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1
Valic, Zoran, Edward H. Vidruk, Stephen B. Ruble, John B. Buckwalter, and Philip S. Clifford. "Parasympathetic innervation of canine tracheal smooth muscle." Journal of Applied Physiology 90, no. 1 (January 1, 2001): 23–28. http://dx.doi.org/10.1152/jappl.2001.90.1.23.
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To investigate whether efferent parasympathetic fibers to the tracheal smooth muscle course through the pararecurrent nerve rather than the recurrent or the superior laryngeal nerve, we stimulated all three nerves in anesthetized dogs. We also recorded the pararecurrent nerve activity response to bronchoconstrictor stimuli and compared it with pressure changes inside a saline-filled cuff of an endotracheal tube. Electrical stimulation (30 s, 100 Hz, 0.1 ms, 10 mA) increased tracheal cuff pressure by 21.0 ± 3.2 and 1.3 ± 0.7 cmH2O for the pararecurrent and the recurrent laryngeal nerve, respectively. Stimulation of the superior laryngeal nerve increased tracheal cuff pressure before, but not after, sectioning of the ramus anastomoticus, which connects it to the pararecurrent nerve. Intravenous administration of sodium cyanide increased pararecurrent nerve activity by 208 ± 51% and tracheal cuff pressure by 14.4 ± 3.5 cmH2O. Elevation of end-tidal Pco 2 to 50 Torr increased pararecurrent nerve activity by 49 ± 19% and tracheal cuff pressure by 8.4 ± 3.6 cmH2O. Further elevation to 60 Torr increased pararecurrent nerve activity by 101 ± 33% and tracheal cuff pressure by 11.3 ± 2.9 cmH2O. These results lead us to the conclusion that parasympathetic efferent fibers reach the smooth muscle of the canine trachea via the pararecurrent nerve.
2
Canning, B. J., and A. Fischer. "Localization of cholinergic nerves in lower airways of guinea pigs using antisera to choline acetyltransferase." American Journal of Physiology-Lung Cellular and Molecular Physiology 272, no. 4 (April 1, 1997): L731—L738. http://dx.doi.org/10.1152/ajplung.1997.272.4.l731.
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Primary antiserum to choline acetyltransferase (ChAT), a specific marker for cholinergic nerves, was used to characterize the distribution of cholinergic nerve fibers and nerve cell bodies in guinea pig airways. ChAT immunoreactive nerve fibers were localized to the smooth muscle throughout the conducting airways and in the lamina propria of the trachea and large bronchi. Likewise, all nerve cell bodies in the ganglia intrinsic to the trachea and bronchi displayed a cholinergic phenotype. By contrast, ChAT immunoreactive nerve fibers were infrequently seen in the lamina propria of the peripheral airways and were absent in the airway epithelium. No evidence for colocalization of ChAT and the enzyme synthesizing the putative relaxant neurotransmitter nitric oxide was observed. These results provide further evidence for the key role played by cholinergic nerves in regulating airway smooth muscle tone and bronchial blood flow and provide further evidence that acetylcholine is not coreleased with the neurotransmitter(s) mediating relaxations of airway smooth muscle.
3
Undem, B. J., A. C. Myers, H. Barthlow, and D. Weinreich. "Vagal innervation of guinea pig bronchial smooth muscle." Journal of Applied Physiology 69, no. 4 (October 1, 1990): 1336–46. http://dx.doi.org/10.1152/jappl.1990.69.4.1336.
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We isolated the guinea pig right bronchus with the vagus nerves intact and evaluated the changes in isometric tension of the smooth muscle in response to nerve stimulation. Brief (10-s) trains of electrical field stimulation or vagus nerve stimulation caused a biphasic contraction: the "first phase" sensitive to atropine and the "second phase" sensitive to capsaicin. The two phases could be dissociated by adjusting the stimulus intensity; greater stimulus intensities (pulse durations or voltage) were required to evoke the capsaicin-sensitive phase. When stimulated at 30-min intervals, the magnitude of both phases of the contractions declined over a 2-h period of repeated stimulation; however, this was prevented by indomethacin. Stimulation of the left vagus nerve resulted in a monophasic contraction of the right bronchus, with little evidence of a capsaicin-sensitive phase. Blocking neurotransmission through the bronchial ganglion, as monitored by intracellular recording techniques, abolished the first-phase contraction but had no effect on the capsaicin-sensitive phase. Selective blockade of muscarinic M1 receptors had no effect on vagus nerve-mediated contractions. The results demonstrate that the left and right vagus nerves carry preganglionic fibers to the right bronchial ganglion. The right but not the left vagus nerve also carries capsaicin-sensitive afferent fibers that, when stimulated, result in a persistent contraction of the right bronchus. Finally, we provide functional and electrophysiological evidence supporting the hypothesis that capsaicin-sensitive afferent neurons communicate with postganglionic motoneurons within the bronchus.
4
Mitchell, R. A., D. A. Herbert, and D. G. Baker. "Inspiratory rhythm in airway smooth muscle tone." Journal of Applied Physiology 58, no. 3 (March 1, 1985): 911–20. http://dx.doi.org/10.1152/jappl.1985.58.3.911.
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In anesthetized paralyzed open-chested cats ventilated with low tidal volumes at high frequency, we recorded phrenic nerve activity, transpulmonary pressure (TPP), and either the tension in an upper tracheal segment or the impulse activity in a pulmonary branch of the vagus nerve. The TPP and upper tracheal segment tension fluctuated with respiration, with peak pressure and tension paralleling phrenic nerve activity. Increased end-tidal CO2 or stimulation of the carotid chemoreceptors with sodium cyanide increased both TPP and tracheal segment tension during the increased activity of the phrenic nerve. Lowering end-tidal CO2 or hyperinflating the lungs to achieve neural apnea (lack of phrenic activity) caused a decrease in TPP and tracheal segment tension and abolished the inspiratory fluctuations. During neural apnea produced by lowering end-tidal CO2, lung inflation caused no further decrease in tracheal segment tension and TPP. Likewise, stimulation of the cervical sympathetics, which caused a reduction in TPP and tracheal segment tension during normal breathing, caused no further reduction in these parameters when the stimulation occurred during neural apnea. During neural apnea the tracheal segment tension and TPP were the same as those following the transection of the vagi or the administration of atropine (0.5 mg/kg). Numerous fibers in the pulmonary branch of the vagus nerve fired in synchrony with the phrenic nerve. Only these fibers had activity which paralleled changes in TPP and tracheal tension. We propose that the major excitatory input to airway smooth muscle arises from cholinergic nerves that fire during inspiration, which have preganglionic cell bodies in the ventral respiratory group in the region of the nucleus ambiguus and are driven by the same pattern generators that drive the phrenic and inspiratory intercostal motoneurons.
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Huizinga, Jan D., David E. Reed, Irene Berezin, Xuan-Yu Wang, Diana T. Valdez, Louis W. C. Liu, and Nicholas E. Diamant. "Survival dependency of intramuscular ICC on vagal afferent nerves in the cat esophagus." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 294, no. 2 (February 2008): R302—R310. http://dx.doi.org/10.1152/ajpregu.00398.2007.
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Interstitial cells of Cajal (ICC) have been proposed as stretch receptors for vagal afferent nerves in the stomach based on immunohistochemical studies. The aim of the present study was to use electron microscopy and the anterograde degeneration technique to investigate ultrastructural features and survival dependency of ICC associated with vagal afferent innervation of the cat esophagus. This is the first report on the ultrastructural characteristics of ICC in the cat esophagus. Intramuscular ICC (ICC-IM) were identified throughout the musculature, whereas ICC in the myenteric plexus were rare. ICC-IM were particularly numerous in septa aligned with smooth muscle bundles. They were in synapse-like contact with nerve varicosities and in gap junction contact with smooth muscle cells. Smooth muscle cells also made contact with ICC through peg and socket junctions. Precision damage through small-volume injection of saline in the center of the nodose ganglion from the lateral side, known to selectively affect sensory nerves, was followed within 24 h by degeneration of a subset of nerve varicosities associated with ICC-IM, as well as degeneration of the associated ICC-IM. Smooth muscle cells were not affected. Nerves of Auerbachs plexus and associated ICC were not affected. In summary, ICC-IM aligning the esophageal muscle bundles form specialized synapse-like contacts with vagal afferent nerves as well as gap junction and peg-and-socket contacts with smooth muscle cells. This is consistent with a role of ICC-IM as stretch receptors associated with vagal afferent nerves; the ICC-vagal nerve interaction appears essential for the survival of the ICC.
6
Conklin, J. L., and C. Du. "Guanylate cyclase inhibitors: effect on inhibitory junction potentials in esophageal smooth muscle." American Journal of Physiology-Gastrointestinal and Liver Physiology 263, no. 1 (July 1, 1992): G87—G90. http://dx.doi.org/10.1152/ajpgi.1992.263.1.g87.
