P2X7 pre-synaptic receptors in adult rat cerebrocortical nerve terminals: a role in ATP-induced glutamate release
Article first published online: 28 FEB 2008
© 2008 The Authors. Journal Compilation © 2008 International Society for Neurochemistry
Journal of Neurochemistry
Volume 105, Issue 6, pages 2330–2342, June 2008
How to Cite
Marcoli, M., Cervetto, C., Paluzzi, P., Guarnieri, S., Alloisio, S., Thellung, S., Nobile, M. and Maura, G. (2008), P2X7 pre-synaptic receptors in adult rat cerebrocortical nerve terminals: a role in ATP-induced glutamate release. Journal of Neurochemistry, 105: 2330–2342. doi: 10.1111/j.1471-4159.2008.05322.x
- Issue published online: 28 FEB 2008
- Article first published online: 28 FEB 2008
- Received December 28, 2007; revised manuscript received February 13, 2008; accepted February 19, 2008.
- cerebrocortical synaptosomes;
- glutamate release;
- human embryonic kidney 293 cells;
- P2X7 receptors
Although growing evidence suggests that extracellular ATP might play roles in the control of astrocyte/neuron crosstalk in the CNS by acting on P2X7 receptors, it is still unclear whether neuronal functions can be attributed to P2X7 receptors. In the present paper, we investigate the location, pharmacological profile, and function of P2X7 receptors on cerebrocortical nerve terminals freshly prepared from adult rats, by measuring glutamate release and calcium accumulation. The preparation chosen (purified synaptosomes) ensures negligible contamination of non-neuronal cells and allows exposure of ‘nude’ release-regulating pre-synaptic receptors. To confirm the results obtained, we also carried out specific experiments on human embryonic kidney 293 cells which had been stably transfected with rat P2X7 receptors. Together, our findings suggest that (i) P2X7 receptors are present in a subpopulation of adult rat cerebrocortical nerve terminals; (ii) P2X7 receptors are localized on glutamatergic nerve terminals; (iii) P2X7 receptors play a significant role in ATP-evoked glutamate efflux, which involves Ca2+-dependent vesicular release; and (iv) the P2X7 receptor itself constitutes a significant Ca2+-independent mode of exit for glutamate.