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|Title:||Metabotropic glutamate receptors modulate [3H]acetylcholine release from cultured amacrine-like neurons||Authors:||Caramelo, Olga L.
Santos, Paulo F.
Carvalho, Arsélio P.
Duarte, Carlos B.
|Issue Date:||1999||Citation:||Journal of Neuroscience Research. 58:4 (1999) 505-514||Abstract:||Retinal amacrine cells express metabotropic glutamate receptors (mGluRs), but their physiological role is unknown. We investigated the effect of mGluR on [3H]acetylcholine release ([3H]ACh) from cultured chick amacrine-like neurons. Activation of group III mGluR with the agonist L(+)-2-amino-4-phosphonobutyric acid (L-AP4) inhibited [3H]ACh release evoked by 25 mM KCl in a dose-dependent manner, and this effect was sensitive to pertussis toxin. In contrast, activation of group I or II mGluR with (S)-3,5-dihydroxyphenylglycine (DHPG) and (2S,2primeR,3primeR)-2-(2prime,3prime-dicarboxycyclopropyl)glycine (DCG-IV), respectively, did not affect significantly [3H]ACh release. The effect of L-AP4 on [3H]ACh release was sensitive to nitrendipine, suggesting that it is, at least in part, due to inhibition of L-type Ca2+ channels. Activation of group III mGluR also partly inhibited ω-conotoxin GVIA-sensitive Ca2+ channels, coupled to [3H]ACh release. The L-AP4 did not affect the cAMP levels measured in amacrine-like neurons depolarized with 25 mM KCl or stimulated with forskolin, indicating that the effect of group III mGluR on [3H]ACh release is not due to inhibition of adenylyl cyclase activity. Inhibition of protein kinase A with KT-5720 was without effect on [3H]ACh release evoked by 25 mM KCl, further indicating that the effect of group III mGluR on [3H]ACh release cannot be attributed to the inhibition of the kinase. The effect of L-AP4 on [3H]ACh release was reversed by DHPG or by DCG-IV, and activation of group II mGluR also partially inhibited cAMP production stimulated by forskolin. Taken together, our results show that the effect of group III mGluR on [3H]ACh release may be due to a direct inhibition of L- and N-type Ca2+ channels and is modulated by group I and group II mGluR. J. Neurosci. Res. 58:505-514, 1999. © 1999 Wiley-Liss, Inc.||URI:||http://hdl.handle.net/10316/8329||DOI:||10.1002/(SICI)1097-4547(19991115)58:4<505::AID-JNR4>3.0.CO;2-J||Rights:||openAccess|
|Appears in Collections:||FCTUC Ciências da Vida - Artigos em Revistas Internacionais|
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