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Biomedical subjects

S Brailowsky

Publications and source records attributed to S Brailowsky.

52 records · Page 3Linked to original sources
PubMed1978

Myoclonus developing after vermisectomy in photosensitive Papio papio.

Two vermisectomized photosensitive baboons exhibited two different types of myoclonus, one induced by intermittent light stimulation (ILS) and the other occuring "spontaneously". The characteristics of these two types of myoclonus are described from a clinical and from an ECoG point of view. Myoclonus induced by ILS (ML) started at the eyelids and secondarily invaded the face and body; it was always preceded by frontorolandic spike-waves or polyspike-waves. The "spontaneous" myoclonus which followed vermisectomy (MV) was "massive", but involved firstly the trunk and secondarily the face and limbs; no ECoG paraoxysm accompanied this myoclonus, but we observed a parietal evoked potential of small amplitude, 10--15 msec after its onset. If MLs can be considered as consequences of the fronto-rolandic paroxysmal discharges, MVs seem to originate in the brain stem but appear similar to action myoclonus. This experimental situation showing two types of myoclonus resembles human hereditary degenerative syndromes (dyssynergic cerebellar myoclonus, progressive myoclonic epilepsy), without being exactly comparable. The conditions in which MVs were seen and their modifications during sleep and by different drugs are described. The relationships between MVs and MLs and myoclonic epilepsy are discussed.

Animals↗
PubMed1976

Effects of melatonin on the photosensitive epilepsy of the baboon, Papio papio.

The acute pharmacological effects of melatonin (5-methoxy-N-acetyl-tryptamine) were evaluated on behaviour and electrographic signs in the photosensitive baboon (Papio papio), including visually evoked potentials VEPs). Doses of 5 and 10 mg/kg i.v. had little effect, contrasting with the enhancement of spontaneous paroxysmal activity and latency of clinical signs elicited by intermittent light stimulation (ILS) produced by the 20 and 50 mg/kg doses. Moreover, a modification of the electrographic pattern of discharge during ILS-induced myoclonic responses was observed. These observations indicate a slight decrease of light sensitivity after melatonin. Only frontal VEPs were modified, with increase in amplitude of their late components for all doses tested. These effects lasted for 2-4 h. The participation of serotoninergic mechanisms involved in melatonin effect and in this model of experimental epilepsy are discussed.

Animals↗
PubMed1976

Effects of drugs modifying brain levels of catecholamines on photically induced epilepsy in Papio papio.

The behavioral and electrographic effects of DL-amphetamine, disulfiram, FLA-63, and propranolol on the photically induced epilepsy of the Senegalese baboon were evaluated. Amphetamine produced somatic hypokinesia with enhancement of eye movements, diminution of spontaneous paroxysmal activity, and little change in photosensitivity. The acute effects of disulfiram and FLA-63 were poor, but the latter was lethal in the days following administration. Propranolol showed no consistent effects. Participation of catecholamine processes in this type of experimental reflex epilepsy are discussed.

Amphetamine↗
PubMed1975

[Indole alkaloids induction of tremors: effect on photosensible epilepsy in Papiopapio].

Harmaline and ibogaine i.v. administration induced in the photosensitive baboon restlesness and tremor (8-12 Hz). The former increased the EEG frequency particularly in central regions with appearance of bursts at 20-24 c/s and blocked by somatic movement. The latter produced a slight enhancement of frontal fast rhythms. Both drugs blocked the spontaneous paroxysmal activity with little effect on photosensitivity. These effects lasted for 2-4 hrs. Vincamine produced agitation during 15 min. post-i.v.-administration and showed an "hypervigilant" EEG. Nor vincamine or Hydergine altered the degree of photosensitivity. Cerebellar involvement in the action of harmaline and ibogaïne is discussed.

Alkaloids↗
PubMedDate not supplied

Auditory evoked potentials from the primary auditory cortex of the cat: topographic and pharmacological studies.

