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F Marrosu

Publications and source records attributed to F Marrosu.

At least 37 records · Page 2Linked to original sources
PubMed1989

Antagonism of ethanol effects by Ro 15-4513: an electrophysiological analysis.

Ethanol (ETH) and general anesthetics have been reported to facilitate the chloride channel opening, possibly, or at least partly, through an interaction with the GABA-benzodiazepine (BZ) receptor-gated chloride ionophore "supramolecular complex". Recently Ro 15-4513, a novel BZ ligand, has been indicated as a potent and selective antagonist of various ETH-induced behavioral and biochemical effects. However, since its precise characterization is still a matter of debate, we have tested and compared the effect of Ro 15-4513, as well as its antagonism against ETH, in two objective electrophysiological parameters, i.e., the electroencephalograph (EEG) pattern in freely moving rats and single unit activity of reticulata neurons. Ro 15-4513 produced an EEG state of alertness and antagonized the behavioral impairment and the EEG deterioration by ETH. However, while its protective action was consistent against moderate doses (2 g/kg) of ETH, it was much less evident versus higher doses (4 and 8 g/kg). On reticulata cells, Ro 15-4513 potently stimulated their spontaneous firing and reversed the depression by both ETH and Na-pentobarbital. Moreover, the beta-carboline DMCM also had similar effects. The "pure" BZ antagonist Ro 15-1788 was completely inefective against ETH, yet fully cancelled the reversing actions of Ro 15-4513 and DMCM upon ETH or Na-pentobarbital effects. It is concluded that Ro 15-4513 behaves as a BZ inverse agonist, so that its opposition to ETH and Na-pentobarbital is probably the result of its "negative" coupling with the BZ recognition site that triggers the closing of chloride channels. It suggests that BZ inverse agonists might constitute, in the near future, a new class of analeptic drugs.

Action Potentials↗
PubMed1989

Epidemiological study of myasthenia gravis in Sardinia, Italy (1958-1986).

From 1.1.1958 to 31.12.1986, 110 cases of MG were observed in Sardinia, with a mean annual incidence of 2.5 x 1,000,000 inhabitants and prevalence rates of 7.5, 17.6, 31.4 and 45.0 x 1,000,000 inhabitants respectively (prevalence days: 15.10.1961, 24.10.1971, 25.10.1981 and 31.12.1986). The disease was found to be more frequent in women. There were no differences in the distribution of MG in various areas of the island. The muscle group more frequently involved at onset was the ocular. In 6.4% of patients an association with thyroid disorders was observed. The mortality of MG patients was significantly higher than expected. Removal of the thymus, carried out in 58 patients, was shown to be useful in the treatment of the disease, particularly in patients without thymomas. No familial cases were observed.

Adult↗
PubMed1988

The benzodiazepine recognition site inverse agonists Ro 15-4513 and FG 7142 both antagonize the EEG effects of ethanol in the rat.

The aim of the present study was to compare the ability of Ro 15-4513 and FG 7142, two inverse agonists for benzodiazepine recognition sites, to antagonize the EEG effects of ethanol in freely moving rats. Ethanol (2.5 g/kg, p.o.) induced sedation and ataxia associated with a progressive suppression of the fast cortical activities and an enhancement of low frequencies in both cortical and hippocampal tracings. In contrast, Ro 15-4513 (2 mg/kg, i.p.) and FG 7142 (10 mg/kg, i.p.) both caused a state of alertness associated with desynchronized cortical activity and theta hippocampal rhythm as well as spiking activity which was predominantly observed in the cortical tracings. When rats were treated with FG 7142 or RO 15-4513 either before or after ethanol, a reciprocal antagonism of the behavioral and EEG effects of ethanol and of the partial inverse agonists was observed. These data support the view that the anti-ethanol effects of Ro 15-4513 may be related to its partial inverse agonist properties.

Animals↗
PubMed1987

Different epileptogenic activities of murine and ovine corticotropin-releasing factor.

The behavioral and EEG effects of rat and ovine corticotropin releasing factor (r- and o-CRF) were compared. Both peptides were injected intracerebroventricularly into rats through chronically implanted cannulae. At the doses of 0.1 and 1 microgram both peptides activated the EEG and stimulated motor activity. At the dose of 10 micrograms they produced spiking activity. However, while o-CRF-induced spiking activity was present both in the hippocampus and in the cortical leads and was associated with generalized myoclonic movements, that induced by r-CRF was confined in the hippocampus and was not accompanied by myoclonic movements. Spiking activity induced by r-CRF was suppressed by verapamil, but was not influenced by naloxone.

