Nitric oxide regulates spike frequency accommodation in nodose neurons of the rabbit.

University of Maryland, Baltimore, Baltimore, Maryland, United States
Neuroscience Letters (Impact Factor: 2.06). 06/1994; 173(1-2):17-20. DOI: 10.1016/0304-3940(94)90140-6
Source: PubMed

ABSTRACT A Ca(2+)-dependent slow spike after hyperpolarization (AHPslow) is present in about 35% of the neurons in the nodose ganglion. Although the AHPslow profoundly affects spike frequency accommodation of these neurons, the mechanisms that control the generation and the duration of the AHPslow are unclarified. N omega-Nitro-L-arginine methyl ester (L-NAME; 10 microM), a specific inhibitor of nitric oxide synthase (NOS), reduced the AHPslow by more than 92%. The L-NAME block of the AHPslow was antagonized by application of 50 microM S-nitroso-N-acetylpenicillamine (SNAP), a nitric oxide donor. The fast, Ca(2+)-dependent, spike after hyperpolarization preceding the AHPslow and the elevation of intracellular Ca2+ accompanying the AHPslow were unaffected by L-NAME treatment. These findings indicate that products of NOS activity might directly or indirectly activate the AHPslow K+ channels at a step beyond Ca2+ influx or intracellular Ca2+ mobilization.

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Available from: Akiva Cohen, Apr 16, 2015
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    ABSTRACT: 1. Standard intracellular recording techniques with 'sharp' micropipettes were used to evoke action potentials (APs) in acutely dissociated adult nodose neurones. 2. APs induced a transient increase in [Ca2+]i (a calcium transient), recorded with fura-2, that was dependent upon [Ca2+]o and the number of APs. Over the range of one to sixty-five APs, the relation between the amplitude of the calcium transient and the number of APs was well fitted by a rectangular hyperbola (chi 2 = 3.53, r = 0.968). From one to four APs, the calcium transient-AP relation can be described by a line with a slope of 9.6 nM AP-1 (r = 0.999). 3. Charge movement corresponding to Ca2+ influx evoked by a single AP was 39 +/- 2.8 pC (mean +/- S.E.M.) and did not change significantly during trains of one to thirty-one APs (P < 0.05). 4. Caffeine (10 mM), a known agonist of the ryanodine receptor, produced an increase in [Ca2+]i. The caffeine-induced rise in [Ca2+]i was attenuated (by > 90%) by lowering [Ca2+]o, and by ryanodine (10 microM), 2,5-di(t-butyl)hydroquinone (DBHQ, 10 microM), or thapsigargin (100 nM). 5. Neurones incubated with ryanodine, DBHQ or thapsigargin required at least eight APs to evoke a detectable calcium transient. These reagents did not significantly affect Ca2+ influx (P < 0.05). In the presence of these inhibitors, the calcium transient-AP relation exhibited slopes of 1.2, 1.1 and 1.9 nM AP-1 for ryanodine, DBHQ and thapsigargin, respectively. When compared with the slope of 9.6 nM AP-1 in non-treated neurones, it appears that Ca2+ influx produced by a single AP is amplified by ca 5- to 10-fold.
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