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- Title
Nitric oxide decreases the excitability of interstitial cells of Cajal through activation of the BK channel.
- Authors
Yaohui Zhu; Huizinga, Jan D.
- Abstract
Nitrergic nerves are structurally and functionally associated with ICC. To further understand mechanisms of communication, the hypothesis was investigated that NO might affect large conductance K channels. To that end, we searched for IbTX-sensitive currents in ICC obtained through explant cultures from the mouse small intestine and studied effects of the NOS inhibitor omega N-nitro-L-arginine (LNNA) and the NO donor sodium nitroprusside (SNP). IbTX-sensitive currents acquired in the whole-cell configuration through nystatin perforated patches exhibited high noise levels but relatively low amplitude, whereas currents obtained in the conventional wholecell configuration exhibited less noise and higher amplitudes; depolarization from -80 to + 40 mV evoked 357 ± 159 pA current in the nystatin perforated patch configuration and 1075 ± 597 pA using the conventional whole-cell configuration. Immunohistochemistry showed that ICC associated with ganglia and Auerbach's plexus nerve fibers were immunoreactive to BK antibodies. The IbTX-sensitive currents were increased by SNP and inhibited by LNNA. BK blockers suppressed spontaneous transit outward currents in ICC. After block of BK currents, or before these currents became prominent, calcium currents were activated by depolarization in the same cells. Their peak amplitude occurred at -25 mV and the currents were increased with increasing extracellular calcium and inhibited by cobalt. The hypothesis is warranted that nitrergic innervation inhibits ICC excitability in part through activation of BK channels. In addition, NO is an intracellular regulator of ICC excitability.
- Subjects
NITROGEN oxides; SODIUM nitroferricyanide; IMMUNOHISTOCHEMISTRY; NYSTATIN; IMMUNOGLOBULINS; HYPOTHESIS
- Publication
Journal of Cellular & Molecular Medicine, 2008, Vol 12, Issue 5a, p1718
- ISSN
1582-1838
- Publication type
Article
- DOI
10.1111/j.1582-4934.2008.00217.x