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Biomedical subjects

G Nistico

Publications and source records attributed to G Nistico.

At least 37 records · Page 2Linked to original sources
PubMed1987

Behavioural and electrocortical power spectrum effects of 5-methoxytryptoline and other analogs after intraventricular administration in rats.

The behavioural and electrocortical power spectrum effects of tryptoline and the 5-hydroxy and 5-methoxy derivatives were studied after microinjection of the drugs into the third cerebral ventricle in freely moving rats. The three compounds produced a dose-dependent desynchronication in electrocortical activity with a concomitant syndrome of behavioural stimulation. The most potent compound was 5-methoxytryptoline, already active at 4 nmol. When given into the third cerebral ventricle, 5-methoxytryptoline antagonized the sedation and hypothermia induced by reserpine. The relative order of potencies was 5-methoxytryptoline greater than 5-hydroxytryptoline greater than tryptoline. Melatonin, the 5-methoxy-N-acetyl derivative of serotonin, when injected into the third cerebral ventricle, did not produce desynchronization and elicited only mild sedation. The high potency of 5-methoxytryptoline following injection into the third cerebral ventricle and the relative order of potencies with 5-hydroxytryptoline and tryptoline is compared to the affinity of these compounds for the modulatory site of the serotonin transporter which was labelled with [3H]imipramine or [3H]paroxetine.

Animals↗
PubMed1987

Anticonvulsant effect of denzimol in DBA/2 mice.

The anticonvulsant activity of N-[beta-[4-beta-phenylethyl)phenyl]-beta-hydroxyethyl]-imidazole hydrochloride, denzimol, was studied following intraperitoneal administration in DBA/2 mice (seizures induced by sound). Protection against sound-induced seizures was observed after intraperitoneal administration of denzimol (3-15 mg/kg). The ED50 values for the suppression of tonic, clonic and wild running phases of sound-induced seizures were 1.24, 2.61 and 6.03 mg/kg, respectively. This protective action was significantly reduced by pretreatment with aminophylline (25 mg/kg i.p.), CGS 8216 (1 or 5 mg/kg i.p.) and Ro 15-1788 (2.5 mg/kg i.p). The present experiments suggest an involvement of purinergic and benzodiazepine mechanisms in the anticonvulsant action of denzimol.

Acoustic Stimulation↗
PubMed1986

Anticonvulsant properties of flunarizine on reflex and generalized models of epilepsy.

The anticonvulsant activity of 1-bis(4-fluorophenyl)methyl-4-(3-phenyl-2-propenyl)-piperazine, flunarizine, was studied after intraperitoneal administration in DBA/2 mice (seizures induced by sound), intravenous administration in Papio papio (myoclonus induced by photic stimulation) and oral administration in Wistar rats (seizures induced by cefazolin). Protection against sound-induced seizures was observed after intraperitoneal administration of flunarizine (5-40 mg/kg). The ED50 for suppression of tonic, clonic and wild running phases of sound-induced seizures was 3.3, 9.8 and 17.5 mg/kg, respectively. This protective action was significantly reduced by pretreatment with aminophylline (50 mg/kg, i.p.). In photosensitive baboons flunarizine (0.5-1.0 mg/kg, i.v.) provided partial protection against myoclonic responses to stroboscopic stimulation. After flunarizine (2 mg/kg, i.v.) this protection lasted for more than 5 hr (and was complete at 2-3 hr). Cefazolin-induced seizures in rats were prevented by administration of flunarizine (20-40 mg/kg, orally). The ED50 for the suppression of tonic and clonic seizures evoked by subsequent intravenous administration of cefazolin was 25 mg/kg. The protective effects of flunarizine (40 mg/kg, orally) were maximal after 3-6 hr and were maintained for 16-24 hr. Behavioural effects of flunarizine included signs of sedation in both mice and rats. Tolerance to the antiepileptic effects of flunarizine was not seen after chronic treatment in rats. The role of purinergic receptors and of calcium entry blockade in the anticonvulsant action of flunarizine requires further study.

Acoustic Stimulation↗
PubMed1983

Lack of relation between dopaminergic and gabaergic mechanisms in chick retina.

