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Junction Potentials (junction + potential)
Kinds of Junction Potentials Selected AbstractsSynchronization of enteric neuronal firing during the murine colonic MMCTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005Nick J. Spencer DiI (1,1,didodecyl-3,3,3,,3,-tetramethylindocarbecyanine perchlorate) retrograde labelling and intracellular electrophysiological techniques were used to investigate the mechanisms underlying the generation of spontaneously occurring colonic migrating myoelectric complexes (colonic MMCs) in mice. In isolated, intact, whole colonic preparations, simultaneous intracellular electrical recordings were made from pairs of circular muscle (CM) cells during colonic MMC activity in the presence of nifedipine (1,2 ,m). During the intervals between colonic MMCs, spontaneous inhibitory junction potentials (IJPs) were always present. The amplitudes of spontaneous IJPs were highly variable (range 1,20 mV) and occurred asynchronously in the two CM cells, when separated by 1 mm in the longitudinal axis. Colonic MMCs occurred every 151 ± 7 s in the CM and consisted of a repetitive discharge of cholinergic rapid oscillations in membrane potential (range: 1,20 mV) that were superimposed on a slow membrane depolarization (mean amplitude: 9.6 ± 0.5 mV; half-duration: 25.9 ± 0.7 s). During the rising (depolarizing) phase of each colonic MMC, cholinergic rapid oscillations occurred simultaneously in both CM cells, even when the two electrodes were separated by up to 15 mm along the longitudinal axis of the colon. Smaller amplitude oscillations (< 5 mV) showed poor temporal correlation between two CM cells, even at short electrode separation distances (i.e. < 1 mm in the longitudinal axis). When the two electrodes were separated by 20 mm, all cholinergic rapid oscillations and IJPs in the CM (regardless of amplitude) were rarely, if ever, coordinated in time during the colonic MMC. Cholinergic rapid oscillations were blocked by atropine (1 ,m) or tetrodotoxin (1 ,m). Slow waves were never recorded from any CM cells. DiI labelling showed that the maximum projection length of CM motor neurones and interneurones along the bowel was 2.8 mm and 13 mm, respectively. When recordings were made adjacent to either oral or anal cut ends of the colon, the inhibitory or excitatory phases of the colonic MMC were absent, respectively. In summary, during the colonic MMC, cholinergic rapid oscillations of similar amplitudes occur simultaneously in two CM cells separated by large distances (up to 15 mm). As this distance was found to be far greater than the projection length of any single CM motor neurone, we suggest that the generation of each discrete cholinergic rapid oscillation represents a discreet cholinergic excitatory junction potential (EJP) that involves the synaptic activation of many cholinergic motor neurones simultaneously, by synchronous firing in many myenteric interneurones. Our data also suggest that ascending excitatory and descending inhibitory nerve pathways interact and reinforce each other. [source] Excitatory purinergic neurotransmission in smooth muscle of guniea-pig taenia caeciTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005Yong Zhang Non-adrenergic, non-cholinergic (NANC) inhibitory neurotransmission has been an area of intense interest in gut motor physiology, whereas excitatory NANC neurotransmission has received less attention. In order to further explore excitatory NANC neurotransmission, we performed conventional intracellular recordings from guinea-pig taenia caeci smooth muscle. Tissue was perfused with oxygenated Krebs solution at 35°C and nerve responses evoked by either oral or aboral nerve stimulation (NS) (4 square wave pulses, 0.3 ms duration, 20 Hz). Electrical activity was characterized by slow waves upon which one to three action potentials were superimposed. Oral NS evoked an inhibitory junction potential (IJP) at either the valley or peak of the slow wave. Application of nifedipine (1 ,m) abolished slow waves and action potentials, but membrane potential flunctuations (1,3 mV) and IJPs remained unaffected. Concomitant application of apamin (300 nm), a small-conductance Ca2+ -activated K+ channel blocker, converted the IJP to an EJP that was followed by slow IJP. Further administration of NG -nitro- l -arginine methyl ester (l -NAME, 200 ,m), a nitric oxide synthase inhibitor, abolished the slow IJP without affecting the EJP, implying that the slow IJP is due to nitrergic innervation. The EJP was abolished by tetrodotoxin (1 ,m), but was not significantly affected by atropine (3 ,m) and guanethidine (3 ,m) or hexamethonium (500 ,m). Substance P (SP, 1 ,m) desensitization caused slight attenuation of the EJP, but the EJP was abolished by desensitization with ,,,-methylene ATP (50 ,m), a P2 purinoceptor agonist that is more potent than ATP at the P2X receptor subtype, suramin (100 ,m), a non-selective P2 purinoceptor antagonist, and pyridoxal-phosphate-6-azophenyl-2,,4,-disulphonic acid (PPADS, 100 ,m), a selective P2X purinoceptor antagonist. In contrast, the EJP was unaffected by MRS-2179 (2 ,m), a selective P2Y1 receptor antagonist. Aboral NS evoked an apamin- and l -NAME-sensitive IJP, but virtually no NANC EJP. These data suggest the presence of polarized excitatory purinergic neurotransmission in guinea-pig taenia caeci, which appears to be mediated by P2X purinoceptors, most likely the P2X1 subtype. [source] A Reference Electrode for Electrochemical and Cryoelectrochemical Use in Tetrahydrofuran SolventELECTROANALYSIS, Issue 21 2005Christopher Abstract We report a reference electrode for direct use in tetrahydrofuran (THF) at low temperatures. A reference solution containing equimolar amounts of ferrocene/ferrocenium hexafluorophosphate (Fc/Fc+) are prepared to give a 4,mM solution in THF that contains tetrabutylammonium hexafluorophosphate (TBAF) supporting electrolyte thus, minimizing liquid junction potentials. The reference solution is added to a sealed glass tube with a porous frit at one end, and a platinum wire is inserted into the tube. The reference electrode assembly is then inserted into a THF test solution. Potentiometric measurements show that the system responds in the expected Nernstian fashion over the concentration and temperature ranges, 4,mM to 40,,M and 20,°C to ,45,°C respectively. In addition, it is shown by steady,state cyclic voltammetry at a platinum microelectrode that the chemical reactivity of ferrocenium hexafluorophosphate (Fc+) otherwise seen in THF is suppressed by ion-pairing with PF using tetrabutylammonium hexafluorophosphate (TBAF) as the supporting electrolyte. [source] Recent advances in enteric neurobiology: mechanosensitive interneuronsNEUROGASTROENTEROLOGY & MOTILITY, Issue 11 2007T. K. Smith Abstract, Until recently, it was generally assumed that the only intrinsic sensory neuron, or primary afferent neuron, in the gut was the after-hyperpolarizing AH/Type II neuron. AH neurons excited by local chemical and mechanical stimulation of the mucosa appear to be necessary for activating the peristaltic reflex (oral excitation and anal inhibition of the muscle layers) and anally propagating ring like contractions (peristaltic waves) that depend upon smooth muscle tone. However, our recent findings in the guinea-pig distal colon suggest that different neurochemical classes of interneuron in the colon are also mechanosensitive in that they respond directly to changes in muscle length, rather than muscle tone or tension. These interneurons have electrophysiological properties consistent with myenteric S-neurons. Ascending and descending interneurons respond directly to circumferential stretch by generating an ongoing polarized peristaltic reflex activity (oral excitatory and anal inhibitory junction potentials) in the muscle for as long as the stimulus is maintained. Some descending (nitric oxide synthase +ve) interneurons, on the other hand, appear to respond directly to longitudinal stretch and are involved in accommodation and slow transit of faecal pellets down the colon. This review will present recent evidence that suggests some myenteric S interneurons, in addition to AH neurons, behave as intrinsic sensory neurons. [source] Synchronization of enteric neuronal firing during the murine colonic MMCTHE JOURNAL OF PHYSIOLOGY, Issue 3 2005Nick J. Spencer DiI (1,1,didodecyl-3,3,3,,3,-tetramethylindocarbecyanine perchlorate) retrograde labelling and intracellular electrophysiological techniques were used to investigate the mechanisms underlying the generation of spontaneously occurring colonic migrating myoelectric complexes (colonic MMCs) in mice. In isolated, intact, whole colonic preparations, simultaneous