We previously reported that both nerve-released and exogenously applied norepinephrine (NE) elicits a depolarization in cochlear vascular muscle cells that is perhaps mediated partially by a novel but poorly defined γ-adrenoceptor, in addition to the partial mediation by α-adrenoceptors [Jiang,SFN Abstr. 2000]. It is known that chloride currents contribute to NE-induced vasocontraction. Our further intracellular recording study found that: 1) in the presence of α1 & α2 adrenergic antagonists (1 μM prazosin & idazoxan), the residual NE-depolarization was not affected by diphenhydramine, ritanserin or haloperidol (antagonists for H1, 5-HT2 and D2,3,4 receptors, respectively); 2) the depolarization was significantly inhibited by the chloride channel blocker niflumic acid (NFA,0.01-1 mM), IAA-94 (10 μM) or DIDS (0.1-1 mM); 3) the depolarization was enhanced by low extracellular Cl- (60 mM, which shifted ECl from ~-25 to ~0 mV); 4) in the presence of α1 & α2 antagonists plus a P2X antagonist (PPADS,10 μM), the ...