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At least 1,063 records · Page 59Linked to original sources
PubMed1989

Halothane and isoflurane alter acetylcholine activated ion channel kinetics.

The effects of halothane and isoflurane on the acetylcholine activated ion channel were studied in the frog sartorius muscle using the two electrode voltage clamp technique. The miniature end-plate currents (MEPCs) were recorded and evaluated for amplitude, duration of growth phase and time constant of decay (tau). Both halothane and isoflurane decreased tau in a dose dependent manner. Depression of current amplitude was also dose dependent. The ED50 value indicates tau is more affected than the amplitude of MEPC. Biexponential decay phases were seen in a small fraction of cells exposed to a low concentration of halothane but not isoflurane. Biexponential decay, when seen, was more prominent at less negative clamped membrane potential. The normal linear relationship between membrane potential and tau was not altered by anesthetics.

Acetylcholine↗
PubMed1989

Diazepam enhances the inhibitory action of adenosine on transmission at the frog neuromuscular junction.

The effect of diazepam and its interaction with adenosine on evoked endplate potentials (e.p.p.s) and on twitch tension were investigated in innervated sartorius muscles of the frog. Diazepam (100 microM) reversibly decreased the amplitude of the e.p.p.s and the twitch responses evoked by indirect stimulation, and reversibly increased the resting membrane potential recorded from the endplates. In a concentration (30 microM) virtually devoid of an effect on the e.p.p.s, twitch responses, or resting membrane potential of the muscle fibres, diazepam potentiated the inhibitory action of adenosine on neuromuscular transmission, but not that induced by the stable analogue of adenosine 5'-N-ethylcarboxamide adenosine (NECA), which is not a substrate for the adenosine uptake system. The potentiating effect of diazepam was not observed in the presence of dipyridamole, an adenosine uptake blocker which potentiated the effect of adenosine on neuromuscular transmission. Diazepam shifted to the left the concentration-response curve obtained for adenosine in the presence of the adenosine receptor antagonist 8-phenyltheophylline (8-PT). The results suggest that diazepam acts at the frog neuromuscular junction by increasing the level of adenosine at the junction level; this increase probably results from inhibition in the uptake of the nucleoside.

Adenosine↗
PubMed1990

Immunocytochemical evidence for an actin-myosin system in lens epithelial cells.

Since filamentous actin had been shown earlier to exist in lens epithelial and fiber cells, we inquired whether this could represent a contractile system with myosin and other actin-associated proteins. We resolved this question in freshly removed or organ-cultured rabbit and squirrel lens epithelial whole mounts using immunocytochemical techniques and by immunoblots of extracts separated by electrophoresis. In the former, methods were developed using long fixation times and long incubation in primary antibodies and biotinylated second antibodies visualized by streptavidin immunofluorescence and by diaminobenzidine peroxidase. Myosin was found to be localized along the filamentous rays and at central vertices of polygonal arrays situated at the apices of epithelial cells. It was not clear whether myosin and actin occurred together along the same or adjacent filaments in a bundle. Tubulin and vimentin were found deeper in the cells and were not aligned with actin and myosin filaments. Control lens epithelia treated similarly except for deletion of the primary antibodies showed no staining. As positive controls, pieces of glycerinated sartorius muscle exhibited characteristic cross-banded patterns of actin and myosin when incubated with the same reagents used on the lens epithelium. Denatured extracts of rabbit lens epithelium and of cortical fiber cells separated by electrophoresis and transferred to nitrocellulose paper, stained specifically with the same myosin and tubulin antibodies used in the immunocytochemistry experiments. The molecular weight profile of the myosin polypeptide indicated that lens tissue has myosin II. We conclude that a contractile system exists in lens epithelial and cortical fiber cells, although the function is not understood at this time. We conjecture that the system may act to stabilize lens shape by providing contractile tone.

Actins↗
PubMed1984

Effects of vinblastine in the frog neuromuscular junction during repetitive stimulation.

