P2X7 receptors exert a permissive role on the activation of release-enhancing presynaptic α7 nicotinic receptors co-existing on rat neocortex glutamatergic terminals

Content Provider	Semantic Scholar
Author	Patti, Laura Raiteri, Luca Grilli, Massimo Parodi, Monica Marchi, Mario
Copyright Year	2006
Abstract	Adenosine triphosphate (ATP) has been reported to enhance the release of glutamate by acting at P2X presynaptic receptors. Acetylcholine (ACh) can elicit glutamate release through presynaptic nicotinic cholinergic receptors (nAChRs) of the alpha7 subtype situated on glutamatergic axon terminals, provided that the terminal membrane is weakly depolarized. Considering that ATP and ACh are co-transmitters, we here investigate on the possibility that P2X and nAChRs co-exist and interact on the same glutamatergic nerve endings using purified rat neocortex synaptosomes in superfusion. ATP evoked Ca(2+)-dependent release of pre-accumulated D-[(3)H]aspartate ([(3)H]D-ASP) as well as of endogenous glutamate; (-)-nicotine, inactive on its own, potentiated the ATP-evoked release. The ATP analogue benzoylbenzoylATP (BzATP) behaved like ATP, but was approximately 30 times more potent; the potentiation of the BzATP-evoked release was blocked by methyllycaconitine or alpha-bungarotoxin. Adding inactive concentrations of (-)-nicotine, epibatidine or choline together with inactive concentrations of BzATP resulted in significant elevation of the [(3)H]D-ASP release mediated by alpha7 nAChRs. To conclude, P2X(7) receptors and alpha7 nAChRs seem to co-exist and interact on rat neocortex glutamatergic terminals; in particular, P2X(7) receptors exert a permissive role on the activation of alpha7 nAChRs, suggesting that ATP may not only evoke glutamate release on its own, but may also regulate the release of the amino acid elicited by ACh.
Starting Page	705
Ending Page	713
Page Count	9
File Format	PDF HTM / HTML
DOI	10.1016/j.neuropharm.2005.11.016
PubMed reference number	16427662
Journal	Medline
Volume Number	50
Alternate Webpage(s)	https://api.elsevier.com/content/article/pii/S0028390805004041
Alternate Webpage(s)	https://www.sciencedirect.com/science/article/pii/S0028390805004041?dgcid=api_sd_search-api-endpoint
Alternate Webpage(s)	https://doi.org/10.1016/j.neuropharm.2005.11.016
Journal	Neuropharmacology
Language	English
Access Restriction	Open
Content Type	Text
Resource Type	Article