A new neuromodulatory pathway with a glial contribution mediated via A2a adenosine receptors
Article first published online: 23 MAY 2002
Copyright © 2002 Wiley-Liss, Inc.
Volume 39, Issue 2, pages 133–147, August 2002
How to Cite
Nishizaki, T., Nagai, K., Nomura, T., Tada, H., Kanno, T., Tozaki, H., Li, X.X., Kondoh, T., Kodama, N., Takahashi, E., Sakai, N., Tanaka, K. and Saito, N. (2002), A new neuromodulatory pathway with a glial contribution mediated via A2a adenosine receptors. Glia, 39: 133–147. doi: 10.1002/glia.10100
- Issue published online: 23 MAY 2002
- Article first published online: 23 MAY 2002
- Manuscript Accepted: 15 APR 2002
- Manuscript Received: 26 NOV 2001
- Ministry of Education, Science, Sports and Culture (Japan)
- Yamanouchi Foundation for Research on Metabotropic Disorders
- Sankyo Foundation of Life Science
- A2a adenosine receptor;
- glutamate release;
A low concentration (10 nM) of adenosine potentiated hippocampal neuronal activity via A2a adenosine receptors without affecting presynaptic glutamate release or postsynaptic glutamatergic conductance. Adenosine inhibited glutamate uptake through the glial glutamate transporter, GLT-1, via A2a adenosine receptors. In addition, adenosine stimulated GLT-1-independent glutamate release from astrocytes, possibly in response to a rise in intracellular Ca2+, via A2a adenosine receptors involving PKA activation. Those adenosine actions could lead to an increase in synaptic glutamate concentrations responsible for the potentiation of hippocampal neuronal activity. The results of the present study thus represent a novel neuromodulatory pathway with a glial contribution, bearing both inhibition of GLT-1 function and stimulation of glial glutamate release, as mediated via A2a adenosine receptors. GLIA 39:133–147, 2002. © 2002 Wiley-Liss, Inc.