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Biomedical subjects

G Schettini

Publications and source records attributed to G Schettini.

At least 145 records · Page 8Linked to original sources
PubMed1981

Pharmacological evidence of supersensitivity of central serotonergic receptors involved in the control of prolactin secretion.

m-Chlorophenylpiperazine (m-CPP), a serotonin receptor agonist, induced dose-related increase in plasma prolactin levels in the rat. This effect was significantly prevented by pretreatment with metergoline, a serotonin receptor blocker. Long-term degeneration of hypothalamic serotonin nerve endings induced by intraventricular injection of 5, 7-dihydroxytryptamine, significantly enhanced the PRL-releasing action of m-CPP, as revealed by the shift to the left in the dose-response curve that relates the dose of m-CPP to plasma PRL levels. Thus the evidence suggests the possible development of supersensitivity of central serotonin receptors involved in the control of prolactin release.

5,7-Dihydroxytryptamine↗
PubMed1979

Effect of midbrain raphe lesion or 5,7-dihydroxytryptamine treatment on the prolactin-releasing action of quipazine and D-fenfluramine in rats.

The role of brain serotonin in regulating prolactin (PRL) secretion has been investigated by studying the effect of quipazine and D-fenfluramine, two serotonin-like drugs, on plasma PRL levels under various experimental conditions. Quipazine (5, 10 and 20 mg/kg i.p.) and D-fenfluramine (5, 7.5 and 10 mg/kg i.p.) induced dose-related increases in plasma PRL levels in male rats. Intraventricular injection of 5,7-dihydroxytryptamine (5,7-DHT) or electrolytic lesion of the nucleus raphe medianus (MR), which caused a marked and selective depletion of hypothalamic serotonin levels, significantly reduced the PRL-releasing effect of both quipazine and D-fenfluramine. These results suggest that the effect of these drugs on PRL release is mediated through a serotonergic mechanism in the brain.

5,7-Dihydroxytryptamine↗
PubMed1979

Effect of 6-hydroxydopamine treatment on TSH secretion in basal and cold-stimulated conditions in the rat.

6-Hydroxydopamine (6-OHDA) (two doses of 200 micrograms each, administered intraventricularly at a 48 h interval) caused a marked decrease of hypothalamic noradrenaline content and blocked the TSH rise elicited by cold exposure. Clonidine (0.4 mg/kg i.p.), a noradrenaline receptor agonist, was able to reverse the 6-OHDA of cold-induced TSH surge. The plasma TSH levels after cold stress in rats treated with 6-OHDA + clonidine were significantly higher than in vehicle + clonidine-injected animals, thus suggesting the presence of noradrenaline receptor supersensitivity in 6-OHDA-pretreated rats. 6-OHDA did not modify the basal concentrations of TSH but the administration of clonidine to 6-OHDA-injected animals caused a significant increase in thyrotropin secretion when compared with the vehicle + clonidine group.

Animals↗
PubMed1979

Lack of evidence for an inhibitory role played by tuberoinfundibular dopaminergic neurons on TSH secretion in the rat.

The role of dopamine (DA) in the control of thyroid stimulating hormone (TSH) secretion in basal or cold stimulated conditions was investigated by using pharmacological or neurosurgical tools. The intraventricular injection of DA (5 micrograms/animal) or the subcutaneus (s.c.) injection of a dopaminomimetic agent failed to induce changes of TSH plasma levels in normal or in cold stimulated conditions. The same results were obtained by intraperitoneal (i.p.) administration of haloperidol, a blocker of dopaminergic receptors. The complete deafferentation of hypothalamus, which causes degeneration of norepinephrinergic nerve endings and leaves the DA tuberoinfundibular system unaffected, prevented the TSH release evoked by cold exposure. alpha-Methyl-p-tyrosine (alpha-MpT) (250 mg/kg i.p.), which causes a remarkable reduction of DA in the median eminence (ME) of deafferented animals, was unable to restore the TSH response to cold. Collectively these results seem to suggest that DA does not play a significative role in the control of TSH secretion in the rat.

Animals↗
PubMed1979

Pharmacological evidence of an interaction between serotonergic and dopaminergic neurons in the control of prolactin secretion in male rats.