intracellular electrical recordings were made from pairs of circular muscle (CM) cells during colonic MMC activity in the presence of nifedipine (1,2 ,m). During the intervals between colonic MMCs, spontaneous inhibitory junction potentials (IJPs) were always present. The amplitudes of spontaneous IJPs were highly variable (range 1,20 mV) and occurred asynchronously in the two CM cells, when separated by 1 mm in the longitudinal axis. Colonic MMCs occurred every 151 ± 7 s in the CM and consisted of a repetitive discharge of cholinergic rapid oscillations in membrane potential (range: 1,20 mV) that were superimposed on a slow membrane depolarization (mean amplitude: 9.6 ± 0.5 mV; half-duration: 25.9 ± 0.7 s). During the rising (depolarizing) phase of each colonic MMC, cholinergic rapid oscillations occurred simultaneously in both CM cells, even when the two electrodes were separated by up to 15 mm along the longitudinal axis of the colon. Smaller amplitude oscillations (< 5 mV) showed poor temporal correlation between two CM cells, even at short electrode separation distances (i.e. < 1 mm in the longitudinal axis). When the two electrodes were separated by 20 mm, all cholinergic rapid oscillations and IJPs in the CM (regardless of amplitude) were rarely, if ever, coordinated in time during the colonic MMC. Cholinergic rapid oscillations were blocked by atropine (1 ,m) or tetrodotoxin (1 ,m). Slow waves were never recorded from any CM cells. DiI labelling showed that the maximum projection length of CM motor neurones and interneurones along the bowel was 2.8 mm and 13 mm, respectively. When recordings were made adjacent to either oral or anal cut ends of the colon, the inhibitory or excitatory phases of the colonic MMC were absent, respectively. In summary, during the colonic MMC, cholinergic rapid oscillations of similar amplitudes occur simultaneously in two CM cells separated by large distances (up to 15 mm). As this distance was found to be far greater than the projection length of any single CM motor neurone, we suggest that the generation of each discrete cholinergic rapid oscillation represents a discreet cholinergic excitatory junction potential (EJP) that involves the synaptic activation of many cholinergic motor neurones simultaneously, by synchronous firing in many myenteric interneurones. Our data also suggest that ascending excitatory and descending inhibitory nerve pathways interact and reinforce each other. [source] Rho kinase inhibitors reduce neurally evoked contraction of the rat tail artery in vitroBRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2005Melanie Yeoh The effects of Rho kinase inhibitors (Y27632, HA-1077) on contractions to electrical stimulation and to application of phenylephrine, clonidine or ,,, -methylene adenosine 5,-triphosphate (,,, -mATP) were investigated in rat tail artery in vitro. In addition, continuous amperometry and intracellular recording were used to monitor the effects of Y27632 on noradrenaline (NA) release and postjunctional electrical activity, respectively. Y27632 (0.5 and 1 ,M) and HA-1077 (5 ,M) reduced neurally evoked contractions. In contrast, the protein kinase C inhibitor, Ro31-8220 (1 ,M), had little effect on neurally evoked contraction. In the absence and the presence of Y27632 (0.5 ,M), the reduction of neurally evoked contraction produced by the , -adrenoceptor antagonists prazosin (10 nM) and idazoxan (0.1 ,M) was similar. The P2-purinoceptor antagonist, suramin (0.1 mM), had no inhibitory effect on neurally evoked contraction in the absence or the presence of Y27632 (1 ,M). In the presence of Y27632, desensitization of P2X-purinoceptors with ,,, -mATP (10 ,M) increased neurally evoked contractions. Y27632 (1 ,M) and H-1077 (5 ,M) reduced sensitivity to phenylephrine and clonidine. In addition, Y27632 reduced contractions to ,,, -mATP (10 ,M). Y27632 (1 ,M) had no effect on the NA-induced oxidation currents or the purinergic excitatory junction potentials and NA-induced slow depolarizations evoked by electrical stimulation. Rho kinase inhibitors reduce sympathetic nerve-mediated contractions of the tail artery. This effect is mediated at a postjunctional site, most likely by inhibition of Rho kinase-mediated ,Ca2+ sensitization' of the contractile apparatus. British Journal of Pharmacology (2005) 146, 854,861. doi:10.1038/sj.bjp.0706377 [source] Role of sarcoplasmic reticulum in control of membrane potential and nitrergic response in opossum lower esophageal sphincterBRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2003Yong Zhang We previously demonstrated that a balance of Ca2+ -activated Cl, current (ICl(Ca)) and K+ current activity sets the resting membrane potential of opossum lower esophageal sphincter (LES) circular smooth muscle at ,,41 mV, which leads to continuous spike-like action potentials and the generation of basal tone. Ionic mechanisms underlying this basal ICl(Ca) activity and its nitrergic regulation remain unclear. Recent studies suggest that spontaneous Ca2+ release from sarcoplasmic reticulum (SR) and myosin light chain kinase (MLCK) play important roles. The current study investigated this possibility. Conventional intracellular recordings were performed on circular smooth muscle of opossum LES. Nerve responses were evoked by electrical square wave pulses of 0.5 ms duration at 20 Hz. In the presence of nifedipine (1 ,M), substance P (1 ,M), atropine (3 ,M) and guanethidine (3 ,M), intracellular recordings demonstrated a resting membrane potential (MP) of ,38.1±0.7 mV (n=25) with spontaneous membrane potential fluctuations (MPfs) of 1,3 mV. Four pulses of nerve stimulation induced slow inhibitory junction potentials (sIJPs) with an amplitude of 6.1±0.3 mV and a half-amplitude duration of 1926±147 ms (n=25). 1H -[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ), a specific guanylyl cyclase inhibitor, abolished sIJPs, but had no effects on MPfs. Caffeine, a ryanodine receptor agonist, hyperpolarized MP and abolished sIJPs and MPfs. Ryanodine (20 ,M) inhibited the sIJP and induced biphasic effects on MP, an initial small hyperpolarization followed by a large depolarization. sIJPs and MPfs were also inhibited by cyclopiazonic acid, an SR Ca2+ ATPase inhibitor. Specific ICl(Ca) and MLCK inhibitors hyperpolarized the MP and inhibited MPfs and sIJPs. These data suggest that (1) spontaneous release of Ca2+ from the SR activates ICl(Ca), which in turn contributes to resting membrane potential; (2) MLCK is involved in activation of ICl(Ca); (3) inhibition of ICl(Ca) is likely to underlie sIJPs induced by nitrergic innervation. British Journal of Pharmacology (2003) 140, 1097,1107. doi:10.1038/sj.bjp.0705537 [source] Involvement of T-type calcium channels in excitatory junction potentials in rat resistance mesenteric arteriesBRITISH JOURNAL OF PHARMACOLOGY, Issue 6 2002Qi Xi We investigated the role of voltage-operated calcium channels in sympathetic transmission and depolarization-induced contractions in the rat mesenteric artery. In particular, we investigated the role of the T-type voltage-operated calcium channels (T-channels) in mediating excitatory junction potentials (EJPs). EJPs were evoked by electrical field stimulation (trains of five stimuli at 0.9 Hz) in small mesenteric arteries. The average resting membrane potential was ,59.8±0.5 mV (n=65). Trains of stimuli evoked individual EJPs with the peak EJP of 6±0.2 mV (n=34) occurring with the second stimulus. Trains of EJPs were inhibited 90% by tetrodotoxin (0.1 ,M) or by ,-conotoxin GVIA (GVIA, 10 nM) indicating their neural origin. The EJPs were not inhibited by the L-type calcium channel blocker nicardipine at 0.1 ,M, a concentration sufficient to abolish the contraction to potassium depolarization. However, mibefradil (3 ,M), considered a relatively selective T-channel antagonist, inhibited the EJPs by about 50%. This concentration of mibefradil did not inhibit GVIA-sensitive electrically-evoked twitches of the rat vas deferens. Thus the action of mibefradil in reducing EJPs is unlikely to be due to either inhibition of L- or N-type channels but is probably due to inhibition of T-channels. The finding that Ni2+ (300 ,M), an inhibitor of T-type calcium channels, also reduced EJP amplitude by about 80% but did not block electrically-evoked twitches in the rat vas deferens, further supports an important role of T-channels in mediating small depolarizations associated with the EJPs evoked by sympathetic nerve stimulation. British Journal of Pharmacology (2002) 137, 805,812. doi:10.1038/sj.bjp.0704943 [source] Effects of a selective neuropeptide Y Y2 receptor antagonist, BIIE0246, on Y2 receptors at peripheral neuroeffector junctionsBRITISH JOURNAL OF PHARMACOLOGY, Issue 4 