Wave VI (8.4 msec) of the brain-stem auditory evoked potential (BAEP) was maximal in a discrete region of primary auditory cortex (AI) of the anesthetized cat. Wave VI underwent rapid amplitude decrease over millimeter distances in the AI region and followed high stimulation rates. Wave VI did not show intracortical polarity inversion nor was it abolished by epicortical or intracortical GABA administration. The data are compatible with a wave VI source in the terminal axons of the thalamo-cortical radiations. Middle latency auditory responses (MAEPs) generated 10-40 msec after auditory stimulation were also recorded in a circumscribed area of AI. In contrast to wave VI, these primary auditory cortex potentials (Pa 18.3 msec; Nb 31.9 msec) underwent transcortical polarity inversion, correlated with intracortical multi-unit activity in the AI region and were reversibly altered or abolished by epicortical or intracortical GABA administration to the AI region. The data suggest that the Pa and Nb components of the cat MAEP are intracortically generated by neuronal elements in the AI region.

Acoustic Stimulation↗
PubMedDate not supplied

Recovery from GABA-mediated hemiplegia in young and aged rats: effects of catecholaminergic manipulations.

We investigated the participation of catecholaminergic mechanisms in the functional recovery from motor cortex lesions in young (9 months) and aged (26 months) rats. The animals were studied during the recovery period from an hemiplegic syndrome secondary to small motor cortex lesions potentiated by the localized, chronic (7 days) infusion of GABA into the lesion site. Acute administration of haloperidol (0.1 mg/kg IP) to these recovered animals induced a re-emergence of the contralateral motor syndrome in both groups. In the young group, the haloperidol-induced hemiplegia lasted one day whereas in the aged animals the deficit was significantly prolonged lasting three days. Apomorphine administration (0.5 mg/kg IP) prior to or immediately after haloperidol injection failed to prevent or reverse the reappearance of the motor deficit. Adult animals recovered from motor cortex aspirations performed 7 to 12 months prior were refractory to haloperidol effects. Amphetamine administration to young rats treated chronically with saline or GABA infusion into the somatomotor region also failed to alter the clinical evolution of the motor deficit. The evidence suggests that dopaminergic mechanisms are involved in the functional recovery from brain lesions and that these mechanisms are most susceptible to neuroleptic blockade during the early post-lesional period. The deleterious effects of dopaminergic blockade are heightened in aged populations. The use of dopaminergic antagonists in brain-lesioned subjects, and particularly in geriatric populations, is considered potentially harmful, particularly in the early stages of the recovery process.

Aging↗
PubMedDate not supplied

Epileptic discharges induced by intermittent light stimulation in photosensitive baboons: a current source density study.

The current source density (CSD) method was applied to the study of paroxysmal discharges (PDs) induced by intermittent light stimulation (ILS) in Papio papio baboons made photosensitive by a subconvulsant dose of allylglycine. CSD was studied in the motor and premotor areas (4 and 6). Laminar profiles of sinks and sources are similar in both areas. Nevertheless, the motor area seems to become involved first since it shows the earliest and most prominent sink in layer III. Such a sink, correlated with the PD spike, moves progressively upward to the cortical surface. The localization and other experimental arguments obtained by the same method suggest that this sink could be mainly of dendritic origin. The cortico-cortical afferents to the superficial layers of the motor area might thus determine the generation of this sink. A smaller sink, detected at the same latency between layers V and VI could correspond to synaptic activations due to thalamo-cortical afferents probably arriving on the pyramidal cells which project to the spinal cord. Intense sinks correlated with the PD wave in layer V could be passive, due to active sources lying just above and/or below, because in previous studies an inhibition of the cellular discharges was always observed in correlation with the wave. It is suggested that ILS triggered PDs involve visual cortico-cortical afferents directed mainly to the superficial layers of the motor area provoking an intense synaptic activation of the cellular elements situated at this level.

Allylglycine↗
PubMedDate not supplied

Ethanol, GABA and epilepsy.

