Chronic experiments on Krushinskii–Molodkina rats, which have an inborn predisposition to audiogenic convulsions, and Wistar rats, which are resistant to the convulsive actions of sound, recorded electrograms from the somatosensory, auditory, and visual areas of the cortex, the caudate nucleus, the hippocampus, and the mediodorsal nucleus of the thalamus during formation of generalized convulsive status epilepticus (SE) in a lithium-pilocarpine model of epilepsy. SE was found to occur in Krushinskii–Molodkina rats after i.m. administration of pilocarpine at a minimal dose of 15 mg/kg and in Wistar rats after a dose of 25 mg/kg. Six EEG patterns characteristic of sequentially substituting phases in the development of SE are described, from its initiation to its completion. Behavioral signs of convulsions were identified for each phase in the development of SE. The sequence and main EEG characteristics in rats of both strains coincided, as did their behavioral convulsive manifestations, with the exception of the latent period of onset of phase 1: in Krushinskii–Molodkina rats, this was significantly longer than in Wistar rats (12.8 ± 1.1 versus 22.5 ± 0.7 min). Rats with an innate predisposition to audiogenic convulsions thus had greater sensitivity to the effects of pilocarpine.
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