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Biomedical subjects

C Menini

Publications and source records attributed to C Menini.

At least 19 recordsLinked to original sources
PubMed1992

Influence of cholinergic system on myoclonus in myoclonic epilepsies.

The effect of two drugs upon multifocal myoclonic jerks was evaluated. The drugs influence the central cholinergic system in opposite ways. Eight patients with progressive and nonprogressive myoclonic epilepsy were tested. The single blind test was used. The number of myoclonic jerks after intravenous physostigmine (mean dose 0.02 mg/kg) and that after atropine (0.04 mg/kg) was compared to number of myoclonic jerks in the drug-free periods and with placebo. Placebo was without an effect. Physostigmine slightly increased the number of jerks. Atropine decreased the number significantly. In most patients the results were not striking. It is suggested that the cholinergic system may participate in the physiopathology of the studied myoclonus in a rather indirect, perhaps modulating way.

Adolescent↗
PubMed1992

Burst generation in neocortical neurons after GABA withdrawal in the rat.

1. gamma-Aminobutyric acid (GABA) withdrawal syndrome (GWS) represents a particular model of focal epilepsy consecutive to the interruption of a chronic intracortical GABA infusion and is characterized by the appearance of focal epileptic electroencephalographic (EEG) discharges and localized clinical signs on withdrawal of GABA. Effects of Ca2+ channel blockers and N-methyl-D-aspartate (NMDA) antagonists were evaluated in living rats presenting a GWS after interruption of a 5-day GABA infusion into the somatomotor cortex and in neocortical slices obtained from such rats. Bursting properties and morphology of neurons were also analyzed in slices. 2. In living rats, the noncompetitive NMDA antagonist phencyclidine [1-(1-phenylcyclohexyl)piperidine] and the Ca2+ antagonist flunarizine [E-1 (bis(4fluorophenyl)methyl)-4(3phenyl2-propenyl)-piperazine] were administered systemically to two groups of rats. Rats in the first group (n = 12) were injected with the drug 30-60 min before discontinuation of the GABA infusion. In this case, phencyclidine (10 mg/kg ip) prevented the development of GWS (n = 5), whereas flunarizine (40 mg/kg ip) had no consistent effect on the GWS appearance and characteristics (n = 7). Rats in the second group (n = 12) were injected 60-90 min after GABA discontinuation, i.e., during a fully developed GWS. In that case, neither drug suppressed GWS. 3. Neuronal activities in the epileptic focus were studied in slices with conventional intracellular recording and stimulation techniques. From the 65 neurons recorded, 29 responded with EPSPs and paroxysmal depolarization shifts (PDSs) to white matter stimulation (synaptic bursting or SB cells). Nineteen other neurons presented, in addition to synaptically induced PDSs, bursts of action potentials (APs) induced by intracellular depolarizing current injection (intrinsic bursting or IB cells). The remaining 17 neurons presented no bursting properties to either synaptic stimulation or depolarizing current injection (nonbursting or NB cells). 4. The recorded neurons were located 0.7-1.2 mm distant from the lesion because of the penetration of the GABA infusion cannula. Intracellular injection of neurons (n = 4) with biocytin or Lucifer yellow revealed that both SB and IB neurons were large, spiny pyramidal neurons localized in layer V of the sensorimotor cortex. 5. Bath application of the selective antagonist of NMDA receptors DL-2amino-5phosphonovalerate or DL-2amino-7phosphonoheptanoate (10-50 microM) reversibly reduced the amplitude (by 25-50%) and the duration (by 20-25%) of PDSs in all cases (n = 17).(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1991

Metabolic anatomy of the focal epilepsy produced by cessation of chronic intracortical GABA infusion in the rat.

