effect of GABA, that of methysergide failed to produce any change. It is concluded that stimulation of the MRn inhibits the proestrous surge of LH by activating a serotonergic pathway and that the effect is mediated by GABAergic neurons.

Animals↗

PubMed1978

Stimulatory and inhibitory effects of ovarian steroids on gonadotrophin secretion in ovariectomized rats after anterior hypothalamic deafferentation.

The effect of frontal hypothalamic deafferentation on the release of LH and FSH was studied in ovariectomized rats. Frontal cuts were placed just in front of the arcuate nucleus, at the posterior border of the optic chiasma (RCS), at the level of the anterior commissure (POS) and in front of the optic chiasma (PCS). Animals with RCS and POS cuts showed vaginal smears with persistent cornification; the other groups had irregular cycles. The concentrations of LH and FSH in the serum increased after ovariectomy in deafferentated animals, but after 4 weeks the levels were lower than in the animals without hypothalamic lesions except for the PCS group. The more caudally that the cuts were located, the lower were the concentrations of hormones in the serum. The injection of repeated doses of oestradiol benzoate resulted in a decrease in serum gonadotrophin of both rats without hypothalamic lesions and RCS rats. Although a greater decrease was observed in the lesioned than in the intact rats, it is believed that such an effect does not indicate an increased sensitivity of deafferentated animals to this steroid. The stimulatory effect of progesterone on LH and FSH release was studied in ovariectomized rats primed with oestradiol benzoate. The responses were unchanged in PCS animals but failed to occur in POS and RCS rats. Measurement of the level of gonadotrophin-releasing hormone in frontal hypothalamic slices from RCS animals showed a decreased level behind the cut and an increased one in front of it, suggesting that perikarya located in front of the section were sending their axons to the mediobasal hypothalamus. It is believed that the blockade of the stimulatory effect on gonadotrophins by frontal hypothalamic deafferentation is due to the transection of these axons. Cuts placed immediately in front of the arcuate nucleus, however, permitted progesterone-induced gonadotrophin release because of incoming neurones containing gonadotrophin-releasing hormone, which end in structures immediately rostral to the cut. The results indicate that effects of both inhibitory and stimulatory ovarian steroid feedback are impaired by frontal hypothalamic deafferentation.

Afferent Pathways↗

PubMed1977

Further evidence on the role of the hypothalamic afferents on the estrogen-induced prolactin release.

Serum prolactin (Prl) concentrations in ovariectomized rats were low without significant differences between morning and afternoon values. These levels were not affected by either frontal or caudal hypothalamic deafferentation. However, they increased after lesioning the hypothalamic median eminence (ME). Three days after the injection of 20 microgram estradiol benzoate (EB) into ovariectomized non-lesioned rats, a rise in serum Prl occurred in the afternoon but not in the morning. In animals with ME lesions estrogen enhanced both morning and afternoon values. The animals with caudal hypothalamic deafferentation and those which had undergone sham operation showed the same pattern as the normal animals. On the contrary, after estrogen treatment of rats with frontal hypothalamic deafferentation high serum Prl concentration during the morning and low levels in the afternoon were observed. It is concluded that estrogen effects on Prl secretion are in part mediated by frontal neural afferents to the hypothalamus. They would facilitate Prl inhibiting factor (PIF) secretion in the morning and inhibit PIF secretion in the afternoon.

Afferent Pathways↗

PubMed1976

The role of hypothalamic afferents in the release of prolactin induced by ovarian steroids.

The importance of frontal and caudal afferents to the hypothalamus in the release of prolactin induced by estrogen and progesterone was studied in gonadectomized female and male rats. The serum prolactin levels 2 or 3 days after the injection of 20 mug estradiol benzoate (EB) into ovariectomized rats were significantly lower in animals with retrochiasmatic section interrupting the anterior inputs to the hypothalamus than in control animals, whereas the prolactin secretion induced by progesterone (2 mg) injection in EB-primed animals was not affected. On the contrary, interruption of caudal afferents to the hypothalamus had no effect on the increase in serum prolactin induced by EB injection. A hypersensitive prolactin response to the injection of estrogen or progesterone occurred in animals with frontal hypothalamic deafferentation. It is concluded that prolactin secretion induced by estrogen injection depends not only on the activation of hypothalamic and pituitary mechanisms, but also on the stimulation of frontal neural afferents to the hypothalamus. The latter mechanism does not operate in male rats.

Animals↗

PubMed1974