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Chonnam Med J. 2000 Jun;36(2):129-138. Korean. Original Article.
Jeong HS , Lee GO , Kim JH , Heo T , Moon JY , Park JS .
Department of Physiology, Chonnam National University Medical School, Kwangju, Korea.
Department of Pharmacology, Chonnam National University Medical School, Kwangju, Korea.
Department of Emergency Medicine, Chonnam National University Medical School, Kwangju, Korea.
Abstract

The effect of the nitrix oxide (NO) pathway on voltage-dependent potassium currents in rat vestibular nuclear neurons was investigated by using the whole cell patch clamp technique. When cells were held at -70 mV and depolarized from -60 mV to + 40 mV in 10 mV increments, sustained outward potassium currents were evoked. The outward potassium currents were decreased by the addition of 10 microM sodium nitroprusside (SNP). And 1 mM 8-bromoguanosine 3',5'-cyclic monophosphate (8-Br-cGMP) produced a similar effects to those of 10 microM SNP. High EGTA containing pipette solution (11 mM) reduced the control currents and inhibited SNP induced outward potassium currents reduction. 1H-[1,2,4]oxadiazolo[4,3-a]quinozalin-1-one (ODQ), a specific inhibitor of soluble guanylyl cyclase, significantly blocked SNP induced reduction. These results suggest that nitric oxide blocks Ca2+-activated K+ channels in the medial vestibular nuclear neuron by activating guanylyl cyclase.

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