scholarly journals Dystrophin is expressed in smooth muscle and afferent nerve fibers in the rat urinary bladder

2019 ◽  
Vol 60 (2) ◽  
pp. 202-210 ◽  
Author(s):  
Judith M. Lionarons ◽  
Govert Hoogland ◽  
Ruben G. F. Hendriksen ◽  
Catharina G. Faber ◽  
Danique M. J. Hellebrekers ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Nerve Fibers ◽  
Afferent Nerve ◽  
Rat Urinary Bladder ◽  
Afferent Nerve Fibers

CGRP-immunoreactive primary afferent nerve fibers in the rat urinary bladder: Effects of dorsal rhizotomy and MK-801

1992 ◽  
Vol 118 (3) ◽  
pp. 317-323 ◽  
Author(s):  
Daniel L. McNeill ◽  
Clifford H. Harris ◽  
Jeffrey M. Holzbeierlein ◽  
Ronald L. Shew ◽  
Neil E. Traugh ◽  
...  
Keyword(s):  
Urinary Bladder ◽  
Nerve Fibers ◽  
Afferent Nerve ◽  
Primary Afferent ◽  
Rat Urinary Bladder ◽  
Mk 801 ◽  
Dorsal Rhizotomy ◽  
Afferent Nerve Fibers ◽  
Primary Afferent Nerve

Spontaneous action potential generation due to persistent sodium channel currents in simulated carotid body afferent fibers

2008 ◽  
Vol 104 (5) ◽  
pp. 1394-1401 ◽  
Author(s):  
David F. Donnelly
Keyword(s):  
Carotid Body ◽  
High Sensitivity ◽  
Nerve Fibers ◽  
Afferent Nerve ◽  
Random Pattern ◽  
Nerve Terminals ◽  
Discharge Rates ◽  
Afferent Nerve Fibers ◽  
Axonal Diameter ◽  
Spontaneous Action

The mechanism by which action potentials (APs) are generated in afferent nerve fibers in the carotid body is unknown, but it is generally speculated to be release of an excitatory transmitter and synaptic depolarizing events. However, previous results suggested that Na+ channels in the afferent nerve fibers play an important role in this process. To better understand the potential mechanism by which Na+ channels may generate APs, a mathematical model of chemoreceptor nerve fibers that incorporated Hodgkin-Huxley-type Na+ channels with kinetics of activation and inactivation, as determined previously from recordings of petrosal chemoreceptor neurons, was constructed. While the density of Na+ channels was kept constant, spontaneous APs arose in nerve terminals as the axonal diameter was reduced to that in rat carotid body. AP excitability and pattern were similar to those observed in chemoreceptor recordings: 1) a random pattern at low- and high-frequency discharge rates, 2) a high sensitivity to reductions in extracellular Na+ concentration, and 3) a variation in excitability that increased with AP generation rate. Taken together, the results suggest that an endogenous process in chemoreceptor nerve terminals may underlie AP generation, a process independent of synaptic depolarizing events.

scholarly journals Expression and functional role of Rho-kinase in rat urinary bladder smooth muscle

2003 ◽  
Vol 138 (5) ◽  
pp. 757-766 ◽  
Author(s):  
Alexandra Wibberley ◽  
Zunxuan Chen ◽  
Erding Hu ◽  
J Paul Hieble ◽  
Timothy D Westfall
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Functional Role ◽  
Rho Kinase ◽  
Bladder Smooth Muscle ◽  
Rat Urinary Bladder ◽  
Urinary Bladder Smooth Muscle

scholarly journals Voltage-gated K+ channels sensitive to stromatoxin-1 regulate myogenic and neurogenic contractions of rat urinary bladder smooth muscle

2010 ◽  
Vol 299 (1) ◽  
pp. R177-R184 ◽  
Author(s):  
Muyan Chen ◽  
Whitney F. Kellett ◽  
Georgi V. Petkov
Keyword(s):  
Smooth Muscle ◽  
Urinary Bladder ◽  
Electrical Field Stimulation ◽  
Resting Membrane Potential ◽  
Bladder Smooth Muscle ◽  
Membrane Excitability ◽  
Molecular Fingerprints ◽  
Rat Urinary Bladder ◽  
Voltage Gated ◽  
Urinary Bladder Smooth Muscle

Members of the voltage-gated K+ (KV) channel family are suggested to control the resting membrane potential and the repolarization phase of the action potential in urinary bladder smooth muscle (UBSM). Recent studies report that stromatoxin-1, a peptide isolated from tarantulas, selectively inhibits KV2.1, KV2.2, KV4.2, and KV2.1/9.3 channels. The objective of this study was to investigate whether KV channels sensitive to stromatoxin-1 participate in the regulation of rat UBSM contractility and to identify their molecular fingerprints. Stromatoxin-1 (100 nM) increased the spontaneous phasic contraction amplitude, muscle force, and tone in isolated UBSM strips. However, stromatoxin-1 (100 nM) had no effect on the UBSM contractions induced by depolarizing agents such as KCl (20 mM) or carbachol (1 μM). This indicates that, under conditions of sustained membrane depolarization, the KV channels sensitive to stromatoxin-1 have no further contribution to the membrane excitability and contractility. Stromatoxin-1 (100 nM) increased the amplitude of the electrical field stimulation-induced contractions, suggesting also a role for these channels in neurogenic contractions. RT-PCR experiments on freshly isolated UBSM cells showed mRNA expression of KV2.1, KV2.2, and KV9.3, but not KV4.2 channel subunits. Protein expression of KV2.1 and KV2.2 channels was detected using Western blot and was further confirmed by immunocytochemical detection in freshly isolated UBSM cells. These novel findings indicate that KV2.1 and KV2.2, but not KV4.2, channel subunits are expressed in rat UBSM and play a key role in opposing both myogenic and neurogenic UBSM contractions.

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