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Biomedical subjects

L Caligaris

Publications and source records attributed to L Caligaris.

At least 19 recordsLinked to original sources
PubMed1993

Intraventricular injection of agents that enhance cyclic adenosine monophosphate formation leads to inhibition of proestrous luteinizing hormone surge in rats.

The effect of increasing hypothalamic levels of 3',5'-cyclic adenosine monophosphate (cAMP) on the preovulatory surge of luteinizing hormone (LH) and ovulation was studied in cycling rats. Animals hearing chronically implanted guiding cannulae into the third ventricle were injected with agents known to enhance the cellular levels of cAMP. Hourly blood samples from the unanesthetized, unrestrained rats were obtained between 11.00 and 17.00 h through a plastic cannula inserted into the jugular vein. Intraventricular injections of serotonin (7.5 mg/ml; 2 microliters) in the morning of proestrous blocked the preovulatory surge of LH and ovulation. This effect was assigned to an increased neuronal level of cAMP because it was prevented by a serum anti-cAMP. Third-ventricle injections of 2 microliters of forskolin (0.5 mmol/l), guanosine 5'-O-(3-thiotriphosphate)(2 mmol/l) or dibutyryl-cAMP (1 mmol/l) at 11.00 h on the day of proestrus mimicked the inhibitory effect of serotonin on the proestrous release of LH. It is suggested that serotonin inhibits LH surge by acting directly on LH-releasing hormone neurons and/or on neurons that provide inputs to these neurons involving cAMP as a second messenger. Neurons releasing gamma-aminobutyric acid (GABA) may serve as interneurons sensitive to serotonin, as well as to cAMP, inasmuch as the inhibitory effect of forskolin on the release of LH was partially blocked by the GABA antagonists, picrotoxin and bicuculline.

Animals↗
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↗
PubMed1983

Lesions of the hypothalamic region of the fetus and length of gestation in the guinea-pig.

A lesion was placed in the hypothalamic region of the brain of one fetus in each of 25 guinea-pigs on days 39-41 of pregnancy. Thirteen females were killed before delivery and the fetuses collected for histological examination of the brain. The young of twelve other females were killed immediately after delivery in order to determine the nature and extent of any brain damage, and the findings in both groups were compared with those recorded from a series of 23 similarly operated control animals in which lesions were not made. Delivery was not consistently advanced by the brain lesions and the results do not confirm those of an earlier study in which lesions of the hypothalamus of the fetus caused premature delivery.

Animals↗
PubMed1983

Prolactin release induced by stress and the influence of oestrogen and progesterone treatments, sex and daily rhythm.

The effect of sex, ovarian steroids and time of the day on the release of prolactin induced by stress was studied. Albino rats were bled by heart puncture and immediately anaesthetized with ether; 10 min later they were bled again. Ovariectomized, oestrogen-primed rats showed a daily rhythm in the stress (bleeding plus ether) induced prolactin release with maximal concentration of prolactin in the serum at night (01.00 h) and minimum in the morning (09.00 h). IN ovariectomized, oestrogen-treated rats the rise of prolactin in the serum after stress was higher than in the non-treated rats both in the morning and at night. However in the afternoon (17.00 h), when the pre-stress levels of prolactin were high, the response to stress was reversed and prolactin levels declined. A similar effect was seen in the ovariectomized, oestrogen-primed rats 4 h after the injection of progesterone. In these animals the concentration of prolactin in serum was high and declined after stress. However 28 h after injection of progesterone stress failed to induce any change in prolactin release. Progesterone injected into ovariectomized, non-primed rats did not influence the response to stress. In male rats, both intact and castrated, the increase of prolactin concentration in serum after stress was lower than in females and failed to exhibit a circadian rhythm. These results show the importance of the hormonal background and the time of the day in the magnitude of prolactin release induced by stress.

Animals↗
PubMed1982

Lack of effect of treatment with oestrogen in advancing puberty in the guinea-pig.

Guinea-pigs were injected with 500 ng oestradiol benzoate or 0.1 ml arachis oil at 0, 5, 10, 20 or 25 days of age, or 2 microgram oestradiol benzoate/100 g body wt at 25 days, in order to determine whether puberty would be advanced, as in the rat. It was not. Repeated injections of 100 ng oestradiol benzoate or 0.1 ml arachis oil for 5 days beginning at 0, 10, 20 or 25 days of age, or 2 microgram oestradiol benzoate/100 g body wt beginning at 25 days, were similarly ineffective.

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↗