The effects of apomorphine and bromocriptine on GABA content, GAD and GABA-T activities in the chick retina, both in conditions of a light cycle of 12 h/day and in conditions of light deprivation for 72 h, were studied. In addition, the effects of a treatment with 2 neuroleptics, having a different action on dopamine receptors, i.e. haloperidol and sulpiride, on the same biochemical parameters were examined. The present results show that all the pharmacological manipulations at the dopaminergic transmission by means of agonists and antagonists at dopamine receptors did not affect GABAergic mechanisms in the chick retina and seem to suggest a lack of relations between dopaminergic and GABAergic mechanisms at this level.

4-Aminobutyrate Transaminase↗
PubMed1980

Behavioral and electrocortical effects after intrastriatal cefazolin in rats are antagonized by drugs enhancing GABA-ergic transmission.

Cefazolin, a semisynthetic cephalosporin, reported to reproduce in several animal species an experimental model of epilepsy, was microinjected into the head of the caudate nucleus in rats. The effects on behavior, electrocortical activity and the antagonism by GABA receptor agonists and GABA-transaminase activity inhibitors were studied. Cefazolin given into the III cerbral ventricle produced an intense pattern of behavioral and locomotor stimulation culminating into several episodes of wild-running crisis, myoclonic jerks of the limbs and in some occasions generalized clonic seizures, these effects lasting over 2 h. At the same time bursts of electrocortical high-voltage spikes followed bu intermittent high-voltage single spikes were recorded. Similarly cefazolin, given into the caudate nucleus produced contralateral circling, an increase locomotor activity, myoclonic jerks of contralateral limbs, intense stereotyped behavior and occasionally generalized clonic convulsions. In addition postural changes consisting in tonic contralateral head-neck deviation were observed. This picture was accompanied by epileptic electrocortical changes, i.e. high-voltage spikes, spike-waves complexes, recruiting polyspikes. The subsequent intraventricular or intrastriatal infusion of GABA, GABOB, muscimol or of GABA-transaminase inhibitors, ethanolamine-o-sulphate and GABA-vinyl-GABA was able to antagonize clinical and electrocortical changes evoked by cefazolin. In conclusion, the present results suggest that cefazolin motor and electrocortical effects are due to an impairment of GABA-ergic transmission.

Animals↗
PubMed1980

Antagonism by classical antiepileptics and sodium valproate of cefazolin in induced experimental epilepsy in rats.

The effects of cefazolin, a semisynthetic cephalosporin, on rat behavior, electrocortical activity and on electrocortical spectrum power were evaluated. In addition, the possible antagonism by some antiepileptic agents was studied. Cegazolin, given intravenously in rats, produced generalized convulsions, electrocortical high-voltage spikes and other electrocortical abnormalities similar to those described to occur in human epilepsy. Power spectrum analysis of the electrocortical activity revealed a significant increase in total voltage output during electrocortical epileptogenic discharges. In addition high-voltage spikes induced by cefazolin were easily counted and lasted approximately 90 min. Classical antiepileptic drugs (diphenylhydantoin, phenobarbital and clonazepam as well as sodium valproate were able to counteract electroclinical disorders induced by cefazolin.

Animals↗
PubMed1977

Effects of gaba, gabob and some anticonvulsant drugs on dibutyryl cyclic AMP evoked seizures.

The present experiments were undertaken to study the possible effects of Gaba, Gabob, phenobarbitone, diphenylhydantoin, and diazepam given systemically on convulsant activity evoked in chicks by intrahypothalamic injection of dibutyryl cyclic AMP (cAMP). Diphenylhydantoin and phenobarbitone antagonized the effect of dibutyryl cAMP but unfortunately the effects of Gaba and Gabob were complicated by osmotic effects. Diazepam, an anticonvulsant benzodiazepine, did not affect dibutyryl cAMP-induced electrocortical spiking. The dibutyryl cAMP-induced syndrome seems to be of limited value as a model for assessing the activity of anticonvulsant drugs are present.

Aminobutyrates↗
PubMed1977

Lack of hypertensive and hyperglycemic effect of diazoxide after intraventricular injection.

In adult fowls intravenous but not intraventricular injection of diazoxide produced hypotension and a rise in blood glucose concentration. Since noradrenaline microinfused into the hypothalamus produced a fall in blood pressure, it does not seem that hypotensive effects of diazoxide are mediated through release of noradrenaline in areas of the luain accessible from the ventriculus tertius cerebri. Present experiments also indicate that the hyperglycemic effects of diazoxide is unlikely to be due to an action on central adrenergic receptors.

Animals↗