Expressão imunohistoquimica da isoforma neuronal da sintase do oxido nitrico no neocortex cerebral humano normal e em displasias corticais

AUTOR(ES)

Cesar Augusto Bueno Zanella

DATA DE PUBLICAÇÃO

2002

RESUMO

Nitric oxide (NO) is a diffusible and reactive molecular messenger in the nervous, vascular and immune systems. NO is not stored, but rather synthesized on demand from the amino acid L-arginine by a family of isoenzymes, the nitric oxide synthases (NOS). NO is a mediator of many physiological roles. In the brain, NO acts as a neurotransmitter/neuromodulator and regulate many cerebral functions. NO also plays patophysiological roles such as in epilepsy and some neurodegenerative diseases. The heading of cortical dysplasia groups heterogenous disorders of development often associated with epilepsy. Some neocortical dysplasias are considered disorders of neuronal migration, which have variously been classified regarding their morfology or putative etiology. We describe here cytoarchitetonic alterations in displatic tissue from patients affected by pharmacologically resistant epilepsy, which were obtained at surgery for epilepsy. This study shows the distribution of nNOS immunoreactivity-like structures in displastic and normal neocortex. Normal cortex was obtained from patients without history of neurologic disease and evidence of neuropathologic changes. In the displastic cortex, cortical laminar disorganization was found in all cases. The strongest nNOS immunoreactivity was detected in the cytoplasm and nucleus of neurons in the deepest cortical layers and in the white matter. The normal cortex showed nNOS immunoreactivity predominantly in neurons of layers III e V. Varicose fibers were detected throughout both the normal and displastic cortex. Assuming that the nNOS immunoreactivity in the deepest cortical neurons of displastic neocortex corresponds to a catalytically active form of the enzyme, we suggest that the release of NO by them might additively activate target neurons, possibly via soluble guanylate cyclase, thereby leading to their hypersynchronization, and eventually triggering an epileptic discharge

ASSUNTO(S)

oxido nitrico cerebro

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