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Electrical field stimulation (EFS) of nerves intrinsic to the opossum lower esophageal sphincter (LES) produces LES relaxation, an increase in its guanosine 3',5'-cyclic monophosphate (cGMP) content, and hyperpolarization of its circular muscle membrane potential difference. Activation of esophageal nerves produces an analogous hyperpolarization of the circular esophageal smooth muscle. These studies test the hypothesis that cGMP is an intracellular mediator of this hyperpolarization. The transmembrane potential difference of circular smooth muscle cells was recorded with glass microelectrodes. Nerve-mediated smooth muscle hyperpolarization was evoked by EFS (1 ms, 50 V pulses). Forskolin, an activator of adenylate cyclase, and sodium nitroprusside, an activator of guanylate cyclase, produced hyperpolarization. Cystamine and methylene blue, inhibitors of guanylate cyclase, blocked the hyperpolarization elicited by sodium nitroprusside, but not that by forskolin. Both also reversibly abolished the hyperpolarization evoked by EFS. Membrane-permeable derivatives of cGMP produced a concentration-dependent hyperpolarization. These data support the hypothesis that cGMP is an intracellular mediator of nerve-induced esophageal smooth muscle hyperpolarization.
7
Stauss, Harald M., Erling A. Anderson, William G. Haynes, and Kevin C. Kregel. "Frequency response characteristics of sympathetically mediated vasomotor waves in humans." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 4 (April 1, 1998): H1277—H1283. http://dx.doi.org/10.1152/ajpheart.1998.274.4.h1277.
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In a recent study, we demonstrated that transmission from peripheral sympathetic nerves to vascular smooth muscles is strongest in the frequency band from 0.2 to 0.5 Hz in conscious rats. In contrast, sympathetic modulation of vasomotor tone in humans is suggested to be reflected in the power spectrum of arterial blood pressure in a frequency range centered around ∼0.1 Hz. Therefore, we addressed whether frequency response characteristics of sympathetic transmission from peripheral sympathetic nerves to vascular smooth muscles in humans differ from those in rats. In 12 male subjects, skin-sympathetic fibers of the left median nerve were electrically stimulated via microneurography needles with stimulation frequencies ranging from 0.01 to 0.5 Hz. Simultaneously, blood flow in the innervated skin area at the palm of the ipsilateral hand was recorded by a laser-Doppler device. The skin blood flow in the same area of the contralateral hand was recorded as a control. Median nerve stimulation produced transient decreases in skin blood flow in the ipsilateral hand. At frequencies ranging from 0.025 to 0.10 Hz, median nerve stimulation evoked high-power peaks at the same frequencies in the skin blood flow power spectra of the ipsilateral but not of the contralateral hand. The greatest responses were found in the frequency range from 0.075 to 0.10 Hz. Therefore, these data indicate that the transmission from peripheral sympathetic nerves to cutaneous vascular smooth muscles in humans is slower than in rats. In addition, the frequency range believed to be most important in sympathetic modulation of vasomotor activity in humans corresponds to the frequency band of the greatest response of cutaneous vascular smooth muscle contraction to sympathetic nerve stimulation.
8
Du, C., J. Murray, J. N. Bates, and J. L. Conklin. "Nitric oxide: mediator of NANC hyperpolarization of opossum esophageal smooth muscle." American Journal of Physiology-Gastrointestinal and Liver Physiology 261, no. 6 (December 1, 1991): G1012—G1016. http://dx.doi.org/10.1152/ajpgi.1991.261.6.g1012.
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Activation of intrinsic nonadrenergic noncholinergic (NANC) esophageal nerves during peristalsis or by electrical field stimulation (EFS) in vitro produces a hyperpolarization followed by a depolarization of the circular smooth muscle of the opossum esophagus. N omega-nitro-L-arginine (L-NNA), an inhibitor of nitric oxide synthase, and nitric oxide (NO) were used to test the hypothesis that NO or a NO-containing compound is a mediator of this NANC nerve-induced hyperpolarization of circular esophageal smooth muscle. The transmembrane potential difference of esophageal circular smooth muscle cells was recorded with glass microelectrodes. Nerve-mediated membrane responses were evoked by single electrical pulses of 0.5 ms duration and 50 V amplitude. L-NNA abolished the initial hyperpolarization and reduced the amplitude of and the time to maximal depolarization. L-Arginine (1 mM), the substrate for NO synthase, antagonized the effect of L-NNA. Exogenous NO produced hyperpolarization of the smooth muscle membrane potential and attenuated the amplitudes of EFS-induced hyperpolarization and depolarization. The effect of NO was blocked neither by L-NNA nor by tetrodotoxin (1 microM). The data support the hypothesis that NO or a NO-containing compound mediates NANC nerve-induced responses of the esophageal smooth muscle membrane.
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Wu, Zhong-Xin, Brian E. Satterfield, and Richard D. Dey. "Substance P released from intrinsic airway neurons contributes to ozone-enhanced airway hyperresponsiveness in ferret trachea." Journal of Applied Physiology 95, no. 2 (August 2003): 742–50. http://dx.doi.org/10.1152/japplphysiol.00109.2003.
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Exposure to ozone (O3) induces airway hyperresponsiveness mediated partly through the release of substance P (SP) from nerve terminals in the airway wall. Although substantial evidence suggests that SP is released by sensory nerves, SP is also present in neurons of airway ganglia. The purpose of this study was to investigate the role of intrinsic airway neurons in O3-enhanced airway responsiveness in ferret trachea. To remove the effects of sensory innervation, segments of ferret trachea were maintained in culture conditions for 24 h before in vitro exposure to 2 parts/million of O3 or air for 1 h. Sensory nerve depletion was confirmed by showing that capsaicin did not affect tracheal smooth muscle responsiveness to cholinergic agonist or contractility responses to electrical field stimulation (EFS). Contractions of isolated tracheal smooth muscle to EFS were significantly increased after in vitro O3 exposure, but the constrictor response to cholinergic agonist was not altered. Pretreatment with CP-99994, an antagonist of the neurokinin 1 receptor, attenuated the increased contraction to EFS after O3 exposure but had no effect in the air exposure group. The number of SP-positive neurons in longitudinal trunk ganglia, the extent of SP innervation to superficial muscular plexus nerve cell bodies, and SP nerve fiber density in tracheal smooth muscle all increased significantly after O3 exposure. The results show that release of SP from intrinsic airway neurons contributes to O3-enhanced tracheal smooth muscle responsiveness by facilitating acetylcholine release from cholinergic nerve terminals.
10
Gonda, T., E. E. Daniel, T. J. McDonald, J. E. Fox, B. D. Brooks, and M. Oki. "Distribution and function of enteric GAL-IR nerves in dogs: comparison with VIP." American Journal of Physiology-Gastrointestinal and Liver Physiology 256, no. 5 (May 1, 1989): G884—G896. http://dx.doi.org/10.1152/ajpgi.1989.256.5.g884.
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The distribution of nerves containing galanin-immunoreactive (GAL-IR) material was compared to the distribution of neurons containing vasoactive intestinal polypeptide (VIP) immunoreactivity in the canine gastrointestinal tract. The actions of intra-arterially administered galanin and VIP on motility in the gastric antrum and corpus and the intestines were also studied. All sphincter muscles contained galanin- and VIP-immunoreactive nerve profiles. VIP-immunoreactive nerve profiles were present in all layers of the stomach, small intestine, and colon. GAL-IR nerve somata were common in the submucous plexus of ileum and colon and in the myenteric plexus of the terminal antrum, as were nerve processes in various layers. In the small intestine, galanin inhibited contractile responses to field stimulation of intrinsic nerves and also reduced the contractions after nerve blockade with tetrodotoxin (TTX). VIP often enhanced field-stimulated contractions at low doses but inhibited these and the contractions after TTX at higher doses. In the stomach and colon, both peptides inhibited responses to field stimulation; whether these effects were due to actions on smooth muscle was not tested. The distribution and actions of galanin in gut are consistent with the hypothesis that it acts at smooth muscle sites and possibly at prejunctional sites.
11
Herrera, Gerald M., Bud Etherton, Bernhard Nausch, and Mark T. Nelson. "Negative feedback regulation of nerve-mediated contractions by KCa channels in mouse urinary bladder smooth muscle." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 289, no. 2 (August 2005): R402—R409. http://dx.doi.org/10.1152/ajpregu.00488.2004.
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When the urinary bladder is full, activation of parasympathetic nerves causes release of neurotransmitters that induce forceful contraction of the detrusor muscle, leading to urine voiding. The roles of ion channels that regulate contractility of urinary bladder smooth muscle (UBSM) in response to activation of parasympathetic nerves are not well known. The present study was designed to characterize the role of large (BK)- and small-conductance (SK) Ca2+-activated K+ (KCa) channels in regulating UBSM contractility in response to physiological levels of nerve stimulation in UBSM strips from mice. Nerve-evoked contractions were induced by electric field stimulation (0.5–50 Hz) in isolated strips of UBSM. BK and SK channel inhibition substantially increased the amplitude of nerve-evoked contractions up to 2.45 ± 0.12- and 2.99 ± 0.25-fold, respectively. When both SK and BK channels were inhibited, the combined response was additive. Inhibition of L-type voltage-dependent Ca2+ channels (VDCCs) in UBSM inhibited nerve-evoked contractions by 92.3 ± 2.0%. These results suggest that SK and BK channels are part of two distinct negative feedback pathways that limit UBSM contractility in response to nerve stimulation by modulating the activity of VDCCs. Dysfunctional regulation of UBSM contractility by alterations in BK/SK channel expression or function may underlie pathologies such as overactive bladder.
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Canning, Brendan J. "Reflex regulation of airway smooth muscle tone." Journal of Applied Physiology 101, no. 3 (September 2006): 971–85. http://dx.doi.org/10.1152/japplphysiol.00313.2006.