2001Margaret A Smith-White This study investigated the effects of BIIE0246, a novel neuropeptide Y (NPY) Y2 receptor antagonist, on the inhibition of cholinergic neuroeffector transmission in rat heart and guinea-pig trachea and purinergic neuroeffector transmission in guinea-pig vas deferens produced by the NPY Y2 receptor agonist, N-acetyl [Leu28,31] NPY 24-36. In pentobarbitone anaesthetized rats, supramaximal stimulation every 30 s, of the vagus nerve innervating the heart, increased pulse interval by approximately 100 ms. This response was attenuated by intravenous administration of N-acetyl [Leu28,31] NPY 24-36 (10 nmol kg,1). Transmural stimulation of segments of guinea-pig trachea at 1 min intervals with 5 s trains of stimuli at 0.5, 5, 10, 20 and 40 Hz evoked contractions which were reduced in force by N-acetyl [Leu28,31] NPY 24-36 (2 ,M). In guinea-pig vasa deferentia, the amplitude of excitatory junction potentials evoked by trains of 20 stimuli at 1 Hz was reduced in the presence of N-acetyl [Leu28,31] NPY 24-36 (1 ,M). In all preparations BIIE0246 attenuated the inhibitory effect of N-acetyl [Leu28,31] NPY 24-36 but had no effect when applied alone. The findings support the view that the nerve terminals of postganglionic parasympathetic and sympathetic neurones possess neuropeptide Y Y2 receptors which, when activated, reduce neurotransmitter release. British Journal of Pharmacology (2001) 132, 861,868; doi:10.1038/sj.bjp.0703879 [source] ARE GAP JUNCTIONS TRULY INVOLVED IN INHIBITORY NEUROMUSCULAR INTERACTION IN MOUSE PROXIMAL COLON?CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 8 2006Andrei Sibaev SUMMARY 1Gap junctions exist between circular muscle cells of the colon and between interstitial cells of Cajal (ICC) in the myenteric plexus of the gastrointestinal tract. They also probably couple intramuscular ICC with smooth muscle cells. Recent functional evidence for this was found in dye-coupling and myoelectrical experiments. 2In the present study, we tested the hypothesis of gap junctions putatively being involved in neuromuscular interaction in mouse colon by using different classes of gap junction blockers. 3Electrical field stimulation of the myenteric plexus elicited tetrodotoxin-sensitive and hexamethonium-independent fast and slow inhibitory junction potentials (fIJP and sIJP, respectively) in circular smooth muscle cells, as evaluated by intracellular recording techniques in impaled smooth muscle cells. Heptanol produced a time-dependent hyperpolarization of the membrane potential (MP) and abolished fIJP and sIJP. Octanol had no effect on the MP and abolished fIJP and sIJP. Carbenoxolone produced a time-dependent depolarization of the MP without any effect on fIJP or sIJP. The connexin 43 mimetic gap junction blocker GAP-27 had no effect on MP, fIJP or sIJP. 4Based on the presently available gap junction blockers we found no evidence that gap junctions are involved in neuromuscular transmission in mouse colon, as suggested by morphological studies. [source] Ongoing Nicotinic And Non-Nicotinic Inputs To Inhibitory Neurons In The Mouse ColonCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2001Andrew K Powell SUMMARY 1. Intracellular microelectrodes were used to record spontaneous and evoked inhibitory junction potentials (IJP) from the circular muscle layer of the mid-distal region of the mouse isolated colon in the presence of nifedipine (1 ,mol/L) and hyoscine (1 ,mol/L). 2. The length of the tissue preparation (> 1 cm) or the presence of the mucosa had no effect on the frequency of spontaneous IJP. 3. Hexamethonium (500 ,mol/L) reduced the frequency of spontaneous IJP to approximately 70% of the control frequency, whereas D -tubocurarine (280 ,mol/L) reduced the frequency to approximately 17% of control. Apamin (250 nmol/L) abolished all spontaneous IJP activity. 4. The greater inhibition of spontaneous IJP in the presence of D -tubocurarine compared with hexamethonium is discussed as a possible ,apamin-like' effect. 5. Although electrically evoked IJP (single pulse at 15 V, 0.6 msec) were not significantly affected by hexamethonium, D -tubocurarine and apamin reduced the amplitude of evoked IJP to approximately 65 and 50% of control, respectively. 6. These results suggest that the properties of spontaneous IJP cannot be inferred by a study of evoked IJP alone. [source] | ||||||||||