Neurological Sciences

, Volume 34, Issue 7, pp 1189–1195

A sequential impairment of cortical astrocytes and GABAergic neurons during ischemia is improved by mGluR1,5 activation

Authors

  • Zhan Liu
    • Department of NeurologyThe First Affiliated Hospital in Harbin Medical University
  • Wei Huo
    • Department of NeurologyThe First Affiliated Hospital in Harbin Medical University
  • Wei Sun
    • Department of NeurologyThe First Affiliated Hospital in Harbin Medical University
  • Manhua Lv
    • Department of NeurologyThe First Affiliated Hospital in Harbin Medical University
  • Fang Li
    • Department of NeurologyThe First Affiliated Hospital in Harbin Medical University
    • Department of NeurologyThe First Affiliated Hospital in Harbin Medical University
Original Article

DOI: 10.1007/s10072-012-1220-9

Cite this article as:
Liu, Z., Huo, W., Sun, W. et al. Neurol Sci (2013) 34: 1189. doi:10.1007/s10072-012-1220-9

Abstract

Ischemic brain cell death is presumably caused by excitotoxicity. In addition to an increase of glutamate release during ischemia, the deficiency of astrocytic glutamate-reuptake may cause glutamate accumulation, which results in GABAergic neurons being vulnerable to ischemia. To confirm this hypothesis, we studied the pathophysiological changes of cortical astrocytes and GABAergic neurons during ischemia as well as the prevention of their injuries. Ischemia led to the sequential impairments of astrocytic glutamate-transporter currents and GABAergic neuronal excitability. The changes were partially reversed by 3,5-DHPG, an agonist of type-I/V metabotropic glutamate receptors (mGluR). Thus, mGluR1,5 activation may be useful against the sequential impairment of cortical astrocytes and GABAergic neurons in an early stage of ischemia.

Keywords

IschemiamGluRAstrocyteGABA neuronGlutamate transport and action potential

Supplementary material

10072_2012_1220_MOESM1_ESM.doc (144 kb)
Supplementary material 1 (DOC 144 kb)

Copyright information

© Springer-Verlag Italia 2012