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Autonomic nerves in most mammalian species mediate both contractions and relaxations of airway smooth muscle. Cholinergic-parasympathetic nerves mediate contractions, whereas adrenergic-sympathetic and/or noncholinergic parasympathetic nerves mediate relaxations. Sympathetic-adrenergic innervation of human airway smooth muscle is sparse or nonexistent based on histological analyses and plays little or no role in regulating airway caliber. Rather, in humans and in many other species, postganglionic noncholinergic parasympathetic nerves provide the only relaxant innervation of airway smooth muscle. These noncholinergic nerves are anatomically and physiologically distinct from the postganglionic cholinergic parasympathetic nerves and differentially regulated by reflexes. Although bronchopulmonary vagal afferent nerves provide the primary afferent input regulating airway autonomic nerve activity, extrapulmonary afferent nerves, both vagal and nonvagal, can also reflexively regulate autonomic tone in airway smooth muscle. Reflexes result in either an enhanced activity in one or more of the autonomic efferent pathways, or a withdrawal of baseline cholinergic tone. These parallel excitatory and inhibitory afferent and efferent pathways add complexity to autonomic control of airway caliber. Dysfunction or dysregulation of these afferent and efferent nerves likely contributes to the pathogenesis of obstructive airways diseases and may account for the pulmonary symptoms associated with extrapulmonary disorders, including gastroesophageal reflux disease, cardiovascular disease, and rhinosinusitis.
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Reynolds, R. P. E., T. Y. El-Sharkawy, and N. E. Diamant. "Oesophageal peristalsis in the cat: the role of central innervation assessed by transient vagal blockade." Canadian Journal of Physiology and Pharmacology 63, no. 2 (February 1, 1985): 122–30. http://dx.doi.org/10.1139/y85-022.
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Studies were performed on five cats to assess the role of extrinsic vagal innervation in the control of peristalsis in the smooth muscle oesophagus. Transient vagal nerve blockade was accomplished by cooling the cervical vagosympathetic nerve trunks previously isolated in skin loops on each side of the neck. Peristalsis throughout the body of the oesophagus was monitored using a continuously perfused multilumen manometry tube. Striated and smooth muscle portions of the esophagus were delineated by abolishing smooth muscle activity with atropine. Secondary peristalsis was assessed by intra-oesophageal balloon distension studies. The threshold volume for balloon-induced secondary peristalsis was lower in the smooth muscle oesophagus. Unilateral vagal blockade reduced the incidence of primary and secondary peristalsis in the striated muscle oesophagus but not in the smooth muscle oesophagus. Bilateral vagal nerve blockade abolished primary swallow-induced peristalsis and secondary peristalsis in both the smooth and striated muscle cat oesophagus. Administration of cholinergic agents or adrenergic blocking agents failed to restore secondary peristalsis in the smooth muscle oesophagus during vagal cooling. We conclude that connections to the central nervous system via the vagal nerve trunks are required for normal secondary as well as primary peristalsis in both the smooth and striated muscle portions of the cat oesophagus.
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Sanders, K. M., and S. M. Ward. "Nitric oxide as a mediator of nonadrenergic noncholinergic neurotransmission." American Journal of Physiology-Gastrointestinal and Liver Physiology 262, no. 3 (March 1, 1992): G379—G392. http://dx.doi.org/10.1152/ajpgi.1992.262.3.g379.
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Part of the regulation of gastrointestinal (GI) smooth muscles is provided by nonadrenergic noncholinergic (NANC) nerves. Stimulation of these nerves, either by field stimulation or via neural reflex pathways, elicits hyperpolarization of postjunctional smooth muscle membranes referred to as inhibitory junction potentials and relaxation. The transmitter(s) that mediate NANC inhibitory neural transmission have been a controversial topic for nearly 30 years. Recent evidence suggests that nitric oxide (NO) may serve as a NANC inhibitory transmitter in the GI tract. This hypothesis is supported by the following. 1) Immunohistochemical studies have shown that the enzyme necessary for NO synthesis is expressed in enteric neurons. In vitro studies of muscles from nearly all levels of GI tract have also shown that arginine analogues, which inhibit NO synthesis, reduce inhibitory effects of NANC neurotransmission. Effects of arginine analogues can be restored by addition of excess L-arginine, the substrate for NO synthesis. These data suggest that NO can be synthesized by enteric nerves. 2) Bioassays have demonstrated nerve-evoked release of a substance that has been identified as NO during NANC nerve stimulation. Oxyhemoglobin, known to bind to and sequester NO, also blocks NANC responses. These data suggest that NO is released into extracellular fluid during nerve stimulation. 3) Addition of NO causes rapid hyperpolarization of GI smooth muscle cells and relaxes muscles strips. These effects are similar to NANC nerve responses. NO and electrical field stimulation also increase tissue guanosine 3',5'-cyclic monophosphate, which may be the second messenger involved in NANC responses. 4) Removal of NO is easily accomplished by its rapid spontaneous breakdown in physiological solutions. 5) The pharmacology of NO and the NANC neurotransmitter in many preparations is similar, e.g., oxyhemoglobin blocks responses to NANC nerve stimulation and to exogenous NO. In summary, it would appear that many of the criteria necessary for NO to be considered a neurotransmitter have been satisfied.
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Jorgensen, J. C., S. P. Sheikh, A. Forman, M. Norgard, T. W. Schwartz, and B. Ottesen. "Neuropeptide Y in the human female genital tract: localization and biological action." American Journal of Physiology-Endocrinology and Metabolism 257, no. 2 (August 1, 1989): E220—E227. http://dx.doi.org/10.1152/ajpendo.1989.257.2.e220.
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The distribution, localization, and smooth muscle effects of neuropeptide Y (NPY) were studied in the human female genital tract. High concentrations of NPY immunoreactivity were demonstrated in the uterine artery, the ovary, the fallopian tube, cervix, and the vagina. The NPY immunoreactivity was confined to nerve fibers. The highest density of nerve fibers was observed in relation to blood vessels, although some NPY-immunoreactive nerves were also seen close to nonvascular smooth muscle. The NPY-immunoreactive material throughout the genital tract was identical to synthetic amidated human NPY with regard to size, hydrophobicity, and charge as evaluated by gel filtration, high-performance liquid chromatography, and isoelectric focusing. NPY (10(-10) to 10(-6) M) exerted a direct vasoconstrictory effect on small arteries dissected from the cervix and an additive effect of NPY and norepinephrine responses was observed. Exogenous NPY did not have a direct effect on nonvascular smooth muscle specimens from the fallopian tube or the myometrium. The close relation between NPY-immunoreactive nerves and blood vessels, the presence of NPY-immunoreactive material identical to amidated synthetic human NPY, and the vasoconstrictory effects of NPY indicate that NPY is involved in the regulation of the blood flow in the human female genital tract.
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Barbe, Mary F., Courtney L. Testa, Geneva E. Cruz, Nagat A. Frara, Ekta Tiwari, Lucas J. Hobson, Brian S. McIntyre, et al. "Nerve transfer for restoration of lower motor neuron-lesioned bladder function. Part 2: correlation between histological changes and nerve evoked contractions." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 320, no. 6 (June 1, 2021): R897—R915. http://dx.doi.org/10.1152/ajpregu.00300.2020.
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We determined the effect of pelvic organ decentralization and reinnervation 1 yr later on urinary bladder histology and function. Nineteen canines underwent decentralization by bilateral transection of all coccygeal and sacral (S) spinal roots, dorsal roots of lumbar (L)7, and hypogastric nerves. After exclusions, eight were reinnervated 12 mo postdecentralization with obturator-to-pelvic and sciatic-to-pudendal nerve transfers, then euthanized 8-12 mo later. Four served as long-term decentralized only animals. Before euthanasia, pelvic or transferred nerves and L1–S3 spinal roots were stimulated and maximum detrusor pressure (MDP) recorded. Bladder specimens were collected for histological and ex vivo smooth muscle contractility studies. Both reinnervated and decentralized animals showed less or denuded urothelium, fewer intramural ganglia, and more inflammation and collagen, than controls, although percent muscle was maintained. In reinnervated animals, pgp9.5+ axon density was higher compared with decentralized animals. Ex vivo smooth muscle contractions in response to KCl correlated positively with submucosal inflammation, detrusor muscle thickness, and pgp9.5+ axon density. In vivo, reinnervated animals showed higher MDP after stimulation of L1–L6 roots compared with their transected L7–S3 roots, and reinnervated and decentralized animals showed lower MDP than controls after stimulation of nerves (due likely to fibrotic nerve encapsulation). MDP correlated negatively with detrusor collagen and inflammation, and positively with pgp9.5+ axon density and intramural ganglia numbers. These results demonstrate that bladder function can be improved by transfer of obturator nerves to pelvic nerves at 1 yr after decentralization, although the fibrosis and inflammation that developed were associated with decreased contractile function.
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Goyal, Raj K., and Arun Chaudhury. "Mounting evidence against the role of ICC in neurotransmission to smooth muscle in the gut." American Journal of Physiology-Gastrointestinal and Liver Physiology 298, no. 1 (January 2010): G10—G13. http://dx.doi.org/10.1152/ajpgi.00426.2009.
