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Glutamate release by neurons evokes a purinergic inhibitory mechanism of osmotic glial cell swelling in the rat retina: Activation by neuropeptide Y
Author(s) -
Uckermann Ortrud,
Wolf Antje,
Kutzera Franziska,
Kalisch Folke,
BeckSickinger Annette G.,
Wiedemann Peter,
Reichenbach Andreas,
Bringmann Andreas
Publication year - 2006
Publication title -
journal of neuroscience research
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.72
H-Index - 160
eISSN - 1097-4547
pISSN - 0360-4012
DOI - 10.1002/jnr.20760
Subject(s) - purinergic receptor , glutamate receptor , purinergic signalling , microbiology and biotechnology , metabotropic receptor , metabotropic glutamate receptor , adenosine , neuroglia , retina , biology , chemistry , receptor , neuroscience , adenosine receptor , biochemistry , extracellular , central nervous system , agonist
Glial cell swelling is a central cause of ischemic edema in the brain and retina; however, the regulation of glial cell volume by endogenous factors in situ is largely unknown. In slices of the postischemic retina of the rat, the somata of glial (Müller) cells swell upon hypotonic stress that is not observed in slices of control retinas. We describe an endogenous signaling pathway that leads to inhibition of the osmotic glial cell swelling, and that is evoked by the release of glutamate from retinal neurons upon application of neuropeptide Y. Glutamate activates metabotropic glutamate receptors on swollen glial cells, which evokes a Ca 2+ ‐independent purinergic signaling cascade that involves release of ATP, P2Y 1 receptor activation, and transporter‐mediated release of adenosine. Activation of A1 receptors causes the inhibition of osmotic glial cell swelling, by a protein kinase A‐dependent activation of K + and Cl − channels. It is proposed that the glutamate‐evoked purinergic receptor signaling of glial cells is crucially involved in the cell volume homeostasis of the retina, and that this mechanism may contribute to the protective effect of adenosine in the ischemic tissue. © 2006 Wiley‐Liss, Inc.