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Regulation of K + channels underlying the slow afterhyperpolarization in enteric afterhyperpolarization‐generating myenteric neurons: Role of calcium and phosphorylation
Author(s) -
Vogalis Fivos,
Harvey John R,
Neylon Craig B,
Furness John B
Publication year - 2002
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.2002.03755.x
Subject(s) - afterhyperpolarization , calcium , chemistry , phosphorylation , microbiology and biotechnology , myenteric plexus , endocrinology , p type calcium channel , neuroscience , biophysics , medicine , biology , voltage dependent calcium channel , biochemistry , t type calcium channel , immunohistochemistry
Summary 1. Myenteric afterhyperpolarization‐generating myenteric (AH) neurons serve as intrinsic primary afferent neurons of the enteric nervous system and generate prolonged or slow afterhyperpolarizing potentials (slow AHP). The slow AHP is generated by an increase in a Ca 2+ ‐activated K + conductance (g K‐Ca ) and is inhibited by enteric neurotransmitters leading to increased excitability. 2. Using cell‐attached patch‐clamp recordings from AH neurons, we have shown that K + channels with an intermediate unitary conductance (IK channels) open following action potential firing. 3. In excised patches from AH neurons, we have identified an IK‐like channel that can be activated by submicromolar levels of cytoplasmic Ca 2+ and is not voltage dependent. 4. Application of the catalytic subunit of cAMP‐dependent protein kinase to the cytoplasmic surface of inside‐out patches inhibits the opening of IK‐like channels previously activated by Ca 2+ . 5. The IK‐like channels are resistant to external tetraethylammonium (5 mmol/L) and apamin (0.3–1 µmol/L), but are inhibited by clotrimazole (10 µmol/L). 6. Our present data support the idea that an increase in the open probability of IK‐like channels in AH neurons following an increase in cytoplasmic [Ca 2+ ] is responsible for the slow AHP and their opening is modulated by kinases.