Fig. 3.

Various receptor antagonists and calcium channel blockers fail to prevent hydroxylamine-induced membrane depolarization of striatal cholinergic interneurons. A, The membrane depolarization produced by 100 μm hydroxylamine (a) was not altered in the presence of 30 μm MK-801 and 10 μm CNQX (7 min) to block both NMDA and non-NMDA glutamate receptors (b). Resting membrane potential was −58 mV. B, Application of the DA D1 receptor antagonist SCH 23390 (10 μm, 7 min) (a) failed to affect the membrane response produced in control medium by 100 μm hydroxylamine (b). Resting membrane potential was −58 mV.C, Summary of pharmacological experiments on 100 μm hydroxylamine-induced membrane depolarization of striatal cholinergic interneurons. Cocktail solution contained: ω-conotoxin GVIA, nifedipine, ω-agatoxin TK, MCPG, and [d--Arg¹,d--Pro²,d--Trp^7,9,Leu¹¹]-SP. Concentrations were: MK-801 30 μm, CNQX 10 μm, SCH 23390 10 μm, TTX 1 μm, ω-conotoxin GVIA 1 μm, nifedipine 20 μm, ω-agatoxin TK 20 nm, MCPG 300 μm, and [d--Arg¹,d--Pro²,d--Trp^7,9,Leu¹¹]-SP 10 μm.