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This Article Full Text Full Text (PDF) All Versions of this Article: 580/1/103    most recent jphysiol.2006.125724v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Momiyama, T. Articles by Fukazawa, Y. Search for Related Content PubMed PubMed Citation Articles by Momiyama, T. Articles by Fukazawa, Y. Related Collections Neuroscience

¹ Division of Cerebral Structure, National Institute for Physiological Sciences, Okazaki 444-8787, Japan
² Core Research for Evolutional Science and Technology (CREST), Japan Science and Technology Corporation, Kawaguchi, Japan

Whole-cell patch-clamp recordings of non-NMDA glutamatergic EPSCs were made from identified cholinergic neurones in slices of basal forebrain (BF) of young rats (P13–P18), to investigate the subtypes of calcium channels involved in dopamine D₁-like receptor-mediated presynaptic inhibition of the EPSCs. The BF cholinergic neurones were pre-labelled by intracerebroventricular injection of a fluorescent marker, Cy3-192IgG. A D₁-like receptor agonist, SKF 81297 (30 µM) suppressed the EPSCs reversibly by about 30%, and this inhibition was reproducible. Calcium channel subtypes involved in the glutamatergic transmission were elucidated using selective Ca²⁺ channel blockers. The N-type Ca²⁺ channel blocker -conotoxin (-CgTX, 3 µM) suppressed the EPSCs by 57.5%, whereas the P/Q-type channel selective blocker -agatoxin-TK (-Aga-TK, 200 nM) suppressed the EPSCs by 68.9%. Simultaneous application of both blockers suppressed the EPSCs by 96.1%. The R-type Ca²⁺ channel blocker SNX-482 (300 nM) suppressed the EPSCs by 18.4%, whereas nifedipine, the L-type Ca²⁺ channel blocker (10 µM), had little effect. In the presence of -Aga-TK, SKF 81297, a dopamine D₁-like receptor agonist, had no effect on the EPSCs. On the other hand, SKF 81297 could still inhibit the EPSCs in the presence of either -CgTX, SNX-482 or nifedipine. SKF 81297 had no further effect on the EPSCs when external Ca²⁺ concentration was raised to 7.2 mM in the presence of -Aga-TK, but could still inhibit the EPSCs in high Ca²⁺ solution after -CgTX application. Forskolin (FK, 10 µM), an activator of adenylyl cyclase pathway, suppressed the EPSCs, and the FK-induced effect was mostly blocked in the presence of -Aga-TK but not that of -CgTX. These results suggest that D₁-like receptor activation selectively blocks P/Q-type calcium channels to reduce glutamate release onto BF cholinergic neurones.

(Received 28 November 2006; accepted after revision 11 January 2007; first published online 18 January 2007)
Corresponding author T. Momiyama: Division of Cerebral Structure, National Institute for Physiological Sciences, Okazaki 444-8787, Japan. Email: tmomi{at}nips.ac.jp

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