[Experimental comparative study of the acute toxicity of quinidine in normal and digitalized guinea pigs].
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Biomedical subjects
Publications and source records attributed to M Lamarche.
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In slices of rat sensorimotor cortex, extracellular field potentials evoked by electrical stimulation of the white matter were recorded at various cortical depths. In order to determine the nature of the various components, experiments were performed in 3 situations: in a control perfusion medium, in a solution in which calcium ions had been replaced by magnesium ions to block synaptic transmission, and in cortices in which the pyramidal neurons of layer V had been previously induced to degenerate. In the control situation, the response at or near the surface was a positive-negative wave. From a depth of about 150 microns downwards, the evoked response consisted usually of 6 successive components, 3 positive-going, P1, P3 and P6 and 3 negative-going, N2, N4 and N5. P1 and N4 were apparent in superficial layers only. The amplitude of the remaining waves was variable in the cortex but all diminished near the white matter. The early part of the surface positive wave arises from a non-synaptic activation of superficial elements, probably apical dendrites. The late part of the surface positive wave and the negative wave are due to the synaptic activation of neurons located probably in layer III. The large negative wave N2 represents principally the antidromic activation of cell bodies and possibly of proximal dendrites of neurons situated in layers III, IV and V, though the compound action potentials of afferent and efferent fibers may contribute to a reduced part to its generation. The late components N4 to P6 are post-synaptic responses. The negative component N5, the amplitude of which is largest in layers III and IV, represents excitatory responses of neurons located at various depths in the cortex. The nature of the positive component P6 is less clear, although the underlying mechanism might be inhibitory synaptic potentials.
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Several observations in Man as well as in animals have stressed the importance of specific afferents in triggering some focal cortical fits. The authors report an analysis of the role of various afferents on the activity of a precentral focus in the monkey. The chronic focus was created on one adult female monkey by subpial injection of alumina cream in the motor area of the left foot. Typical seizures were clonic and local. The most striking feature was that movement or, more generally, proprioceptive afferents from the concerned leg could elicit and maintain these motor fits. This assumption was verified by curaryzing the animal with succinyl-choline. In this condition, the number of attacks was strongly reduced. Since there was no lowering of excitability at the central level, as shown by direct stimulation of the perifocal area, this decrease seems to result from the lack of triggering mechanisms. If this is the case, one should be able to elicit seizures by proprioceptive afferent volleys coming from the concerned leg. In fact, although passive motion was not very effective (the reason probably being the decrease of the back-ground activity of stretch receptors under curare), direct electrical intramuscular stimulation was always followed by an attack. Similar stimulation of the opposite leg was ineffective. These results are discussed. The role of the "motor cortex proprioceptive feedback" in jacksonian progression of motor seizures is debated. The same concept is applied to "startle epilepsy", for which a physiological hypothesis is purposed.