Journal
NEUROSCIENCE RESEARCH
Volume 47, Issue 2, Pages 225-232Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/S0168-0102(03)00201-3
Keywords
Ca2+-activated non-selective cation current (I-CAN); calmodulin; CaMKII; fulfenamic acid; slice; rat
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It is well known that midbrain dopamine (DA) neurons receive massive projection from cholinergic neurons in the brainstem. In our preceding report, we showed that Ca2+-influx through nicotinic acetylcholine (ACh) receptors in the DA neurons subsequently activated an inward current that was sensitive to fulfenamic acid (FFA) and phenytoin, presumably a Ca2+-activated non-selective cation current. The FFA-sensitive current exhibited a negative slope conductance and predominantly enhanced the depolarizing responses of DA neurons. In this study, we showed that the inward FFA-sensitive current was eliminated by antagonists of Ca2+/calmodulin (Ca2+/CaM), N-(6-aminobexyl)-5-chloro-1-naphthalene-sulfonamide hydrochloride (W-7; 1 muM), trifluoperazine (TFP; 1.5 muM) and calmidazolium (100 nM). Application of W-7 and TFP reduced the ACh-induced inward current and the current component suppressed by these drugs exhibited negative slope conductance, as well as the FFA-sensitive current. Further, intracellular application of KN-93, an antagonist of Ca2+/CaM-dependent protein kinase II (CaMKII), but not KN-92 eliminated the FFA-sensitive current. All these results suggest that Ca2+/CaM-CaMKII pathway is involved in an activation of the FFA-sensitive current. (C) 2003 Elsevier Ireland Ltd and the Japan Neuroscience Society. All rights reserved.
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