Vinblastine (10(-5) to 10(-4) M) applied in a Mg-blocked sciatic nerve-sartorius muscle preparation of the frog at the beginning of 20 min of repetitive stimulation of the nerve at 10 Hz, markedly inhibited the facilitation period. There was a smaller increase of end-plate potential amplitude, of quantal content, and of miniature end-plate potential (MEPP) frequency in comparison with that found in experiments without the drug. This depressant effect was more evident when the preparation was preincubated in vinblastine: synaptic responses often disappeared after a few minutes, whereas MEPP frequency attained a maximum at the 5th min. The results suggest a multiple site of action for vinblastine. First, an alteration of both vesicle and plasmalemma membrane, as revealed by the increase of MEPP frequency and by the change of the binomial release features. Second, the drug could damage the intracellular transport system, interfering with the mobilization of the vesicles toward the nerve endings, as shown by the very low or absent facilitation.

Animals↗
PubMed1983

The ionic channel of the nicotinic acetylcholine receptor is unable to differentiate between the optical antipodes of perhydrohistrionicotoxin.

The enantiomers of perhydrohistrionicotoxin were studied in their effects on endplate currents recorded at the junctional region of sartorius muscles of Rana pipiens. The two optical antipodes progressively decreased the peak amplitude of the endplate currents and were indistinguishable from each other at all times. The enantiomers shortened equally the time constants for endplate current decay, but did not alter their voltage sensitivities. Although perhydrohistrionicotoxin contains 4 chiral centers, complete steric inversion does not alter its effects on the acetylcholine receptor-ion channel complex. By contrast the recognition site of the AcChR is extremely sensitive to any change in the chirality of agonists.

Amphibian Venoms↗
PubMed1987

The neurotoxin histrionicotoxin interacts with the putative ion channel of the nicotinic acetylcholine receptors in the central nervous system.

Perhydrohistrionicotoxin at micromolar concentrations blocked the nicotine-evoked transmitter release from perfused striatal (dopaminergic) and hippocampal (cholinergic) nerve terminals. Perhydrohistrionicotoxin failed to compete with [3H]nicotine for its high-affinity binding site in rat brain, suggesting that the action of this toxin on central nicotinic receptors is noncompetitive. From the dose-response curve, 50% inhibition of nicotine-evoked striatal dopamine release occurred at 5 microM perhydrohistrionicotoxin, a value similar to that obtained in frog sartorius muscle and Electrophorus electroplax. This close agreement may suggest that the ionic channel of the presynaptic nicotinic acetylcholine receptor of brain neurons has similar properties to those of the peripheral receptor.

Acetylcholine↗
PubMed1985

Verapamil alters the amplitude and time course of miniature endplate current.

The effect of verapamil on neuromuscular transmission was examined by recording miniature endplate currents (mepcs) in voltage-clamped frog sartorius muscle fibres. In the presence of 100 microM verapamil, the amplitude and time constant of decay of the mepcs (tau D) were reduced to 68% and 55% of control respectively, and the normal voltage dependency of tau D was decreased. Part of the decrease in amplitude of the mepc was independent of changes in tau D because, on washout, recovery of tau D was more rapid than that of amplitude, and in some cells smaller concentrations of verapamil (1 and 10 microM) decreased amplitude without affecting tau D. Evidence of open and closed channel blockade by verapamil (5-20 microM) was obtained from ionophoretic end-plate current trains and it is proposed that these effects are mediated via an allosteric mechanism.

Animals↗
PubMed1986

Effects of delta-9-tetrahydrocannabinol, 11-hydroxy-delta-9-tetrahydrocannabinol and cannabidiol on neuromuscular transmission in the frog.

Intracellular recording techniques were used on neuromuscular junctions of the sartorius muscle of the frog, in vitro, to define the synaptic pharmacology of delta-9-tetrahydrocannabinol (THC), 11-hydroxy-THC and cannabidiol (CBD). The frequency of miniature endplate potentials was increased by THC, decreased by CBD and was unaffected by 11-hydroxy-THC, whereas the amplitude of the miniature endplate potentials was depressed by all three cannabinoids. In addition, the mean quantum content of the endplate potential (m) was first increased and then decreased by THC and 11-hydroxy-THC, but CBD produced only depression. Changes in m and the frequency of the miniature endplate potential indicated presynaptic sites of drug action and reduction of the amplitude of the miniature endplate potential suggested a postsynaptic site. The findings suggest possible mechanisms of action for the central excitatory and depressant properties of the cannabinoids.

