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Biomedical subjects

A Quattrone

Publications and source records attributed to A Quattrone.

At least 181 records · Page 10Linked to original sources
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

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

Decreased anticonvulsant activity of carbamazepine in 6-hydroxydopamine-treated rats.

An intraventricular injection of 6-hydroxydopamine, which produced a marked decrease of catecholamines in the forebrain, significantly lowered the electroconvulsive threshold in rats. The anticonvulsant effect of carbamazepine was also significantly reduced in the animals treated with 6-hydroxydopamine. The results are consistent with the hypothesis that brain catecholamines may play an important role in seizure susceptibility as well as in the anticonvulsant activity of carbamazepine in rats.

Animals↗
PubMed1976

Antinociceptive action of quipazine: relation to central serotonergic receptor stimulation.

Quipazine, a serotonin receptor stimulant, inhibited the response of rats to painful stimuli in two methods currently used to measure antinociception in these animals: the hot plate and tail compression test. The antinocicptive action was observed with doses ranging from 5 to 20 mg/kg i.p according to the test situation. The effect was significantly antagonized by a pretreatment with methergoline, a potent serotonin antagonist. An electrolytic lesion placed in the nucleus raphe medianus, which produced a marked decrease of serotonin in the forebrain did not, or only slightly, affected the effect of quipazine, depending on the method used to measure antinociception. It is suggested that quipazine can produce antinociceptive action in rats by interacting with a serotonergic mechanism. The action appears to be due mainly to a direct action on postsynaptic serotonin receptors, although a presynaptic component can also contribute to the effect of quipazine.

Analgesia↗
PubMedDate not supplied

Computerized analysis of eye movements as a function of age.

Vertical and horizontal saccadic (SEMv, SEMh) and smooth pursuit eye movements (SPEM) were recorded in 66 normal subjects of different ages using a computerized system. No difference was found in SEMh recordings for the right versus the left eye or for gaze direction. In contrast, SEMv recordings of upgaze vs. downgaze showed a significant difference in performance index (peak velocity) and delay. SEMh and SEMv performance index and delay were significantly slowed in elderly subjects, although accuracy was not affected. SPEM analysis also revealed a decrease in velocity in elderly people indicating diminished tracking ability as a result of the aging process. These data suggest that senescence may influence some SEM and SPEM parameters. We thus emphasize the usefulness of having reliable normative data corrected for age.

Journal Article↗
PubMedDate not supplied

Sequential occurrence of benign partial epilepsy and childhood absence epilepsy in three patients.

We first report 3 patients who experienced absence epilepsy (mean age at onset: 6.3 years; range: 4-9) 1-4 years after recovering from an electroclinical picture characteristic of benign childhood partial epilepsy (BCPE). All patients were put on monotherapy with sodium valproate, and their long-term course was excellent with remission of absences and normalization of EEG recordings. The exceptionality of our observation favors the hypothesis that BCPE and absence epilepsy are distinct entities.

Adolescent↗
PubMedDate not supplied

Exclusion of the SCN2B gene as candidate for CMT4B.

Charcot-Marie-Tooth disease type 4B (CMT4B) is a demyelinating autosomal recessive motor and sensory neuropathy characterised by focally folded myelin sheaths in the peripheral nerve. The CMT4B gene has been localised by homozygosity mapping and haplotype sharing in the 11q23 region. A cDNA encoding for the beta 2 subunit of the human brain sodium channel, SCN2B, has been recently assigned to the same chromosomal interval by FISH. The SCN2B gene has been considered a good candidate for CMT4B on the basis of protein homology, chromosomal localisation, and putative biological function of the coded product. In this paper, we report the genomic structure of the SCN2B gene consisting of 4 exons and 3 introns spanning a region of approximately 12 Kb. In addition, a search for mutations in patients affected with CMT4B as well as a refined physical localisation excludes SCN2B as the CMT4B gene.

Base Sequence↗
PubMedDate not supplied

Carbamazepine-induced nonepileptic myoclonus in a child with benign epilepsy.

Myoclonic jerks involving the proximal limb musculature and tic-like movements (sniffing, coughing, or sighing) were observed in an 11-year-old boy with benign occipital epilepsy treated with carbamazepine (CBZ). The involuntary movements disappeared a few days after withdrawal of CBZ and reappeared with CBZ reintroduction. Plasma CBZ levels were always within the therapeutic range. Polygraphic studies failed to show any electroencephalogram (EEG) changes during myoclonic jerks. Appearance of nonepileptic myoclonus in epileptic children treated with CBZ should be carefully evaluated to prevent worsening of the clinical picture. The coexistence of other involuntary movements (tics) could suggest the correct diagnosis.

Carbamazepine↗