Mechanism of intercellular cornrnunication inhibition after induction of nitric oxide synthase in astrocytes during development

Authors

  • J. P. Bolaños
  • B. VERA
  • L. SÁNCHEz-ABARCA

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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Published

1996-12-20

How to Cite

1.
Bolaños JP, VERA B, SÁNCHEz-ABARCA L. Mechanism of intercellular cornrnunication inhibition after induction of nitric oxide synthase in astrocytes during development. Ars Pharm [Internet]. 1996 Dec. 20 [cited 2025 Jul. 28];37(4):971-9. Available from: https://revistaseug.ugr.es/index.php/ars/article/view/21764

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Special Articles