Animals↗
PubMed1991

Acid-base regulation in the toad Bufo marinus during environmental hypoxia.

Gas exchange and the correlated changes in blood and tissue metabolic and acid-base status were investigated during long term exposure of the toad Bufo marinus to graded levels of hypoxia. During hypoxia, PCO2 values in blood and tissues fell, leading to a transient alkalosis in the extracellular but not in the intracellular space. A reduction in blood perfusion of the skin during hypoxia may explain why PCO2 was low in sartorius muscle under normoxia, but approached the PCO2 values found in other tissues (gastrocnemius muscle, ventricle) under hypoxia. At PO2 values below the critical PO2, lactate was formed and the decrease in total CO2 was accelerated. Lactate levels in the plasma were higher than in the intracellular space of the skeletal muscles, a finding attributed to the pH-dependent distribution of lactic acid across the cell membrane. The comparison of metabolic proton quantities with those found in the extra- and intracellular acid-base status suggests that CO2 release was accelerated by anaerobic proton formation. The alkalizing effect of decreasing PCO2 in the skeletal musculature was compensated for by a release of base equivalents into the blood. The resulting alkalosis in the blood was probably compensated for by the release of base equivalents into the environment.

Acid-Base Equilibrium↗
PubMed1984

Interactions of lead and cadmium on acetylcholine release at the frog neuromuscular junction.

The interactive effects of Cd2+ and Pb2+ on evoked and spontaneous transmitter release were studied in the sciatic nerve-sartorius muscle preparation of the frog (Rana pipiens). Either Pb2+ or Cd2+ competitively inhibited the actions of Ca2+ in bringing about evoked release, as measured by the endplate potential (EPP) amplitude. Combinations of Pb2+ and Cd2+ were additive in their effects on the EPP. The rate of spontaneous transmitter release was measured as the miniature endplate potential (MEPP) frequency. In contrast to their effects on the EPP, exposure of preparations to combinations of Pb2+ and Cd2+ actually increased the MEPP frequency less than exposures of the preparations to Pb2+ alone. The degree of reduction in MEPP frequency produced by Cd2+ depended upon the relative ratio of Pb2+ and Cd2+ ions. These results suggest that Pb2+ and Cd2+ ions competed for a common presynaptic receptor site during evoked release. They also suggest that Pb2+ ions may enter the nerve terminal, possibly through the Ca2+ channel, and that this entry is inhibited by Cd2+.

Acetylcholine↗
PubMed1990

Neuropeptide Y mimics a non-adrenergic component of sympathetic vasoconstriction in the bullfrog.

The effects of preganglionic sympathetic nerve stimulation and exogenous agents upon vascular tone were observed in hindlimb preparations of pithed adult bullfrogs. Repetitive electrical stimulation of the sympathetic C, but not the B, system elicited arterial vasoconstriction and reduced blood flow in vascular beds supplying the sartorius muscle and the skin. Close-arterial injections of epinephrine and neuropeptide Y each mimicked neurogenic vasoconstriction. After close-arterial injection of phentolamine, an alpha-adrenergic antagonist, the maximal effects of nerve stimulation were delayed in onset and reduced in magnitude, but not eliminated. Pretreatment with phentolamine blocked the vasoconstriction caused by injection of epinephrine, and produced a mild reduction in responses to neuropeptide Y. These observations demonstrate the vasomotor function of the sympathetic C system and they support the hypothesis that neuropeptide Y and epinephrine function as cotransmitters in postganglionic C neurons.

Animals↗
PubMed1992

Effects of toki-shakuyaku-san (Tsumura TJ-23) on electrical activity in neuroblastoma cells and frog neuromuscular junctions.

