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INTRODUCTION: Identification of the interaction between excitatory foci and their complexes in the cortex is important for understanding functional organization of the regions they arise from and help learn the pathophysiological mechanisms of various CNS pathologies development. AIM(S): We aimed to identify the types and mechanisms of interactions between excitatory foci with variable intensity and their complexes in the neocortex. METHOD(S): We used adult male cats and rats for applications of strychnine, penicillin, and acetylcholine with proserin to produce excitatory foci. In this experiment, we used different drug concentrations and application zones in the neocortex. RESULTS: We established two main types of interactions: the determinant and the dominant. A focus of more powerful excitation may enhance and synchronize the activity in the weaker foci, integrate them in a single functional complex and define the pattern of its activity (determinant relations). Phenobarbital or surgical excision of the neocortical region with hyperactive foci can suppress determinant foci and destroy the complex. The hyperactive focus may also suppress the activity of previously created foci (dominant relationships). We observed the latter form of interaction in either transitional stage during complex formation or it had an independent meaning. The interaction between foci did not depend on their neurochemical background and localization in the cortex. In cortex isolé and preparations with mesencephalic sections of the stem, a more rapid formation of functional complexes occurred underthe effect of the determinant complex. CONCLUSIONS: These findings demonstrate two types of functional interaction both between separate foci and between their complexes. Complete elimination of the afferent and thalamic-cortical interactions does not hinder hypersynchronization of cortical neuronal elements or formation of functional complexes and generalization of seizure activity over the cortex.
The cerebellum is a potent anti‑epileptic target for deep brain stimulation in patients with drug‑resistant epilepsy. The effects of such stimulation, however, may also favor seizure activity. Our goal was to investigate the effect of cerebellar electrical stimulation (ES) alone and in combination with the anti‑epileptic drug diazepam (DIA) on seizure outcome. We used a rat model of pentylenetetrazol kindling, which is characterized by seizures followed by deteriorations in central benzodiazepine‑GABAA (BDZ‑GABAA) receptors. We tested the effects of ES alone and in combination with DIA (0.1 and 1.0 mg/kg) on seizures. Our data demonstrated: 20 ES trials can prevent the recurrence of clonic‑tonic kindled seizures, administration of either DIA‑0.1 or ES (5 trials) alone is ineffective on seizures, and combining DIA‑0.1 and 5 ES or DIA‑1.0 and 5 ES caused an additive effect, prolonged the latency to seizure onset, and prevented recurrence of clonic‑tonic seizures. We also observed that ES alone produced either facilitation or inhibition of seizures on EEG. In contrast, the same ES inhibited EEG seizures when delivered after a combination of DIA‑1.0 and 5 ES and ultimately prevented the facilitation of the discharges. Lastly, we demonstrated that seizure suppression is intensified when cortical ES is performed after DIA administration. Our data supported the hypothesis that both BDZ‑GABAA receptor activity along with cerebellar output comprise the potential mechanisms underlying the peculiar effects of deep brain stimulation in the cerebellum on seizures.
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