Presented at the Australian Neuroscience Society Symposium on K Channels, Sydney, February 2002. The papers in these proceedings have been peer reviewed.
Regulation of K+ channels underlying the slow afterhyperpolarization in enteric afterhyperpolarization-generating myenteric neurons: Role of calcium and phosphorylation
Article first published online: 5 SEP 2002
Clinical and Experimental Pharmacology and Physiology
Volume 29, Issue 10, pages 935–943, October 2002
How to Cite
Vogalis, F., Harvey, J. R., Neylon, C. B. and Furness, J. B. (2002), Regulation of K+ channels underlying the slow afterhyperpolarization in enteric afterhyperpolarization-generating myenteric neurons: Role of calcium and phosphorylation. Clinical and Experimental Pharmacology and Physiology, 29: 935–943. doi: 10.1046/j.1440-1681.2002.03755.x
- Issue published online: 5 SEP 2002
- Article first published online: 5 SEP 2002
- Received 25 April 2002; accepted 29 April 2002.
- Ca2+-activated K+ channels;
- intermediate conductance;
- myenteric plexus;
- sensory neurons
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 Ca2+-activated K+ conductance (gK-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 Ca2+ 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 Ca2+.
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 [Ca2+] is responsible for the slow AHP and their opening is modulated by kinases.