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Post-junctional Regulation Of Sensitivity To Cholinergic Motor Neurotransmission In The Murine Gastric Fundus | 25208
Journal of Gastrointestinal & Digestive System
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Increasing the Ca2+ concentration [Ca2+]i initiates smooth muscle contraction. A given increase in [Ca2+]i can yield more
or less contractile force by increasing the myofilament sensitivity to Ca2+ through the regulation of MYPT1 and CPI-17
phosphorylation, which results in inhibition of myosin light chain phosphatase (MLCP) activity. Ca2+ sensitization of smooth
muscle contraction has typically been studied by bath application of contractile agonists to smooth muscles. Stimulating
gastrointestinal (GI) smooth muscles by bath applied agonists may not be equivalent to neurotransmitter release because
these different modes of stimulation may activate different post-junctional receptors. It was found that bath applied carbachol
activates different Ca2+ sensitization mechanisms in gastric fundus smooth muscles than cholinergic neurotransmission.
Carbachol increased both CPI-17 and MYPT1 phosphorylation, while cholinergic neurotransmission only increased CPI-
17 phosphorylation. In the presence of the cholinesterase inhibitor neostigmine, cholinergic neurotransmission increased
both CPI-17 and MYPT1 phosphorylation. In gastric fundus muscles of W/Wv mice, which lack intramuscular interstitial
cells of Cajal (ICC-IM), cholinergic neurotransmission alone increased both CPI-17 and MYPT1 phosphorylation. Inhibiting
Rho kinase (ROCK) or protein kinase C (PKC) blocked the increases in MYPT1 and CPI-17 phosphorylation, respectively.
These findings suggest that cholinergic neurotransmission only activates PKC-dependent CPI-17 phosphorylation, while bathapplied
carbachol recruits ROCK-dependent MYPT1 phosphorylation due to exposure of the agonist to a wider population of
muscarinic receptors. These are the first findings demonstrating that bath applied carbachol and cholinergic neurotransmission
elicit different biochemical responses in GI smooth muscles and that ICC-IM and transmitter metabolism restrict the volume
of influence of enteric motor neurotransmitters.
Brian Perrino received his PhD at the age of 30 years from Boston University School of Medicine and performed his postdoctoral studies at the Vollum Institute,
Oregon Health Sciences University. He is a project leader in the Smooth Plasticity COBRE grant, and Co-Investigator on 3 NIH R01 grants. He has published
more than 40 papers in peer-reviewed journals, has been invited several times to be a seminar speaker, has presented findings at many national and international
scientific conferences, and serves as a reviwer for several leading peer-reviewed scientific journals.
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