Animals↗
PubMed1985

Aminophylline antagonizes diazepam-induced anesthesia and EEG changes in humans.

General anesthesia was induced in eight subjects by the slow IV injection of 60 mg diazepam. During the anesthetic effect, the EEG was characterized by 3-5 Hz high voltage activity. Immediate recovery of consciousness and reversal of the EEG pattern to fast low voltage activity was obtained after the IV injection of 60 mg aminophylline. On the other hand, three diazepam-treated subjects who received IV saline instead of aminophylline recovered from anesthesia 73-120 min after saline.

Adult↗
PubMed1983

Increased paroxysmal activity of partial seizures in man by apomorphine.

In order to study the role of dopamine (DA) in the regulation of seizure mechanisms in man, a non-emetic dose of apomorphine, a direct stimulant of DA receptors, was administered to eight patients effected by different types of epilepsy. The EEG changes induced by apomorphine administration in comparison to those elicited by promazine or placebo were evaluated in a double blind cross-over study. Similarly to promazine treatment, apomorphine worsened the EEG recordings of some patients. The apomorphine-induced increase in paroxysmal activity was observed in patients affected by partial epilepsy and was not related to the sleep-inducing properties of the drug. This effect is interpreted as being the result of a stimulation of DA autoreceptors, mediating a decrease of dopaminergic activity in the central nervous system. The use of apomorphine as an EEG activating agent is suggested.

Adolescent↗
PubMedDate not supplied

Localized epileptiform activity induced by murine CRF in rats.

Murine corticotropin releasing factor (rCRF), injected intracerebroventricularly into rats at a dose of 10 micrograms produced increased motor activity, grooming, and recurrent episodes of epileptic activity localized in the hippocampal leads. Such activity persisted for approximately 5 h and was characterized by recurrent trains of biphasic spikes never associated with behavioral signs of epilepsy. The intraperitoneal administration of carbamazepine (15 and 30 mg/kg) reduced the epileptic activity for approximately 90 and 120 min, respectively, whereas that of naloxone (8 mg/kg) was ineffective. The results suggest that rCRF-induced spiking activity might be a model of temporal lobe epilepsy.

Animals↗
PubMedDate not supplied

Neonatal monosodium glutamate abolishes corticotropin-releasing factor-induced epileptogenic activity in rats.

Intracerebroventricular (i.c.v.) injection of rat corticotropin-releasing factor (rCRF) at doses of 5-20 micrograms in rats induces epileptogenic activity characterized by pacemaker-like spikes localized in the hippocampal leads. Such an effect was still present in rats neonatally treated with saline but was absent in those neonatally treated with monosodium glutamate (MSG), a treatment that caused marked changes in the concentration of several brain neurotransmitters and neuropeptides in hypothalamic nuclei where CRF is highly concentrated and is believed to induce endocrinologic and behavioral effects. The present results suggest the rCRF-induced spiking activity is mediated by activation of neuronal pathways sensitive to MSG neurotoxic effect.

Animals↗
PubMedDate not supplied

Clonidine prevents corticotropin releasing factor-induced epileptogenic activity in rats.

Studies have shown that intracerebroventricular (i.c.v.) injection (10-20 micrograms) of corticotropin releasing factor (CRF) in rats induces epileptiform activity characterized by a regular (pacemaker-like) spiking pattern located in hippocampal leads. CRF has also been shown to increase the firing rate of noradrenergic neurons in the locus ceruleus. Our experiments clarified the possible role of norepinephrine (NE) in mediating hippocampal activity of CRF. Intraperitoneal (i.p.) injection of the alpha 2-agonist clonidine at a dose of 0.5-5 micrograms/kg prevented, in a dose-related manner, the hippocampal epileptiform activity induced by CRF (20 micrograms i.c.v.). Our results suggest a possible role of NE in CRF-induced spiking activity.

Animals↗
PubMedDate not supplied

Paradoxical reactions elicited by diazepam in children with classic autism.

Administration of diazepam (10 mg i.m.) to seven children (two girls and five boys) affected by infantile autism elicited paradoxical behavioural responses. Mainly, anxiogenic effect, unsocialized aggressive behaviour and explosive aggression were dramatically increased in comparison with the same symptoms present before and after treatment. The results show for the first time that benzodiazepines may elicit paradoxical behavioural response in autistic children. The possible involvement of an altered function at the level of GABA/benzodiazepine receptor complex is discussed.

Aggression↗