Studies in Wistar rats in conditions of free behavior showed that low-frequency stimulation of the paleocerebellar cortex (nodulus, uvula) (10-12 Hz, 0.5 msec) was accompanied by activation of spike discharges induced by systematic application of benzylpenicillin sodium (3,000,000 IU/kg). Facilitation of the formation of ictal discharges was also seen. High-frequency electrical stimulation (100-300 Hz, 0.25 msec) of the same structure was accompanied by suppression of the generation of spike potentials and prevented the development of ictal potentials. The antiepileptic effect of electrical stimulation was seen in conditions of relatively low levels of convulsive activity. Electrical stimulation decreased the frequency and amplitude of spike potentials in the interstimulus intervals and decreased the total duration of epileptic foci. Repeated electrical stimulation of the paleocerebellum after electrocoagulation did not produce any changes in convulsive activity.
Acute experiments on rats showed that the ED100 of NMDA for induction of clonic convulsions was 0.53 microgram, while the ED100 of NMDA for inducing tonic extension of the forelimbs was 5.02 micrograms/animal. Determination of these parameters after administration of delta-sleep-inducing peptide (100 micrograms/kg, i.p.) revealed 2.3- and 4.46-fold increases. These results provide evidence for a neuroprotective role of delta-sleep-inducing peptide in relation to excitatory amino acid receptor agonists.
Data are presented in this paper on the influence of the delta-sleep-inducing peptide (DSIP) on various forms of convulsive activity. The capacity of this peptide to suppress convulsive activity in foci created in the cerebral cortex by the application of strychnine has been demonstrated in experiments on cats. It has been established in experiments on rats that DSIP determines the later development of the convulsive kindling syndrome, and prevents the development of convulsions in mice induced by bicuculline, picrotoxin, and corazol, but is devoid of such action in relation to thiosemicarbazide and strychnine. It was demonstrated that the anticonvulsant action of DSIP is associated with its influence on the reticular portion of the substantia nigra. The lowest level of this peptide itself has been discovered, in the reticular portion of the substantia nigra at the late stages of pharmacological kindling. It is inferred that DSIP may represent one of the factors of the endogenous control of the excitability of the brain.
In 1.5 months after modeling of streptozotocin-induced diabetes mellitus, superoxide dismutase and catalase activities decreased by 40.7 and 32.0%, respectively, in comparison with the corresponding values in Wistar rats without diabetes. Electric stimulations (100 Hz, 0.25 msec, 50-100 μA, 2.5 sec) of the paleocerebellar cortex (V-VII lobules) were conducted 3 times a day over 1 month. These stimulations prevented the decrease in antioxidant enzyme activity in rats with experimental diabetes.
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