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Biomedical subjects

S Sagratella

Publications and source records attributed to S Sagratella.

85 records · Page 5Linked to original sources
PubMed1984

Influence of morphine and cyclazocine on the cortical epileptic foci in rabbits.

The effects of morphine, cyclazocine and naloxone on penicillin- and strychnine-induced epileptic foci were studied in rabbits. The intracortical injection of penicillin (75, 150 and 300 units) elicited isolated spikes followed by repeated ictal events. The application of strychnine (0.062 and 0.125%) over the cortical surface of one side induced appearance of ipsilateral spiking spreading to the contralateral cortex. Administration of morphine (0.25-0.75 mg/kg i.v.) or cyclazocine (0.05-3.0 mg/kg i.v.) inhibited the occurrence or the duration of the EEG and motor manifestations induced by penicillin (75 and 150 units) and strychnine (0.062 and 0.125%), while it did not influence the effect of 300 units of penicillin. High doses of morphine (up to 10 mg/kg i.v.) failed to affect the epileptic responses to penicillin and strychnine and at the same time significantly reduced the pO2 in arterial blood. Naloxone per se potentiated the effects of the lower doses of penicillin and strychnine. Only at very high doses (20 mg/kg i.v.) displayed a weak antagonism towards the anticonvulsant effect of the two opiates. A full antagonism is only observed towards the effect of cyclazocine (2 mg/kg i.v.) administered after penicillin. Present data provide additional evidence of the heterogeneity of regulation by opioids of convulsive phenomena. One can hypothesize that the anticonvulsant effect of the two opiate agonists is mediated by naloxone-insensitive opiate receptors, while the proconvulsant-convulsant effect of naloxone might be related to an inhibition of GABA and glycine-mediated transmission.

Animals↗
PubMed1983

An EEG investigation on the effects of phencyclidine on pentylentetrazol convulsions in rats and rabbits.

The present work deals with an EEG and behavioral study of the effect of phencyclidine against the convulsions due to pentylentetrazol in rats and rabbits. The effects of phencyclidine were compared to those of phenobarbital and trimethadione. A dissociation between the behavioral and electrocortical manifestations of chemically-induced convulsions in the presence of several anticonvulsant drugs has been found.

Animals↗
PubMed1982

Convulsant and anticonvulsant effects of opioids: relationship to GABA-mediated transmission.

The convulsant benzodiazepine Ro 5-3663, bicuculline and picrotoxin induced electroencephalographic (EEG) and behavioural convulsions. In rabbits, the EEG modifications consisted, with increasing doses, of three different patterns: slow waves in the optic lead, spike- and wave-complexes in the sensorimotor cortex, and grand-mal generalized seizures. These EEG effects were terminated by administration of diazepam (1 mg/kg) and morphine (0.25-1.0 mg/kg). Naloxone, in doses of 5-10 mg/kg, potentiated the effects of the three convulsant drugs. This potentiating phenomenon was also antagonized by the administration of diazepam and morphine. In membrane preparations, obtained from rat cortex, deprived of endogenous modulators of [3H]GABA binding, naloxone but not morphine, was able to inhibit [3H]GABA binding to its specific recognition sites. These data agree with previous findings indicating a GABA-antagonistic effect of naloxone, and support the hypothesis that the anticonvulsant effect of morphine might be, at least in part, due to an increase in GABAergic activity at the synaptic level.

Animals↗
PubMedDate not supplied

NMDA antagonists: antiepileptic-neuroprotective drugs with diversified neuropharmacological profiles.

In conclusion, NMDA antagonists as anticonvulsants are especially active in preventing the generalization of the behavioural and electrical seizures and display a typical spectrum of in vitro antiepileptiform activities. In addition, based on in vitro and in vivo limbic kindled studies, the drugs should be regarded more as an antiepileptiform than as an anticonvulsant drugs. As neuroprotective drugs, NMDA antagonists are effective against many types of neuronal injury and show a window of activity which does not exceed 1-2 h, thus suggesting an influence of NMDA receptors in the 'early' or 'acute' mechanisms of brain damage. Among NMDA antagonists, glycine antagonists or the morphinans dextromethorphan and dextrorphan showed a spectrum of antiepileptiform and neuroprotective activities broader than other NMDA antagonists. The primary pharmacological activities of NMDA antagonists are accompanied by some effects including perturbation of many sensory, psychological or motor processes. Typical behavioural and EEG changes were also induced by the drugs. In spite of the side-effects elicited by the drugs, differential effects detected among the various classes of NMDA antagonists (i.e. lack of induction of typical EEG-behavioural effects and of typical cortical neurotoxicity) might render some of these suitable for full clinical application as anticonvulsant-neuroprotective drugs.