Cessation of chronic (5 days), unilateral infusion of GABA into the somatomotor cortex of rats induces focal epileptic spikes which remain limited to the infused site and never evolve into generalized seizures. We have considered this finding as a new model of focal epilepsy and named it "GABA withdrawal syndrome". In the present study, we have measured local cerebral glucose utilization in order to map the cortical and subcortical regions involved in the GABA withdrawal syndrome. Local cerebral glucose utilization increased two- to three-fold in a 1-1.5 mm diameter area, involving all the cortical layers at the GABA-infusion site. This hypermetabolic area contained a central (1-2 mm diameter) hypometabolic zone showing neuronal depopulation in some animals. Except for the epileptic focus, the hemisphere ipsilateral to the infusion site was slightly hypometabolic. However, there was a large increase (three- to five-fold) in some ipsilateral thalamic nuclei (posterior oralis, ventralis postero-lateralis, centralis lateralis, ventralis lateralis and reticularis thalami nucleus). The local cerebral glucose utilization of the contralateral cortex and thalamus were unchanged. The present results confirm the focal nature of the epileptogenic syndrome produced by stopping chronic, intracortical GABA infusion. These results are markedly different from those described in the penicillin focal epilepsy model. Our data also show that specific ipsilateral thalamic relays may, by an as yet unknown mechanism, play a role in maintaining paroxysmal activity during the GABA withdrawal syndrome.

Animals↗
PubMed1990

Unexpected potentializing effect of a tacrine derivative (9-amino-7-methoxy-1,2,3,4 tetrahydroacridine) upon the non-epileptic myoclonus in baboons Papio papio.

1. The influence of 7-methoxytacrine (7-MEOTA) on the non epileptic myoclonus of the Papio papio baboon was studied in 5 animals. 2. This type of myoclonus is thought to depend on a cholinergic system dysfunction since it can be induced by atropine and blocked by physostigmine. 3. 7-MEOTA, a tacrine derivative, is believed to display a conspicuous anticholinesterase activity but, surprisingly, it here potentiated the non epileptic myoclonus occuring either spontaneously or induced by atropine. 4. In baboons not spontaneously presenting the non epileptic myoclonus, 7-MEOTA induced the myoclonus in a fashion similar to atropine; such a myoclonus was blocked by physostigmine. 5. These data indicate a possible antagonist action of tacrine on the muscarinic acetylcholine receptor. From these data, it is suggested that caution is necessary when introducing a tacrine derivative in clinical practice.

Animals↗
PubMed1990

Clinical efficacy of five filters specific for leukocyte removal.

The clinical efficacy of 5 filters specific for leukocyte depletion was evaluated retrospectively. The patient population was composed of 191 thalassemics who received about 15,000 units of filtered blood in 28 months. The frequencies of reactions to filtered blood varied significantly (p less than 0.0001) according to the type of filter and were as follows: Erypur, 0.7%; Imugard, 2.7%; Leucostop, 0.7%; Miropore, 2.1%; Sepacell, 0.6%. There was a notable concordance between the efficacy in the leukocyte removal and the clinical performance of the filters. The 2 polyester filters examined combined good clinical and laboratory results with superior flow properties.

Adolescent↗
PubMed1990

Non-A, non-B hepatitis and anti-HCV antibodies in dialysis patients.

To define the prevalence of non-A, non-B hepatitis, antibodies to HCV were detected in 193 patients on renal replacement therapy (52 transplant and 141 hemodialysis patients) and in 50 staff members of a Nephrology Department. Unequivocal seroconversion was documented in 5 transplant (9.6%) and in 26 dialysis patients (18.4%). In the dialysis population, the prevalence of anti-HCV antibodies was evaluated in patients grouped according to the number of blood transfusions and to the different sections of dialytic treatment. The most striking findings were the marked differences in the prevalence of anti-HCV antibodies among patients treated in different sections (from 0% to 70%), and the presence of a significant increase in alanine-amino-transferase (ALT) concentrations in 14 anti-HCV negative patients. The results suggest that the diffusion of non-A, non-B hepatitis is mainly transfusion-related, with the possibility of significant environmental diffusion related to the violation of infection-control measures. The current immunoassay is probably unable to detect the actual frequency of the infection.

Adult↗
PubMed1990

[Value of the monkey Papio papio for the study of epilepsy].

