Jong-Seong Park1,2 and Han-Seong Jeong1,2,*
1Chonnam National University Research Institute of Medical
Sciences and 2Department of Physiology,
Chonnam National University Medical School, Kwangju 501-190, Korea
*Corresponding author (affiliation #2).ﾊﾊFAX:+82-62-232-1242
E-mail: hsjeong@chonnam.ac.kr
Abstract: The effects of nitric oxide on the vestibular function
recovery following unilateral labyrinthectomy were studied. Male Sprague-Dawley
rats treated with N-omega-nitro-L-arginine
methyl ester (L-NAME),
a nitric oxide synthase (NOS) inhibitor, were subjected to destruction of
the unilateral vestibular apparatus and spontaneous nystagmus was observed.
To explore the role of nitric oxide on the potassium current, the whole
cell patch clamp technique was applied on isolated medial vestibular nuclear
neurons. The frequency of spontaneous nystagmus that appeared in L-NAME-treated
rats was higher and maintained longer than in control animals. Potassium
currents in the isolated medial vestibular nucleus were inhibited by nitric
oxide liberating agents, sodium nitroprusside and S-nitroso-N-acetylpenicillamine.
After blockade of calcium dependent potassium currents by high EGTA (11ﾊmM)-containing
pipette solution, sodium nitroprusside did not inhibit the outward potassium
currents. 8-Bromoguanosine 3,5-cyclic monophosphate, a membrane-permeable
cGMP analogue, produced similar effects to inhibit the outward potassium
currents as sodium nitroprusside. These results suggest that nitric oxide
production after unilateral labyrinthectomy would help to facilitate vestibular
compensation by inhibiting calcium-dependent potassium currents through
increasing intracellular cyclic GMP, thereby increasing excitability in
ipsilateral vestibular nuclear neurons.
Keywords: Vestibular compensation, Nitric oxide, Potassium current
Copyrightｩ The Japanese Pharmacological Society 2000
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