Anticonvulsants↗
PubMedDate not supplied

Differential effects of morphinan drugs on haloperidol-induced catalepsy in rats: a comparative study with an N-methyl-D-aspartate antagonist.

The effects of the morphinan drugs dextrorphan, dextromethorphan and levorphanol were tested towards the cataleptic activity induced by 1 mg/kg of haloperidol i.p. in rats. The influence of the morphinans was compared to that of the N-methyl-D-aspartate competitive antagonist, 2-amino-5-phosphonovaleric acid. 2-Amino-5-phosphonovaleric acid (0.5 mumoles, i.c.v.), dextrorphan (7.5-15 mg/kg, i.p.) and dextromethorphan (15-30 mg/kg, i.p.) significantly reduced the degree of catalepsy in the haloperidol-treated rats within 15 min. Conversely, levorphanol (15-30 mg/kg, i.p.) significantly increased the degree of catalepsy in the haloperidol-treated rats within 15 min. Naloxone (2 mg/kg, i.p.) counteracted the potentiating effects of levorphanol. These findings demonstrate a differential influence of the morphinan stereoisomers dextrorphan and levorphanol on experimental catalepsy, and suggest a potential use of dextromethorphan in the treatment of Parkinson's disease.

2-Amino-5-phosphonovalerate↗
PubMedDate not supplied

Antiepileptic effects of the excitatory amino acid antagonist cis-2,3 piperidine-dicarboxylic acid depend on non-N-methyl-d-aspartate receptors.

The effects of the broad spectrum antagonist of the excitatory amino acid neurotransmission, the cis-2,3 piperidine-dicarboxylic acid (cis-2,3 PDA) were investigated on the epileptiform activity induced in vitro by different treatments on rat hippocampal slices. The drug reduced the bursting duration by 45% and the occurrence of the additional population spikes by 50% compared with controls using 1 microM kainic acid to induce epileptiform bursting. At the same concentrations (50-100 microM) cis-2,3 PDA did not significantly affect the magnesium free-induced epileptiform activity. At higher concentrations (200-400 microM), the drug was able to reduce by 25% the bursting duration and the occurrence of the additional population spikes using 1 mM penicillin to induce epileptiform bursting. Our data indicate that the broad spectrum antagonist of the excitatory amino acid transmission, cis-2,3 PDA, presents a low antiepileptic activity that could be related to an influence on "non N-methyl-d-aspartate" (NMDA) receptors.

Animals↗
PubMedDate not supplied

Influence of adenosinergic drugs on the epileptiform and neurotoxic effects of N-methyl-d-aspartate: comparison with the effects of MK801.

In the present paper, the influence of the adenosine receptor agonist N6-(l-2-phenylisopropyl)adenosine (L-PIA) and of the adenosine receptor antagonist caffeine on the epileptiform and neurotoxic effects of N-methyl-d-aspartate (NMDA) has been tested in rat hippocampal slices. Slice superfusion with 1 microM NMDA changed within 30 min the control CA1 field potentials into an epileptiform bursting in all experiments. Slice superfusion with 0.5-1 microM L-PIA or 50-100 microM caffeine plus 1 microM NMDA inhibited or potentiated, respectively, the CA1 epileptiform bursting duration with respect to a slice superfusion with 1 microM NMDA alone. Slice superfusion with 50-100 microM NMDA induced within a few minutes the appearance of short-lived (1-2 min) additional epileptiform population spikes, followed by an irreversible disappearance of the CA1 population spike. Slice superfusion with 50 microM of the NMDA antagonist dizocilpine (MK801) plus 50-100 microM NMDA prevented in all experiments the irreversible disappearance of the CA1 population spike with respect to a slice superfusion with 50-100 microM alone. Neither in a slice superfusion with 0.5-1 microM L-PIA plus 50-100 microM NMDA nor in a slice superfusion with 50-100 microM caffeine plus 50-100 microM NMDA did this effect occur. The results demonstrate that adenosine receptor ligands modulate the epileptiform but not the neurotoxic effects of NMDA.

Action Potentials↗