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The opposite effect of convulsant drugs on neuronal and endothelial nitric oxide synthase - A possible explanation for the dual proconvulsive/anticonvulsive action of nitric oxide.
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Laboratorio de Bioquímica Farmacológica Departamento de Bioquímica Escuela nacional de Ciencias Biológicas Instituto Politécnico Nacional Carpio y Plan de Ayala S/N, Colonia Casco de Santo Tomás, C.P. 11340 Ciudad de México, México.
Nitric oxide (NO) participates in processes such as endothelium-dependent vasodilation and neurotransmission/neuromodulation. The role of NO in epilepsy is controversial, attributing it to anticonvulsant but also proconvulsant properties. Clarification of this dual effect of NO might lead to the development of new antiepileptic drugs.
View Article and Find Full Text PDFVascular endothelial growth factor up-regulation in the mouse hippocampus and its role in the control of epileptiform activity.
Eur J Neurosci
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Unit of General Physiology, Department of Biology, University of Pisa, via San Zeno 31, 56127 Pisa, Italy.
The vascular endothelial growth factor (VEGF) signalling pathway may represent an endogenous anti-convulsant in the rodent hippocampus although its exact contribution requires some clarification. In mouse hippocampal slices, the potassium channel blocker 4-aminopyridine (4-AP) in the absence of external Mg(2+)(0 Mg(2+)) produces both ictal and interictal activity followed by a prolonged period of repetitive interictal activity. In this model, we demonstrated that exogenous VEGF has clear effects on ictal and interictal activity as it reduces the duration of ictal-like events, but decreases the frequency and intensity of interictal discharges.
View Article and Find Full Text PDFStructural and functional MRI following 4-aminopyridine-induced seizures: a comparative imaging and anatomical study.
Neurobiol Dis
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Section of Anatomy and Histology, Department of Morphological and Biomedical Sciences, Faculty of Medicine, Strada Le Grazie 8, 37134 Verona, Italy.
Structural and functional MRI was used in conjunction with computerized electron microscopy morphometry to study changes 2 h, 24 h and 3 days after 4-aminopyridine-induced seizures lasting 2 h in rats. T2 (relaxation time) values showed changes throughout the cerebral cortex, hippocampus, amygdala and medial thalamus, with a different temporal progression, showing a complete recovery only after 3 days. Two hours after seizures, the apparent diffusion coefficient was decreased throughout the brain compared to control animals, and a further decrease was evident 24 h after seizures.
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