Mechanism of intercellular cornrnunication inhibition after induction of nitric oxide synthase in astrocytes during development
Abstract
Normal brain development requires an active metabolic cooperation among glial
cells through intercellular communications. This communication is regulated by different
factors, such as nitric oxide (-NO) synthase (NOS) activity, which inhibits gap junction
permeability in rat neonatal astrocytes. Since this effect is accompanied by a mitochondrial
dysfunction, we have proposed the possibility that both phenomena are related. Thus,
antimycin-mediated energy deficiency in rat neonatal astrocytes inhibits gap junction
permeability. This effect is reversible and caIcium-dependent. The energy deficiencymediated
inhibition of intercellular communication after -NO synthesis induction in
glial cells may help to clarify the mechanisms causing brain damage by perinatal
hypoxia, and also to the knowledge of the brain pathophysiological development.
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