The baboon Papio papio is the only animal model showing a natural photosensitive epilepsy very similar to that observed in some human epileptic patients. In the baboon, intermittent light stimulation (ILS) induces bilateral and synchronous myoclonic twitches which are associated with paroxysmal discharges (PDs) predominating in the frontal cortex, and can be followed by generalized tonic-clonic seizures. We were able to demonstrate the motor cortical origin of all these manifestations since neuronal generators responsible for paroxysmal discharges are localized there and are activated by visual afferents from the occipital lobe. The corpus callosum is the structure determining the interhemispheric synchronization of PDs. An unbalance of neurotransmitter systems such as GABA or excitatory amino acids should be responsible for the hereditary predisposition of baboons to photosensitive epilepsy. Some Papio papio, either photosensitive or not, may show spontaneous truncular myoclonic twitches, different from those induced by intermittent light stimulation, and resembling the intention myoclonus as observed in some human neurological disorders (post-anoxic syndrome, degenerative encephalopathies such as Ramsay-Hunt syndrome...). Because of the absence of any abnormal electrographic discharge, this myoclonus is considered non epileptic. Until now, we were unable to determine the structure generating this myoclonus. The most probable origin is in the lower brain stem. Experimental data suggest that a local unbalance of the cholinergic neurotransmission could be responsible for the predisposition of baboons to show this type of myoclonus.

Animals↗
PubMed1989

Relationship between tolerance to GABAA agonist and bursting properties in neocortical neurons during GABA-withdrawal syndrome.

The interruption of intracortical, chronic GABA infusion is known to give rise to 'GABA withdrawal syndrome' (GWS) consisting of electroencephalographic paroxysmal focal activities, associated with behavioral epileptic signs. Neocortical slices were obtained from rats presenting the GWS (GWS slices), and intracellular recordings were performed in the vicinity of the gamma-aminobutyric acid (GABA)-infused site. Electrical stimulation of the underlying white matter induced paroxysmal depolarization shifts (PDSs) in virtually all neurons. Bath-applied GABA (1-10 microM) had no effect on these neurons, while the same dose range was found effective in blocking action potentials in saline-infused cortex slices obtained from control rats. In the GWS slices a population of neurons presented, in addition to synaptically induced PDSs, voltage-dependent and cobalt-sensitive PDSs and bursts of action potentials induced by depolarizing current injections. These intrinsic bursting neurons were unresponsive to high doses of GABA (100 microM). Dose-response curves of isoguvacine, a specific GABAA agonist, showed a shift to the right for the intrinsic bursting cells whatever the parameter measured (depolarization or conductance increase): the ED50 was 50-100 times higher for intrinsic bursting cells than for other non-intrinsic bursting cells, thus indicating that intrinsic bursting cells are tolerant to GABAA agonist. This tolerance may result from a decreased number of receptors or from a change in their properties as a consequence of the previous prolonged GABA infusion. The decrease in the GABA efficacy could lead to disinhibition and could thus give the appearance of epileptic events.

Animals↗
PubMed1988

The GABA-withdrawal syndrome: a new model of focal epileptogenesis.

A novel model of focal, cortical epilepsy is described. Chronic (6 h to 14 days), localized application of gamma-aminobutyric acid (GABA) into the somatomotor cortex of rats induces, upon withdrawal, the appearance of epileptogenic activity with maximal electrographic expression circumscribed to the infused site. This GABA-withdrawal syndrome (tested for a 100 micrograms/microliter/h dose) lasted from 24 to 168 h (mean values). A significant correlation was found between infusion time and duration of the excitability rebound, with the longer duration corresponding to the shorter infusion time. A distant lesion effect was observed in the thalamic area of cortical projection. The potential use of this neurotransmitter-induced phenomenon in the study of brain plasticity in general, and of epilepsy in particular, is discussed.

Animals↗
PubMed1988

Local asymptomatic status epilepticus induced by withdrawal of GABA infusion into limbic structures.

Most of the experimental models of status epilepticus result either from administration of a variety of excitatory neurotoxins or repeated electrical stimulation. Here we propose a new model based on the withdrawal of chronic gamma-aminobutyric acid (GABA) infusion into limbic structures via osmotic minipumps. Appearing with a latency of about 50 min, continuous pseudo-rhythmic EEG epileptic spiking was elicited for about 12-24 h after removal of GABA infusion in hippocampus or amygdala. No apparent distant brain damage was observed. This model differs from many others by several features and could result from different mechanisms.

Amygdala↗