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How nerves transmit their signals to regulate activity of smooth muscle is of fundamental importance to autonomic and enteric physiology, clinical medicine, and therapeutics. A traditional view of neurotransmission to smooth muscles has been that motor nerve varicosities release neurotransmitters that act on receptors on smooth muscles to cause their contraction or relaxation via electromechanical and pharmacomechanical signaling pathways in the smooth muscle. In recent years, an old hypothesis that certain interstitial cells of Cajal (ICC) may transduce neural signals to smooth muscle cells has been resurrected. This later hypothesis is based on indirect evidence of closer proximity and presence of synapses between the nerve varicosities and ICC, gap junctions between ICC and smooth muscles, and presence of receptors and signaling pathways for the neurotransmitters and ICC. This indirect evidence is at best circumstantial. The direct evidence is based on the reports of loss of neurotransmission in mutant animals lacking ICC due to c-Kit receptor deficiency. However, a critical analysis of the recent data show that animals lacking ICC have normal cholinergic and purinergic neurotransmission and tachykinergic neurotransmission is actually increased. The status of nitrergic neurotransmission in c-Kit deficient animals has been controversial. However, reports suggest that 1) nitrergic neurotransmission in the internal anal sphincter does not require ICC and 2) the in vivo phenotype of ICC deficiency does not resemble nNOS deficiency. 3) The most recent report, in this issue of the Journal, concludes that impaired nitrergic neurotransmission may be due to smooth muscle defects associated with c-Kit receptor deficiency.
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Kawamoto, Shunsuke, Hadzki Matsuda, Keisuke Ueki, Yoshifumi Okada, and Phyo Kim. "NEUROMUSCULAR CHORISTOMA OF THE OCULOMOTOR NERVE." Neurosurgery 60, no. 4 (April 1, 2007): E777—E778. http://dx.doi.org/10.1227/01.neu.0000255352.56453.8e.
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Abstract OBJECTIVE Neuromuscular choristomas (NMC) are rare benign tumors of the peripheral nerves. We report an NMC affecting the oculomotor nerve. CLINICAL PRESENTATION An 18-year-old girl presented with long-standing intermittent retro-orbital pain and oculomotor paresis. Magnetic resonance imaging scans demonstrated a small nodular lesion on the left oculomotor nerve, similar to the findings for a schwannoma. INTERVENTION The tumor was resected with the parental oculomotor nerve, which was reconstructed using a peroneal nerve graft. Postoperatively, the patient became pain-free, and her oculomotor function partially recovered. Histologically, the lesion consisted of well-differentiated smooth muscle fibers intermingled with mature nerve elements consistent with the diagnosis of an NMC, although the possibility of leiomyoma in this rare location was not excluded completely. CONCLUSION NMC may need histological confirmation for diagnosis if they occur in the intracranial space. The resection is feasible, and the function of the affected nerve can be at least partially restored with the nerve reconstruction.
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Xin, Wenkuan, Ning Li, Vitor S. Fernandes, and Georgi V. Petkov. "Constitutively active PKA regulates neuronal acetylcholine release and contractility of guinea pig urinary bladder smooth muscle." American Journal of Physiology-Renal Physiology 310, no. 11 (June 1, 2016): F1377—F1384. http://dx.doi.org/10.1152/ajprenal.00026.2016.
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Autonomic and somatic motor neurons that innervate the urinary bladder and urethra control the highly coordinated functions of the lower urinary tract, the storage, and the emptying of urine. ACh is the primary excitatory neurotransmitter in the bladder. Here, we aimed to determine whether PKA regulates neuronal ACh release and related nerve-evoked detrusor smooth muscle (DSM) contractions in the guinea pig urinary bladder. Isometric DSM tension recordings were used to measure spontaneous phasic and electrical field stimulation (EFS)- and carbachol-induced DSM contractions with a combination of pharmacological tools. The colorimetric method was used to measure ACh released by the parasympathetic nerves in DSM isolated strips. The pharmacological inhibition of PKA with H-89 (10 μM) increased the spontaneous phasic contractions, whereas it attenuated the EFS-induced DSM contractions. Intriguingly, H-89 (10 μM) attenuated the (primary) cholinergic component, whereas it simultaneously increased the (secondary) purinergic component of the nerve-evoked contractions in DSM isolated strips. The acetylcholinesterase inhibitor, eserine (10 μM), increased EFS-induced DSM contractions, and the subsequent addition of H-89 attenuated the contractions. H-89 (10 μM) significantly increased DSM phasic contractions induced by the cholinergic agonist carbachol. The inhibition of PKA decreased the neuronal release of ACh in DSM tissues. This study revealed that PKA-mediated signaling pathways differentially regulate nerve-evoked and spontaneous phasic contractions of guinea pig DSM. Constitutively active PKA in the bladder nerves controls synaptic ACh release, thus regulating the nerve-evoked DSM contractions, whereas PKA in DSM cells controls the spontaneous phasic contractility.
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Rummings, Wayne, P. Honeycutt, Edward Jernigan, Paul Weinhold, and Reid Draeger. "Effect of Nerve-Cutting Technique on Nerve Microstructure and Neuroma Formation." Journal of Hand and Microsurgery 11, no. 01 (September 27, 2018): 028–34. http://dx.doi.org/10.1055/s-0038-1654751.
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Abstract Background Peripheral neuroma formation results from partial or complete nerve division. Elucidating measures to prevent the development of peripheral neuromas is of clinical importance. The aim of this study was to determine the effect of various surgical nerve-cutting techniques on nerve microstructure and resultant neuroma formation. Methods Twenty Sprague-Dawley rats were randomly assigned to one of the following nerve-cutting techniques: No. 15 scalpel blade with tongue depressor, micro-serrated scissors, nerve-cutting guide forceps with straight razor, and bipolar cauterization. The right sciatic nerve was transected using the assigned nerve-cutting technique. Neuromas were harvested 6 weeks postoperatively, and samples were obtained for histologic analysis. The contralateral sciatic nerve was transected at euthanasia and analyzed with histology and with scanning electron microscopy in a subset of the rats. Results Fifteen of the 20 rats survived the 6-week experiment. Scanning electron microscopy of the No. 15 scalpel blade group showed the most visual damage and disorganization whereas the nerve-cutting guide forceps and micro-serrated scissors groups resulted in a smooth transected surface. Bipolar cauterization appeared to enclose the fascicular architecture within a sealed epineurium. Each neuroma was significantly larger than contralateral controls. There were no significant differences in neuroma caliber between nerve transection groups. No substantial differences in microstructure were evident between transection groups. Conclusion Despite disparate microscopic appearances of the cut surfaces of nerves using various nerve-cutting techniques, we found no significant differences in the caliber or incidence of neuroma formation based on nerve-cutting technique. Nerve-cutting technique used when transecting peripheral nerves may have little bearing on the formation or size of resultant neuroma formation.
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Jacquir, S., S. Binczak, J. P. Gauthier, and J. M. Bilbault. "Emergence of travelling waves in smooth nerve fibres." Discrete & Continuous Dynamical Systems - S 1, no. 2 (2008): 263–72. http://dx.doi.org/10.3934/dcdss.2008.1.263.
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Creedon, D., and J. B. Tuttle. "Nerve growth factor synthesis in vascular smooth muscle." Hypertension 18, no. 6 (December 1991): 730–41. http://dx.doi.org/10.1161/01.hyp.18.6.730.
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van Helden, Dirk F., Ayumi Kamiya, Sam Kelsey, Derek R. Laver, Phillip Jobling, Retsu Mitsui, and Hikaru Hashitani. "Nerve-induced responses of mouse vaginal smooth muscle." Pflügers Archiv - European Journal of Physiology 469, no. 10 (May 27, 2017): 1373–85. http://dx.doi.org/10.1007/s00424-017-1995-x.
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Klarskov, Peter. "Lower urinary tract smooth muscle inhibitory nerve responses." Neurourology and Urodynamics 7, no. 4 (1988): 307–26. http://dx.doi.org/10.1002/nau.1930070402.
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Toda, Noboru, Megumi Toda, Kazuhide Ayajiki, and Tomio Okamura. "Cholinergic nerve function in monkey ciliary arteries innervated by nitroxidergic nerve." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 5 (May 1, 1998): H1582—H1589. http://dx.doi.org/10.1152/ajpheart.1998.274.5.h1582.
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We sought to determine the control of ciliary arterial tone by neurogenic acetylcholine (ACh) acting directly on smooth muscle and in conjunction with vasodilator nerves. Isolated posterior ciliary arteries from monkeys responded to ACh (10−8–10−5M) with dose-related contractions, which were endothelium independent. The response was not affected by cyclooxygenase inhibitors but was abolished by atropine. Relaxations induced at 10−4 M ACh in the atropine-treated arterial strips were abolished by hexamethonium and N G-nitro-l-arginine (l-NNA), andl-arginine (l-Arg) reversed the response suppressed by l-NNA. Similar results were also obtained on the nicotine (10−4 M)-induced relaxation. Contractions due to transmural electrical stimulation in the endothelium-denuded strips treated withl-NNA were potentiated by physostigmine and depressed by atropine; the remaining contraction in the presence of atropine was abolished by prazosin. Relaxations associated with electrical stimulation, sensitive to tetrodotoxin, were abolished or reversed to contractions byl-NNA and restored byl-Arg. Stimulation-induced relaxation was attenuated by exogenous ACh and physostigmine and was potentiated by atropine. ACh did not affect the relaxation caused by nitric oxide (NO). Nerve fibers and bundles containing NADPH diaphorase and acetylcholinesterase were histologically demonstrated in the adventitia of ciliary arteries. We conclude that 1) endogenous and exogenous ACh contracts monkey ciliary arteries by acting on muscarinic receptors in smooth muscle cell membranes, 2) vasodilatation elicited by nerve stimulation with electrical pulses or nicotine is mediated by NO synthesized froml-Arg, 3) neurogenic ACh seems to interfere with the nitroxidergic nerve function by acting on prejunctional muscarinic receptors, and 4) high concentrations of ACh stimulate nicotinic receptors in vasodilator nerve terminals and promote the synthesis and/or release of NO.
