ArticleAmerican journal of physiology. Gastrointestinal and liver physiology2012
CaMKII inhibition hyperpolarizes membrane and blocks nitrergic IJP by closing a Cl(-) conductance in intestinal smooth muscle.
Article in American journal of physiology. Gastrointestinal and liver physiology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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8 citing papers in PubMed, 9 citations in OpenAlex.
- Calmodulin-Dependent Regulation of Overexpressed but Not Endogenous TMEM16A Expressed in Airway Epithelial Cells.Membranes · 2021Article
- Relaxin influences ileal muscular activity through a dual signaling pathway in mice.World journal of gastroenterology · 2018Article
- Orai1 and TRPC1 Proteins Co-localize with CaV1.2 Channels to Form a Signal Complex in Vascular Smooth Muscle Cells.The Journal of biological chemistry · 2016Article
- Vascular CaMKII: heart and brain in your arteries.American journal of physiology. Cell physiology · 2016Review
- CrossTalk opposing view: Interstitial cells are not involved and physiologically important in neuromuscular transmission in the gut.The Journal of physiology · 2016Article
- Rebuttal from Raj K Goyal.The Journal of physiology · 2016Article
- Depolarization-induced depression of inhibitory transmission in cerebellar Purkinje cells.Physiological reports · 2013Article
- Structure activity relationship of synaptic and junctional neurotransmission.Autonomic neuroscience : basic & clinical · 2013Review
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2 authors at 2 institutions in 1 country.
Funding
Abstract
The ionic basis of nitrergic "slow'" inhibitory junction potential (sIJP) is not fully understood. The purpose of the present study was to determine the nature and the role of calmodulin-dependent protein kinase II (CaMKII)-dependent ion conductance in nitrergic neurotransmission at the intestinal smooth muscle neuromuscular junction. Studies were performed in guinea pig ileum. The modified Tomita bath technique was used to induce passive hyperpolarizing electrotonic potentials (ETP) and membrane potential change due to sIJP or drug treatment in the same cell. Changes in membrane potential and ETP were recorded in the same smooth muscle cell, using sharp microelectrode. Nitrergic IJP was elicited by electrical field stimulation in nonadrenergic, noncholinergic conditions and chemical block of purinergic IJP. Modification of ETP during hyperpolarization reflected active conductance change in the smooth muscle. Nitrergic IJP was associated with decreased membrane conductance. The CAMKII inhibitor KN93 but not KN92, the Cl(-) channel blocker niflumic acid (NFA), and the K(ATP)-channel opener cromakalim hyperpolarized the membrane. However, KN93 and NFA were associated with decreased and cromakalim was associated with increased membrane conductance. After maximal NFA-induced hyperpolarization, hyperpolarization associated with KN93 or sIJP was not seen, suggesting a saturation block of the Cl(-) channel signaling. These studies suggest that inhibition of CaMKII-dependent Cl(-) conductance mediates nitrergic sIJP by causing maximal closure of the Cl(-) conductance.
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