The purpose of the present study was to investigate the possible interaction between serotonergic and dopaminergic neurons in regulating prolactin (PRL) secretion. We have examined the effect of quipazine, a drug which has been reported to increase plasma PRL levels by acting through a serotonergic mechanism, on PRL release in rats pretreated with penfluridol or alpha-methyl-p-tyrosine (alpha-MPT). The effect of d-fenfluramine, a serotonin releaser, on plasma PRL levels in animals pretreated with penfluridol was also studied. Penfluridol or alpha-MPT treatments significantly stimulated PRL secretion. Quipazine also increased plasma PRL levels in normal male rats. However, this drug was not able to further stimulate PRL release in animals pretreated with penfluridol or alpha-MPT. Like quipazine, d-fenfluramine increased plasma PRL levels in normal rats but it failed to further stimulate PRL secretion in penfluridol-pretreated animals. These findings support the hypothesis that serotonin may stimulate PRL release through an inhibition of dopaminergic neurons.

Animals↗
PubMed1978

Increased plasma prolactin levels induced in rats by d-fenfluramine: relation to central serotonergic stimulation.

d-Fenfluramine (7.5 and 10 mg/kg i.p.) and quipazine (10 and 20 mg/kg i.p.) increased plasma prolactin levels in male rats. Metergoline (3 mg/kg p.o.) or p-chlorophenylalanine (100 mg/kg X 3, orally) pretreatment markedly blocked the prolactin-releasing effect of both d-fenfluramine and quipazine. This result suggests that the effect of these drugs on prolactin secretion could be mediated through a serotonergic mechanism. Brain serotonin may thus exert a stimulatory role on prolactin secretion in rats.

Animals↗
PubMed1977

The role of central noradrenergic neurons in the control of thyrotropin secretion in the rat.

To investigate the role played by hypothalamic noradrenaline (NE) in the regulation of TRH-TSH release during tonic and cold activated conditions, drugs and surgical procedures able to interfere with central NE tonus were utilized. The time course of the effect of alpha-methyl-para-tyrosine (alpha-MpT) on basal TSH secretion was followed. The tyrosine hydroxylase (TH) inhibitor was unable to modify TSH plasma levels, whereas NE hypothalamic content decreased beginning with the third hour. The acute release of TSH evoked by cold exposure (CE) was prevented by pretreatment with alpha-MpT 1 h before; when alpha-MpT was followed 40 min later by clonidine, a central noradrenergic stimulating agent, TSH response to cold, previously blocked by the TH inhibitor was restored. Intraventricular injection of 10 micrograms of clonidine hydrochloride in unstimulated rats caused a significant rise of basal TSH levels 3, but not 10 min after the administration. Complex deafferentation of the medial basal hypothalamus (MBH), which destroys all the NE fibers afferent to this area, caused no change of thyrotropin secretion in basal conditions. Deafferented animals did not show any acute increase of TSH in response to CE. The results of this study provide evidence that NE may be the catecholamine (CA) mediating the rise in TSH following CE and that the direct stimulation of central NE receptors can evoke a massive TSH release from the anterior pituitary gland also in basal conditions.

Animals↗
PubMed1977

Effects of clonidine on basal and cold-stimulated TSH secretion.

Clonidine, injected i.p. 20 min before cold exposure, is able to counteract the blockade induced by alpha-methyl-p-tyrosine of cold-stimulated release of TSH in rats. Under basal conditions the alpha-adrenoceptor stimulating agent, administered into the lateral cerebral ventricle (10 microgram), produces, at 30 min, a sharp increase in plasma TSH that returns to control levels at 60 min. When the drug is given intraperitoneally (0.4 mg/kg) it causes a significant decrease in plasma TSH 120 min after the treatment.

Animals↗
PubMed1977

Effects of some antineoplastic agents on plasma levels of corticosterone, prolactin and thyroid stimulating hormone.

The effects of 5-fluorouracil (5-FU), 1,3 bis(2-chloroethyl)-1 nitrosurea (BCNU) and cyclophosphamide on plasma levels of corticosterone, prolactin and thyroid stimulating hormone (TSH) were investigated. All the three drugs produce a remarkable adrenocortical activation but the duration of this effect is different. Hypophysectomized rats do not show any increase of plasma corticosterone levels in response to the considered antineoplastic agents. This may be indicative of an action mediated by adrenocorticotropic hormone (ACTH). The same drugs caused a significant fall of plasma TSH. Also the duration of this effect was different for the three compounds. No relevant modifications of plasma prolactin were observed.

Animals↗