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Nausch, Lydia W. M., Adrian D. Bonev, Thomas J. Heppner, Yvonne Tallini, Michael I. Kotlikoff, and Mark T. Nelson. "Sympathetic nerve stimulation induces local endothelial Ca2+ signals to oppose vasoconstriction of mouse mesenteric arteries." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 3 (February 2012): H594—H602. http://dx.doi.org/10.1152/ajpheart.00773.2011.
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It is generally accepted that the endothelium regulates vascular tone independent of the activity of the sympathetic nervous system. Here, we tested the hypothesis that the activation of sympathetic nerves engages the endothelium to oppose vasoconstriction. Local inositol 1,4,5-trisphosphate (IP3)-mediated Ca2+ signals (“pulsars”) in or near endothelial projections to vascular smooth muscle (VSM) were measured in an en face mouse mesenteric artery preparation. Electrical field stimulation of sympathetic nerves induced an increase in endothelial cell (EC) Ca2+ pulsars, recruiting new pulsar sites without affecting activity at existing sites. This increase in Ca2+ pulsars was blocked by bath application of the α-adrenergic receptor antagonist prazosin or by TTX but was unaffected by directly picospritzing the α-adrenergic receptor agonist phenylephrine onto the vascular endothelium, indicating that nerve-derived norepinephrine acted through α-adrenergic receptors on smooth muscle cells. Moreover, EC Ca2+ signaling was not blocked by inhibitors of purinergic receptors, ryanodine receptors, or voltage-dependent Ca2+ channels, suggesting a role for IP3, rather than Ca2+, in VSM-to-endothelium communication. Block of intermediate-conductance Ca2+-sensitive K+ channels, which have been shown to colocalize with IP3 receptors in endothelial projections to VSM, enhanced nerve-evoked constriction. Collectively, our results support the concept of a transcellular negative feedback module whereby sympathetic nerve stimulation elevates EC Ca2+ signals to oppose vasoconstriction.
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Burnstock, G., and P. Sneddon. "Evidence for ATP and noradrenaline as cotransmitters in sympathetic nerves." Clinical Science 68, s10 (January 1, 1985): 89s—92s. http://dx.doi.org/10.1042/cs068s089.
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Sympathetically innervated smooth muscles, including those in some arteries, arterioles, cat nictitating membrane and vas deferens, have α1-adrenoceptors which respond to exogenously applied noradrenaline (NA) by producing contractions which can be abolished by α1-adrenoceptor antagonists such as prazosin. Stimulation of the sympathetic nerves innervating these muscles causes release of NA and a contractile response. However, this contraction is (at least partly) resistant to specific α1-adrenoceptor antagonists. This apparent contradiction could be explained by a variety of ad hoc explanations (such as high transmitter concentrations within the nerve-muscle junction, or prejunctional enhancement of transmitter release by the antagonist due to prejunctional α2-adrenoceptor blockade etc.) but recently two hypotheses have been advanced which may have more fundamental implications for sympathetic neurotransmission. First, Hirst and Neild and their colleagues suggested that the electrical and mechanical responses of some smooth muscles were resistant to α-adrenoceptor antagonists because neuronally released NA was acting not only on α-adrenoceptors but also on a new class of adrenoceptors which they designated γ-receptors, located near the nerve-muscle junction. The crucial experiments in support of this hypothesis were originally performed on the arterioles of the guinea-pig submucosa [1], but the idea has been extended to include many other sympathetically innervated smooth muscles [2], including guinea-pig vas deferens, which was also the smooth muscle preparation in which the experimental evidence for an alternative hypothesis was obtained by Fedan et al. [3]. They proposed that the α-blocker-resistant portion of the contractile response to sympathetic nerve stimulation was mediated by ATP, acting as a cotransmitter with NA. Full details of the early development of the concept of cotransmission in sympathetic nerves have been reviewed previously [4, 6, 7]. The experimental evidence relating to the co-transmission hypothesis is outlined below, drawing mainly on results obtained in guinea-pig vas deferens, where most of the more recent experiments have been performed.
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Daniel, E. E., V. Posey-Daniel, L. P. Jager, I. Berezin, and J. Jury. "Structural effects of exposure of smooth muscle in sucrose gap apparatus." American Journal of Physiology-Cell Physiology 252, no. 1 (January 1, 1987): C77—C87. http://dx.doi.org/10.1152/ajpcell.1987.252.1.c77.
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Structural changes were studied over time of a smooth muscle tissue (opossum esophagus circular muscle) exposed in various compartments of a functioning single sucrose gap. The tissues in the Krebs-perfused compartment were qualitatively normal, possessing nerve profiles with little damage, normal appearing smooth muscle and interstitial cells of Cajal as well as gap junctions between muscle cells and interstitial cells. However, in the sucrose compartment tissues had serious damage to smooth muscle, interstitial cells and nerves, and normal gap junctions disappeared. There was also damage to all these structures in tissues exposed to KCl, but most striking was the disappearance of most interstitial cells. These studies raise serious questions about the assumptions underlying the basis for functioning of multicellular tissues in the sucrose gap.
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Goodman, Barbara E. "Channels active in the excitability of nerves and skeletal muscles across the neuromuscular junction: basic function and pathophysiology." Advances in Physiology Education 32, no. 2 (June 2008): 127–35. http://dx.doi.org/10.1152/advan.00091.2007.
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Ion channels are essential for the basic physiological function of excitable cells such as nerve, skeletal, cardiac, and smooth muscle cells. Mutations in genes that encode ion channels have been identified to cause various diseases and disorders known as channelopathies. An understanding of how individual ion channels are involved in the activation of motoneurons and their corresponding muscle cells is essential for interpreting basic neurophysiology in nerves, the heart, and skeletal and smooth muscle. This review article is intended to clarify how channels work in nerves, neuromuscular junctions, and muscle function and what happens when these channels are defective. Highlighting the human diseases that result from defective ion channels is likely to be interesting to students in helping them choose to learn about channel physiology.
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Bramich, Narelle J. "Electrical behavior of guinea pig tracheal smooth muscle." American Journal of Physiology-Lung Cellular and Molecular Physiology 278, no. 2 (February 1, 2000): L320—L328. http://dx.doi.org/10.1152/ajplung.2000.278.2.l320.
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Intracellular recordings were taken from the smooth muscle of the guinea pig trachea, and the effects of intrinsic nerve stimulation were examined. Approximately 50% of the cells had stable resting membrane potentials of −50 ± 1 mV. The remaining cells displayed spontaneous oscillations in membrane potential, which were abolished either by blocking voltage-dependent Ca2+channels with nifedipine or by depleting intracellular Ca2+stores with ryanodine. In quiescent cells, stimulation with a single impulse evoked an excitatory junction potential (EJP). In 30% of these cells, trains of stimuli evoked an EJP that was followed by oscillations in membrane potential. Transmural nerve stimulation caused an increase in the frequency of spontaneous oscillations. All responses were abolished by the muscarinic-receptor antagonist hyoscine (1 μM). In quiescent cells, nifedipine (1 μM) reduced EJPs by 30%, whereas ryanodine (10 μM) reduced EJPs by 93%. These results suggest that both the release of Ca2+ from intracellular stores and the influx of Ca2+ through voltage-dependent Ca2+channels are important determinants of spontaneous and nerve-evoked electrical activity of guinea pig tracheal smooth muscle.
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Gleason, Neil R., George Gallos, Yi Zhang, and Charles W. Emala. "The GABAA agonist muscimol attenuates induced airway constriction in guinea pigs in vivo." Journal of Applied Physiology 106, no. 4 (April 2009): 1257–63. http://dx.doi.org/10.1152/japplphysiol.91314.2008.
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GABAA channels are ubiquitously expressed on neuronal cells and act via an inward chloride current to hyperpolarize the cell membrane of mature neurons. Expression and function of GABAA channels on airway smooth muscle cells has been demonstrated in vitro. Airway smooth muscle cell membrane hyperpolarization contributes to relaxation. We hypothesized that muscimol, a selective GABAA agonist, could act on endogenous GABAA channels expressed on airway smooth muscle to attenuate induced increases in airway pressures in anesthetized guinea pigs in vivo. In an effort to localize muscimol's effect to GABAA channels expressed on airway smooth muscle, we pretreated guinea pigs with a selective GABAA antagonist (gabazine) or eliminated lung neural control from central parasympathetic, sympathetic, and nonadrenergic, noncholinergic (NANC) nerves before muscimol treatment. Pretreatment with intravenous muscimol alone attenuated intravenous histamine-, intravenous acetylcholine-, or vagal nerve-stimulated increases in peak pulmonary inflation pressure. Pretreatment with the GABAA antagonist gabazine blocked muscimol's effect. After the elimination of neural input to airway tone by central parasympathetic nerves, peripheral sympathetic nerves, and NANC nerves, intravenous muscimol retained its ability to block intravenous acetylcholine-induced increases in peak pulmonary inflation pressures. These findings demonstrate that the GABAA agonist muscimol acting specifically via GABAA channel activation attenuates airway constriction independently of neural contributions. These findings suggest that therapeutics directed at the airway smooth muscle GABAA channel may be a novel therapy for airway constriction following airway irritation and possibly more broadly in diseases such as asthma and chronic obstructive pulmonary disease.