Ethanol exerts its behavioral effects largely by interacting with receptors to brain neurotransmitters. The molecular mechanisms involving these interactions are still not well known since an ideal model for their study is currently unavailable. In addition, responses to alcohol may vary due to factors such as genetic predisposition, ethanol concentration consumed, and stimuli such as stress, socialization, etc. The chronic consumption of alcohol, similar to that of other drugs such as benzodiazepines and barbiturates, is linked to GABAergic neurotransmission. GABA is the predominant inhibitory neurotransmitter in the brain. In a context of substance abuse, these three drugs first cause a gratifying effect, later tolerance and finally, physical and psychological dependence. If consumption is interrupted abruptly, a withdrawal syndrome occurs. The Alcohol Withdrawal Syndrome (AWS) is a state of hyperexcitability characterized by anxiety, fear, muscular rigidity and tonic-clonic seizures with epileptiform-type characteristics. The epileptic seizures seen during AWS are often similar to those seen in experimental epilepsy models such as "kindling" or GABA Withdrawal Syndrome (GWS) models. A possible correlation between these models and AWS will allow for a better understanding of the cellular and molecular effects that alcohol exerts on the brain.

Alcohol Withdrawal Delirium↗
PubMedDate not supplied

Motor function in young and aged hemiplegic rats: effects of a Ginkgo biloba extract.

We have previously shown beneficial effects of a Ginkgo biloba extract (EGb761-IPSEN) in accelerating functional recovery from hemiplegia induced by unilateral motor cortex ablation. Here, we report the behavioral and histological effects of various dose regimes of EGb761. In young rats (3 months), 10 mg/kg/day for 7 days produced an improvement in motor performance, relative to untreated controls, on the last day of treatment. Applying a priming (P)-maintenance (M) dose regime (P-7 = 7 days, M-21 = 21 days), a P-7 of 50 (all doses expressed in mg/kg/day) and a M-21 of 10 promoted recovery from the second day after surgery. However, in aged rats (26-28 months old) this treatment ameliorated motor performance only after the 10th day of treatment. A P-7 of 100 or 200 and a M-21 of 50 or 100 produced an acceleration of behavioral recovery in aged animals. Improvement was evident by the fifth day of treatment and was maintained after the treatment regimen. These two groups also demonstrated reduced glial fibrillary acid protein (GFAP) immunostaining and ex vacuo hydrocephalus. Thus, the confirmed efficacy of EGb in hemiplegic rats can be enhanced by an appropriate posology.

Aging↗
PubMedDate not supplied

Electroencephalographic study of the GABA-withdrawal syndrome in rats.

The spatial and temporal EEG features of the epileptogenic syndrome induced by cessation of chronic intracortical GABA infusion in normal rats are described. In the initial stages, the paroxysmal discharges (PDs) induced by withdrawal from unilateral GABA application may appear either unilaterally or bilaterally, although with greater amplitude on the infused side. PDs are transitorily accompanied by behavioral signs of distal myoclonus of the body territory corresponding to the infused area (contralateral hindlimb). Later, the paroxysmal activity becomes more localized, circumscribed to the cannula-infused site and with ipsilateral propagation to anterior cortical areas. The amplitude of PDs decreases progressively while their frequency increases, reaching its maximal value at about 4 h after the first PDs have appeared. In the final stages of the syndrome, which may last several days, clinical manifestations are absent and PDs are activated by slow-wave sleep and reduced during REM sleep and waking. Chronic intracortical applications of taurine failed to induce any electroclinical changes on withdrawal and were unable to inhibit the focus elicited by GABA withdrawal, whereas reinstatement of GABA infusion into the epileptogenic area was effective in blocking the paroxysmal activity. Intracortical infusion of baclofen induced the appearance of an epileptogenic focus that waned on withdrawal. The GABA-withdrawal syndrome appears to be a new model of focal status epilepticus; it may be useful as an experimental model of human partial epilepsy to investigate the role of GABAergic neurotransmission.

Animals↗
PubMedDate not supplied

[Neurosteroids. Neuromodulators of cerebral excitability].

Steroids which are produced by the brain are called neurosteroids, and they are able to modulate neurotransmissions: GABAergic; glutamatergic; glycinergic, and cholinergic (nicotine receptor). These effects are of short latency and duration, and do not implicate the cellular genome. The interaction of these neurosteroids with membrane receptors contribute to the regulation of neuronal excitability, and their study has allowed a better understanding of cognitive, hormonal, and epileptic phenomena as well as the development of new drugs with anxiolytic, antidepressive, anesthetic and anti-epileptic effects.

Adrenal Cortex Hormones↗