Tyrosine kinase signaling involved in glutamate-induced astrocyte proliferation

Neuroreport. 2001 Nov 16;12(16):3519-22. doi: 10.1097/00001756-200111160-00029.

Abstract

Proliferation of astrocytes is a common response of the CNS to injury and disease. The mechanisms controlling the proliferation of astrocytes are of great interest. In this paper, the signaling pathways underlying glutamate-induced astrocyte proliferation are investigated. Glutamate stimulates the proliferation of non-synchronized, subconfluent cultures of rat cortical astrocytes. Glutamate-induced cell proliferation is not prevented by inhibitors of G protein, protein kinase A, protein kinase C, phosphatidylinositol 3 kinase, extracellular signal-regulated kinase, or phospholipase A2. However, the tyrosine kinase inhibitors Genistein and Herbimycin A inhibit the glutamate-induced proliferation. Moreover, this proliferation is mediated by the activation of glutamate metabotropic receptors. These results suggest that glutamate induces astrocyte proliferation through a tyrosine kinase pathway.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Astrocytes / cytology
  • Astrocytes / drug effects*
  • Astrocytes / enzymology*
  • Cell Division / drug effects
  • Cell Division / physiology
  • Cells, Cultured
  • Cerebral Cortex / cytology
  • Cerebral Cortex / drug effects
  • Cerebral Cortex / enzymology
  • Glutamic Acid / pharmacology*
  • Protein-Tyrosine Kinases / physiology*
  • Rats
  • Rats, Sprague-Dawley
  • Signal Transduction / drug effects
  • Signal Transduction / physiology*

Substances

  • Glutamic Acid
  • Protein-Tyrosine Kinases