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LUNDBORG, G., B. ROSÉN, S. O. ABRAHAMSON, L. DAHLIN, and N. DANIELSEN. "Tubular Repair of the Median Nerve in the Human Forearm." Journal of Hand Surgery 19, no. 3 (June 1994): 273–76. http://dx.doi.org/10.1016/0266-7681(94)90068-x.
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Transected median nerves in the forearm of two male patients, 12 and 21 years of age, were treated with a chamber technique leaving a 3 to 5 mm gap between the nerve ends. The nerve ends were enclosed in a silicone tube of such a dimension that would not cause compression of the nerve. Post-operative examination including sensory evaluation and assessment of muscle contraction force was carried out after 3 years. In both cases there was excellent motor recovery of the thenar muscles. Outgrowth of sensory fibres was remarkably fast, resulting ultimately in functional sensibility allowing almost normal hand function. 2PD was ⩽ 6 mm (12year-old patient) and 8 to 10 mm (21-year-old patient) respectively. In one case the silicone tube was re-explored because of minor local discomfort 2 years after the repair. The former gap was bridged by a smooth continuous nerve-like structure of the same diameter as the adjacent nerve trunk and with no signs of nenroma formation or compression of the nerve.
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Huizinga, Jan D., Louis W. C. Liu, Amanda Fitzpatrick, Elizabeth White, Sandeep Gill, Xuan-Yu Wang, Natalia Zarate, et al. "Deficiency of intramuscular ICC increases fundic muscle excitability but does not impede nitrergic innervation." American Journal of Physiology-Gastrointestinal and Liver Physiology 294, no. 2 (February 2008): G589—G594. http://dx.doi.org/10.1152/ajpgi.00130.2007.
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The motility of the gastrointestinal tract is generated by smooth muscle cells and is controlled to a large extent by an intrinsic neural network. A gap of ∼200 nm usually separates nerve varicosities from smooth muscle cells, which suggests that direct innervation of the smooth muscle by synapses does not occur. Enteric nerves do make synapse-like contact with proposed regulatory cells, the interstitial cells of Cajal (ICC), which in turn may be in gap junction contact with smooth muscle cells. The role played by ICC in enteric innervation is controversial. Experimental evidence has been presented in vitro for the hypothesis that nitrergic inhibitory innervation is strongly reduced in the absence of ICC. However, in vivo data appear to dispute that. The present report provides evidence that explains the discrepancy between in vivo and in vitro data and provides evidence that inhibitory neurotransmitters can reach smooth muscle cells without hindrance when ICC are absent. The fundic musculature shows increased responses to substance P-mediated innervation and shows marked spontaneous activity, which is consistent with increased muscle excitability.
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Gown, A. M., A. M. Vogel, D. Gordon, and P. L. Lu. "A smooth muscle-specific monoclonal antibody recognizes smooth muscle actin isozymes." Journal of Cell Biology 100, no. 3 (March 1, 1985): 807–13. http://dx.doi.org/10.1083/jcb.100.3.807.
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Injection of chicken gizzard actin into BALB/c mice resulted in the isolation of a smooth muscle-specific monoclonal antibody designated CGA7. When assayed on methanol-Carnoy's fixed, paraffin-embedded tissue, it bound to smooth muscle cells and myoepithelial cells, but failed to decorate striated muscle, endothelium, connective tissue, epithelium, or nerve. CGA7 recognized microfilament bundles in early passage cultures of rat aortic smooth muscle cells and human leiomyosarcoma cells but did not react with human fibroblasts. In Western blot experiments, CGA7 detected actin from chicken gizzard and monkey ileum, but not skeletal muscle or fibroblast actin. Immunoblots performed on two-dimensional gels demonstrated that CGA7 recognizes gamma-actin from chicken gizzard and alpha- and gamma-actin from rat colon muscularis. This antibody was an excellent tissue-specific smooth muscle marker.
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Torihashi, S., S. Kobayashi, W. T. Gerthoffer, and K. M. Sanders. "Interstitial cells in deep muscular plexus of canine small intestine may be specialized smooth muscle cells." American Journal of Physiology-Gastrointestinal and Liver Physiology 265, no. 4 (October 1, 1993): G638—G645. http://dx.doi.org/10.1152/ajpgi.1993.265.4.g638.
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The fine structures and properties of cells between the inner and outer circular muscle layers in the canine small intestine were studied by transmission electron microscopy (TEM), immunocytochemistry, and scanning electron microscopy (SEM). A nerve plexus (deep muscular plexus) supported by enteroglial cells, fibroblasts around blood vessels, macrophages, and thin and branched cells previously identified as interstitial cells of Cajal was observed. The interstitial cells of the deep muscular plexus (IC-DMP) were rich in mitochondria, dense bodies, and caveolae, and they were closely associated with nerve fibers. The IC-DMP had incomplete basal laminae. These cells also had numerous interconnecting gap junctions, and they also formed gap junctions with the surrounding smooth muscle cells of the outer circular muscle layer. IC-DMP were rich in myofilaments, which were primarily actin thin filaments, but myosin thick filaments, identified with anti-myosin light-chain antibodies, were also apparent. IC-DMP and circular smooth muscle cells both expressed immunoreactivity to anti-smooth muscle actin antisera, but these two types of cells differed in their intermediate filament proteins: IC-DMP featured vimentin immunopositive filaments, and circular smooth muscle cells featured desmin immunoreactivity. SEM showed that IC-DMP had thin and flat cell bodies with numerous branching processes. These cells came into close contact with nerve fibers and circular smooth muscle cells. The findings that IC-DMP cells contained myosin thick filaments and were immunopositive for anti-smooth muscle actin suggest that they may be more properly categorized as a type of smooth muscle cell.
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Montgomery, Laura E. A., Etain A. Tansey, Chris D. Johnson, Sean M. Roe, and Joe G. Quinn. "Autonomic modification of intestinal smooth muscle contractility." Advances in Physiology Education 40, no. 1 (March 2016): 104–9. http://dx.doi.org/10.1152/advan.00038.2015.
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Intestinal smooth muscle contracts rhythmically in the absence of nerve and hormonal stimulation because of the activity of pacemaker cells between and within the muscle layers. This means that the autonomic nervous system modifies rather than initiates intestinal contractions. The practical described here gives students an opportunity to observe this spontaneous activity and its modification by agents associated with parasympathetic and sympathetic nerve activity. A section of the rabbit small intestine is suspended in an organ bath, and the use of a pressure transducer and data-acquisition software allows the measurement of tension generated by the smooth muscle of intestinal walls. The application of the parasympathetic neurotransmitter ACh at varying concentrations allows students to observe an increase in intestinal smooth muscle tone with increasing concentrations of this muscarinic receptor agonist. Construction of a concentration-effect curve allows students to calculate an EC50 value for ACh and consider some basic concepts surrounding receptor occupancy and activation. Application of the hormone epinephrine to the precontracted intestine allows students to observe the inhibitory effects associated with sympathetic nerve activation. Introduction of the drug atropine to the preparation before a maximal concentration of ACh is applied allows students to observe the inhibitory effect of a competitive antagonist on the physiological response to a receptor agonist. The final experiment involves the observation of the depolarizing effect of K+ on smooth muscle. Students are also invited to consider why the drugs atropine, codeine, loperamide, and botulinum toxin have medicinal uses in the management of gastrointestinal problems.
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Hirst, G. David S., Frank R. Edwards, Dianna J. Gould, Shaun L. Sandow, and Caryl E. Hill. "Electrical properties of iridial arterioles of the rat." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 5 (November 1, 1997): H2465—H2472. http://dx.doi.org/10.1152/ajpheart.1997.273.5.h2465.
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When intracellular recordings were made from iridial arterioles, the cells had membrane potentials of about −65 mV and perivascular nerve stimulation evoked a membrane depolarization. When these cells were labeled with lucifer yellow, all cells that responded to perivascular nerve stimulation had the morphological characteristics of smooth muscle cells. Cells with the morphological characteristics of endothelial cells were never stained. When impaled with two separate recording electrodes, the smooth muscle layer was shown to form an electrical syncytium with a membrane time constant of ∼80 ms and an electrical length constant of ∼900 μm. At the ultrastructural level, areas of close apposition were frequently observed between adjacent smooth muscle cells and between adjacent endothelial cells. On the other hand, at contacts between smooth muscle and endothelial cells, the membranes characteristically had much larger separations. The observations show that individual smooth muscle cells are electrically coupled to their neighbors, but the morphological studies raise the possibility that in these arterioles the endothelial and muscle layers are electrically separate.
