ArticleThe Journal of physiology1998
Apamin- and nitric oxide-sensitive biphasic non-adrenergic non-cholinergic inhibitory junction potentials in the rat anococcygeus muscle.
Article in The Journal of physiology, 1998. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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1 citing paper in PubMed, 8 citations in OpenAlex.
- A KBiomolecules · 2026Article
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3 authors at 1 institution in 1 country.
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Abstract
1. Changes in membrane potential following electrical field stimulation (EFS; 1, 2 and 5 pulses at 5 Hz, 0.5 ms duration, 60-80 V) of non-adrenergic non-cholinergic (NANC) inhibitory nerves in the rat isolated anococcygeus muscle were measured using standard intracellular recording techniques. Resting membrane potential ranged between -60 and -70 mV. 2. In the presence of guanethidine (30 microM), atropine (1 microM), propranolol (1 microM) and phentolamine (0.05 microM) to establish NANC conditions, the membrane potential depolarized to between -40 and -50 mV. Under these conditions, EFS caused pulse-dependent, tetrodotoxin (1 microM)-sensitive biphasic inhibitory junction potentials (IJPs) comprising a fast onset and time-to-peak phase followed by a second, slower phase that delayed repolarization. The duration of NANC IJPs ranged between 10 and 20 s. 3. Inhibition of small-conductance Ca2+-activated K+ channels with apamin (0.1 microM) selectively blocked the first fast phase of the NANC IJP, whereas inhibitors of large-conductance Ca2+-activated K+ channels (charybdotoxin and iberiotoxin) and ATP-sensitive K+ channels (glibenclamide) all had no effect on NANC IJPs. 4. Both the nitric oxide synthase inhibitor N G-nitro-L-arginine (L-NOARG; 100 microM) and the inhibitor of soluble guanylate cyclase 1-H-oxodiazol-[1,2,4]-[4,3-a] quinoxaline-1-one (ODQ; 10 microM) had no effect on the first fast phase of the NANC IJP. Each treatment, however, markedly inhibited the slow phase with the duration of the IJP reduced to between 1 and 3 s. The L-NOARG-resistant fast phase of the NANC IJP was almost abolished by the subsequent addition of apamin (0.1 microM). 5. In conclusion, the present study demonstrates unequivocal NANC nerve-mediated biphasic IJPs in the rat isolated anococcygeus. We propose that nitric oxide (NO), via activation of cGMP-dependent K+ channels, and a non-NO inhibitory factor which activates apamin-sensitive K+ channels contribute to NANC nerve-evoked IJPs in the rat anococcygeus.
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