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Wu, Z. X., K. B. Benders, D. D. Hunter, and R. D. Dey. "Early postnatal exposure of mice to side-steam tobacco smoke increases neuropeptide Y in lung." American Journal of Physiology-Lung Cellular and Molecular Physiology 302, no. 1 (January 1, 2012): L152—L159. http://dx.doi.org/10.1152/ajplung.00071.2011.
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Our recent study showed that prenatal and early postnatal exposure of mice to side-steam tobacco smoke (SS), a surrogate to environmental tobacco smoke (ETS), leads to increased airway responsiveness and sensory innervation later in life. However, the underlying mechanism initiated in early life that affects airway responses later in life remains undefined. The concomitant increase in nerve growth factor (NGF) after exposures suggests that NGF may be involved the regulation of airway innervation. Since NGF regulates sympathetic nerve responses, as well as sensory nerves, we extended previous studies by examining neuropeptide Y (NPY), a neuropeptide associated with sympathetic nerves. Different age groups of mice, postnatal day (PD) 2 and PD21, were exposed to either SS or filtered air (FA) for 10 consecutive days. The level of NPY protein in lung and the density of NPY nerve fibers in tracheal smooth muscle were significantly increased in the PD2–11SS exposure group compared with PD2–11FA exposure. At the same time, the level of NGF in lung tissue was significantly elevated in the PD2–11SS exposure groups. However, neither NPY (protein or nerves) nor NGF levels were significantly altered in PD21–30SS exposure group compared with the PD21–30FA exposure group. Furthermore, pretreatment with NGF antibody or K252a, which inhibits a key enzyme (tyrosine kinase) in the transduction pathway for NGF receptor binding, significantly diminished SS-enhanced NPY tracheal smooth muscle innervation and the increase in methacholine-induced airway resistance. These findings show that SS exposure in early life increases NPY tracheal innervation and alters pulmonary function and that these changes are mediated through the NGF.
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Huizinga, Jan D., Irene Berezin, Edwin E. Daniel, and Edwin Chow. "Inhibitory innervation of colonic smooth muscle cells and interstitial cells of Cajal." Canadian Journal of Physiology and Pharmacology 68, no. 3 (March 1, 1990): 447–54. http://dx.doi.org/10.1139/y90-063.
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The effect of neural inhibition on the electrical activities of circular and longitudinal colonic smooth muscle was investigated. In addition, a comparative study was carried out between circular muscle preparations with and without the "submucosal" and "myenteric plexus" network of interstitial cells of Cajal (ICC) to study innervation of the "submucosal" ICC and to investigate whether or not the ICC network is an essential intermediary system for inhibitory innervation of smooth muscle cells. Electrical stimulation of intrinsic nerves in the presence of atropine caused inhibitory junction potentials (ijps) throughout the circular and longitudinal muscle layers. The ijp amplitude depended on the membrane potential and not on the location of the muscle cells with respect to the ICC network. Neurally mediated inhibition of the colon resulted in a reduction in amplitude and duration of slow wave type action potentials in circular and abolishment of spike-like action potentials in longitudinal smooth muscle, both resulting in a reduction of contractile activity. With respect to mediation by ICC, the study shows (i) "submucosal" ICC receive direct inhibitory innervation and (ii) circular smooth muscle cells can be directly innervated by inhibitory nerves without ICC as necessary intermediaries. The reversal potential of the ijp in colonic smooth muscle was observed to be approximately −76 mV, close to the estimated potassium equilibrium potential, suggesting that the nerve-mediated hyperpolarization is caused by increased potassium conductance.Key words: enteric nerves, potassium conductance, pacemaker activity, VIP, inhibitory junction potential.
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Manders, Ernest K., Gregory C. Saggers, Peter Diaz-Alonso, Laura Finn, James C. Sipio, Thomas Glumac, Victor K. Au, Randcilp K. M. Wong, and Mamdouh Mottaleb. "Elongation of Peripheral Nerve and Viscera Containing Smooth Muscle." Clinics in Plastic Surgery 14, no. 3 (July 1987): 551–62. http://dx.doi.org/10.1016/s0094-1298(20)31525-x.
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Jones, Mirka W., Henry J. Norris, and Eric S. Wargotz. "Smooth Muscle and Nerve Sheath Tumors of the Breast." International Journal of Surgical Pathology 2, no. 2 (October 1994): 85–92. http://dx.doi.org/10.1177/106689699400200202.
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Abou-Al-Shaar, Hussam, Michael Karsy, Ilyas M. Eli, Jayant P. Agarwal, Barbu Gociman, and Mark A. Mahan. "Masseter-to-facial nerve transfer for facial nerve reanimation." Neurosurgical Focus: Video 8, no. 1 (January 2023): V6. http://dx.doi.org/10.3171/2022.9.focvid22107.
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Smooth symmetric facial muscle function is important for social interactions. When lesions of the facial nerve occur, achieving complete restoration of balanced and spontaneous facial function can be challenging. In this video, the authors demonstrate the surgical details and long-term follow-up of a masseter-to-facial nerve transfer in a 3-year-old girl who had insidious onset of a left facial palsy due to a facial nerve schwannoma. After resection, she underwent distal nerve repair with a masseter-to-zygomatic branch transfer. She demonstrated decreased lagophthalmos and good activation and excursion on the left side with near symmetry to the right side, but lacked left frontalis function. The video can be found here: https://stream.cadmore.media/r10.3171/2022.9.FOCVID22107
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Heppner, Thomas J., Nathan R. Tykocki, David Hill-Eubanks, and Mark T. Nelson. "Transient contractions of urinary bladder smooth muscle are drivers of afferent nerve activity during filling." Journal of General Physiology 147, no. 4 (March 14, 2016): 323–35. http://dx.doi.org/10.1085/jgp.201511550.
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Activation of afferent nerves during urinary bladder (UB) filling conveys the sensation of UB fullness to the central nervous system (CNS). Although this sensory outflow is presumed to reflect graded increases in pressure associated with filling, UBs also exhibit nonvoiding, transient contractions (TCs) that cause small, rapid increases in intravesical pressure. Here, using an ex vivo mouse bladder preparation, we explored the relative contributions of filling pressure and TC-induced pressure transients to sensory nerve stimulation. Continuous UB filling caused an increase in afferent nerve activity composed of a graded increase in baseline activity and activity associated with increases in intravesical pressure produced by TCs. For each ∼4-mmHg pressure increase, filling pressure increased baseline afferent activity by ∼60 action potentials per second. In contrast, a similar pressure elevation induced by a TC evoked an ∼10-fold greater increase in afferent activity. Filling pressure did not affect TC frequency but did increase the TC rate of rise, reflecting a change in the length-tension relationship of detrusor smooth muscle. The frequency of afferent bursts depended on the TC rate of rise and peaked before maximum pressure. Inhibition of small- and large-conductance Ca2+-activated K+ (SK and BK) channels increased TC amplitude and afferent nerve activity. After inhibiting detrusor muscle contractility, simulating the waveform of a TC by gently compressing the bladder evoked similar increases in afferent activity. Notably, afferent activity elicited by simulated TCs was augmented by SK channel inhibition. Our results show that afferent nerve activity evoked by TCs represents the majority of afferent outflow conveyed to the CNS during UB filling and suggest that the maximum TC rate of rise corresponds to an optimal length-tension relationship for efficient UB contraction. Furthermore, our findings implicate SK channels in controlling the gain of sensory outflow independent of UB contractility.
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Giannini, Caterina, Carol Reynolds, Jacqueline A. Leavitt, Gregory A. Schultz, James A. Garrity, Michael J. Ebersold, Bernd W. Scheithauer, and Diva R. Salomao. "Choristoma of the Optic Nerve: Case Report." Neurosurgery 50, no. 5 (May 1, 2002): 1125–28. http://dx.doi.org/10.1097/00006123-200205000-00032.
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Abstract OBJECTIVE AND IMPORTANCE: Optic nerve choristoma is a rare lesion composed of adipose tissue and smooth muscle involving the optic nerve. Few cases have been reported. CLINICAL PRESENTATION: A 20-year-old woman presented with a history of slowly progressive visual loss in the left eye. On T1-weighted magnetic resonance imaging studies, after frequency-selective fat saturation, an optic nerve mass was detected at the level of the optic canal with signal characteristics suggesting the diagnosis of optic nerve lipoma. INTERVENTION: At left frontotemporal craniotomy, the intracranial optic nerve appeared thin and atrophic proximally and was covered by abundant adipose tissue distally. Because no cleavage plane could be identified between the fatty lesion and the optic nerve, which appeared splayed within the adipose tissue, the nerve was resected after an intraoperative biopsy. The presence of two heterotopic mesodermal elements, a rim of adipose tissue admixed with bundles of mature smooth muscle, extending into the nerve septa, warranted a diagnosis of optic nerve choristoma. CONCLUSION: Optic nerve choristoma is an uncommon optic nerve lesion. Even if imaging studies are highly suggestive of the diagnosis, pathological confirmation is required because of the high adipose tissue content in the majority of cases. The lesion, most likely malformative and nonneoplastic in nature, can be the cause of progressive visual loss.
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Toda, N., and T. Okamura. "Regulation by Nitroxidergic Nerve of Arterial Tone." Physiology 7, no. 4 (August 1, 1992): 148–52. http://dx.doi.org/10.1152/physiologyonline.1992.7.4.148.
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Nitric oxide plays a crucial role in transmitting information from nonadrenergic, noncholinergic vasodilator nerve to cerebroarterial smooth muscle. Since nitric oxide acts as transmitter, the nerve is termed "nitroxidergic." Mesenteric and temporal arterial tone appears to be regulated by reciprocal nitroxidergic and noradrenergic innervation.
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Motley, E. D., R. J. Paul, and M. A. Matlib. "Role of Na(+)-Ca2+ exchange in the regulation of vascular smooth muscle tension." American Journal of Physiology-Heart and Circulatory Physiology 264, no. 4 (April 1, 1993): H1028—H1040. http://dx.doi.org/10.1152/ajpheart.1993.264.4.h1028.
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To determine the role of the Na(+)-Ca2+ exchange systems of nerve terminal and sarcolemmal membrane on development of tension in rabbit aortic rings, internal or external Na+ concentration was changed with either ouabain or Na(+)-free solution, respectively. Ouabain produced a verapamil-insensitive but external Na(+)- and Ca(2+)-dependent biphasic tension with distinct lag periods both of which were shortened by depolarization with KCl. The first phase of tension was inhibited by prazosin, phentolamine, in vitro neurolysis with 6-hydroxydopamine and in vivo treatment with reserpine to deplete catecholamines in nerve terminals. Therefore, first phase of tension was attributed to catecholamines released from nerve terminals induced by increased axoplasmic Ca2+ concentration mediated by the neural Na(+)-Ca2+ exchanger due to the increased axoplasmic Na+ concentration resulting from inhibition of the Na(+)-Ka+ pump with ouabain. In the absence of the first phase of tension, the second phase of tension was enhanced by caffeine, presumably by preventing sequestration of the sarcolemmal Na(+)-Ca2+ exchanger-mediated increase in cytosolic Ca2+ concentration in vascular smooth muscle cells. The prazosin-insensitive tension was dependent on the external Na+ concentration and was also attributed to the sarcolemmal Na(+)-Ca2+ exchanger of vascular smooth muscle. The magnitude of the increase in tension with ouabain or Na(+)-free solution attributed to the sarcolemmal Na(+)-Ca2+ exchanger of vascular smooth muscle was larger than that mediated by the exchanger of the nerve terminal. It was concluded that the Na(+)-Ca2+ exchange systems of both the nerve terminal and the vascular smooth muscle sarcolemma contribute to the development of tension by different mechanisms and to different extents when internal or external Na+ concentration was changed.
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Mahbub, Zaid Bin, JH Karami, and K. Siddique-e. Rabbani. "Analysis of Evoked EMG using Wavelet Transformation." Bangladesh Journal of Medical Physics 5, no. 1 (April 19, 2013): 41–51. http://dx.doi.org/10.3329/bjmp.v5i1.14667.
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Evoked EMG M-responses obtained from the thenar muscle in the palm by electrical stimulation of the median nerve demonstrate a well-established smooth bipolar shape for normal healthy subjects while kinks are observed in certain neurological disorders, particularly in cervical spondylotic neuropathy. A first differentiation failed to identify these kinks because of comparable values obtained for normally rising and falling segments of the smooth regions, and due to noise. In this study, the usefulness of the wavelet transform (WT), that provides localized measures of non-stationary signals is investigated. The Haar WT was used to analyze a total of 36 M-responses recorded from the median nerves of 6 normal subjects (having smooth shape) and 12 subjects with assumed neurological disorders (having kinks), for two points of stimulation on the same nerve. Features in the time-scale representation of the M-responses were studied using WT to distinguish smooth M-responses from ones with kinks. Variations in the coefficient line of the WT were also studied to allow visualization of WT at different scales (inverse of frequency). The high and low frequency regions in the WT came out distinctively which helped identifications of kinks even of very subtle ones in the M-responses which were difficult to obtain using the differentiated signal. In conclusion, the wavelet analysis may be a technique of choice in identifying kinks in M-responses in relation to time, thus enhancing the accuracy of neurological diagnosis. DOI: http://dx.doi.org/10.3329/bjmp.v5i1.14667 Bangladesh Journal of Medical Physics Vol.5 No.1 2012 41-51
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Xiao, Lan, and Zhong-Xin Wu. "Substance P Regulates Environmental Tobacco Smoke-Enhanced Tracheal Smooth Muscle Responsiveness in Mice." Journal of Allergy 2012 (August 13, 2012): 1–10. http://dx.doi.org/10.1155/2012/423612.
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Environmental tobacco smoke (ETS) is an environmental trigger that leads to airway inflammation and airway hyperresponsiveness (AHR) in susceptible individuals and animals, but the underlying mechanism is not fully understood. Substance P (SP) release from sensory nerve fibers has been linked to AHR. The present experiments characterize the role of SP in tracheal smooth muscle on ETS-increased airway responses. The mice were exposed to either sidestream tobacco smoke (SS), a surrogate to ETS, or filtered air (FA) for 1 day or 5 consecutive days. Contractions of tracheal smooth muscle to SP and electrical field stimulation (EFS) were not significantly altered in 1 of day SS-exposed mice. However, 5 of days SS exposure significantly increased airway smooth muscle contractions to SP and EFS. Administration of CP-99994, an antagonist of the neurokinin (NK)1 receptor, attenuates the SS exposure-enhanced tracheal smooth muscle responses to EFS. Furthermore, the immunohistochemistry showed that SP nerve fibers were increased in tracheal smooth muscle after 5 of days SS exposure. These results suggest that the increased SP production may contribute to SS-enhanced smooth muscle responsiveness in mice trachea.
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Daniel, E. E., Ahmed El Yazbi, Marco Mannarino, Gary Galante, Geoffrey Boddy, Jonathan Livergant, and Tahereh Eteraf Oskouei. "Do gap junctions play a role in nerve transmissions as well as pacing in mouse intestine?" American Journal of Physiology-Gastrointestinal and Liver Physiology 292, no. 3 (March 2007): G734—G745. http://dx.doi.org/10.1152/ajpgi.00428.2006.
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Varicosities of nitrergic and other nerves end on deep muscular plexus interstitial cells of Cajal or on CD34-positive, c- kit-negative fibroblast-like cells. Both cell types connect to outer circular muscle by gap junctions, which may transmit nerve messages to muscle. We tested the hypotheses that gap junctions transmit pacing messages from interstitial cells of Cajal of the myenteric plexus. Effects of inhibitors of gap junction conductance were studied on paced contractions and nerve transmissions in small segments of circular muscle of mouse intestine. Using electrical field stimulation parameters (50 V/cm, 5 pps, and 0.5 ms) which evoke near maximal responses to nitrergic, cholinergic, and apamin-sensitive nerve stimulation, we isolated inhibitory responses to nitrergic nerves, inhibitory responses to apamin-sensitive nerves and excitatory responses to cholinergic nerves. 18β-Glycyrrhetinic acid (10, 30, and 100 μM), octanol (0.1, 0.3, and 1 mM) and gap peptides (300 μM of40Gap27,43Gap26,37,43Gap27) all failed to abolish neurotransmission. 18β-Glycyrrhetinic acid inhibited frequencies of paced contractions, likely owing to inhibition of l-type Ca2+channels in smooth muscle, but octanol or gap peptides did not. 18β-Glycyrrhetinic acid and octanol, but not gap peptides, reduced the amplitudes of spontaneous and nerve-induced contractions. These reductions paralleled reductions in contractions to exogenous carbachol. Additional experiments with gap peptides in both longitudinal and circular muscle segments after NG-nitro-l-arginine and TTX revealed no effects on pacing frequencies. We conclude that gap junction coupling may not be necessary for pacing or nerve transmission to the circular muscle of the mouse intestine.
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Wu, Z. X., B. E. Satterfield, J. S. Fedan, and R. D. Dey. "Interleukin-1β-induced airway hyperresponsiveness enhances substance P in intrinsic neurons of ferret airway." American Journal of Physiology-Lung Cellular and Molecular Physiology 283, no. 5 (November 1, 2002): L909—L917. http://dx.doi.org/10.1152/ajplung.00363.2001.
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Interleukin (IL)-1β causes airway inflammation, enhances airway smooth muscle responsiveness, and alters neurotransmitter expression in sensory, sympathetic, and myenteric neurons. This study examines the role of intrinsic airway neurons in airway hyperresponsiveness (AHR) induced by IL-1β. Ferrets were instilled intratracheally with IL-1β (0.3 μg/0.3 ml) or saline (0.3 ml) once daily for 5 days. Tracheal smooth muscle contractility in vitro and substance P (SP) expression in tracheal neurons were assessed. Tracheal smooth muscle reactivity to acetylcholine (ACh) and methacholine (MCh) and smooth muscle contractions to electric field stimulation (EFS) both increased after IL-1β. The IL-1β-induced AHR was maintained in tracheal segments cultured for 24 h, a procedure that depletes SP from sensory nerves while maintaining viability of intrinsic airway neurons. Pretreatment with CP-99994, an antagonist of neurokinin 1 receptor, attenuated the IL-1β-induced hyperreactivity to ACh and MCh and to EFS in cultured tracheal segments. SP-containing neurons in longitudinal trunk, SP innervation of superficial muscular plexus neurons, and SP nerve fiber density in tracheal smooth muscle all increased after treatment with IL-1β. These results show that IL-1β-enhanced cholinergic airway smooth muscle contractile responses are mediated by the actions of SP released from intrinsic airway neurons.