Toki-shakuyaku-san (Tsumura TJ-23) is a Chinese medicine which has been used for the treatment of gynecological symptoms in aged women. There are several reports on the usefulness of this drug in the treatment of cognitive disorders. We studied the effects of toki-shakuyaku-san on electrical activity in NG108-15 cells, a cell line of differentiated neuroblastoma x glioma hybrid cells, and on frog neuromuscular transmission. In the hybrid cells, an extract of toki-shakuyaku-san slightly depolarized the membrane potential, and strongly decreased the peak heights of the Na+ and Ca2+ current components of the action potential. The order of potency for NG108-15 cells of the 5 ingredients in toki-shakuyaku-san was soujyutsu >> shakuyaku, takusha, toki, senkyu. In voltage-clamped NG108-15 cells, toki-shakuyaku-san and soujyutsu decreased the Na+, K+, and Ca2+ current components. Toki-shakuyaku-san and soujyutsu also induced an increase in the intracellular calcium concentration. However, toki-shakuyaku-san did not affect neuromuscular transmission in the frog sartorius muscle. The results suggest that the effects of toki-shakuyaku-san on neurons are multiple, and tissue- and species-specific, and its effect derives mainly from soujyutsu.

Action Potentials↗
PubMed1981

Peptides isolated from the venom of Conus geographus block neuromuscular transmission.

The effects of a mixture of two peptides (GI and GII), purified from the venom of the marine gastropod, Conus geographus, were studied on neuromuscular transmission in the isolated mouse phrenic nerve--diaphragm and frog sciatic nerve--sartorius muscles. The GI--GII mixture rapidly blocked nerve-evoked contractions of the mouse diaphragm at bath concentrations greater than or equal to 0.2 microM but had no effect on contractions elicited by direct muscle stimulation. Paralytic concentrations of GI--GII had no significant effect on the compound nerve action potential of the bullfrog sciatic nerve. Similar concentrations of GI--GII produced a rapid reduction of endplate potential (epp) and miniature endplate potential amplitudes, apparently by a postsynaptic effect because the decrease in epp amplitude produced by subparalytic doses was not accompanied by significant alteration in the epp quantal content. The GI--GII mixture also inhibited [125I]alpha-bungarotoxin binding to endplate regions of the mouse diaphragm in a dose-dependent manner and was at least 10 times more potent than d-tubocurarine. We conclude that the blockage of vertebrate neuromuscular transmission by GI--GII is in part due to antagonism of acetylcholine binding to its receptor at motor endplates.

Animals↗
PubMed1986

Presynaptic effects of cholecystokinin octapeptide on neuromuscular transmission in the frog.

Intracellular recordings were obtained from the frog sartorius muscle end-plate to investigate the effects of cholecystokinin octapeptide (CCK-8) on cholinergic transmission at the neuromuscular junction. A brief bath-application of CCK-8 (1 microM) produced a depression, followed by a long-lasting facilitation, of the amplitude and the quantal content of the end-plate potential (epp). CCK-8 had a biphasic effect, an initial depression followed by an augmentation of the frequency of the miniature epps. CCK-8 did not affect the sensitivity of the nicotinic receptor at the end-plate. These results suggest a significant role for CCK-8 in cholinergic transmission, possibly as a modulator of the evoked release of acetylcholine from motor nerve terminals.

Animals↗
PubMed1987

Postsynaptic inhibition of the frog neuromuscular transmission by prostaglandin E1.

Intracellular recordings were made from the frog sartorius muscle end plate. Prostaglandin (PG) E1 (100 nM-10 microM) decreased the amplitude of the end plate potential (EPP). PGE1 decreased the quantal size of EPPs, while it rather increased the quantum content. The frequency of miniature (m) EPPs was not affected by PGE1. PGE1 depressed the acetylcholine (ACh)-induced depolarization, as well as the amplitude of mEPPs. These results suggest that PGE1 decreases the sensitivity of nicotinic ACh receptors at the end plate membrane, resulting in postsynaptic depressions of neuromuscular transmission.

Animals↗
PubMed1990

Time course of neostigmine action on the endplate response.

Miniature endplate currents (MEPCs) were focally recorded in frog sartorius muscle. In the presence of 3 microM neostigmine, the amplitude of MEPCs increased, but later, after 45-60 min of treatment, a decrease of the amplitude towards the initial levels appeared. The pronounced lengthening of the falling phase of MEPCs, which accompanied the increased amplitude, suggests that at the beginning the effect is mainly ascribed to cholinesterase inhibition. The final decreased amplitude of MEPC showed a shortening of the time course instead. This suggests that also a direct effect on endplate receptors is involved.

Acetylcholine↗
PubMed1990

Changes in the time course of miniature endplate currents induced by bath-applied acetylcholine.

Bath application of 0.5 and 2 microM acetylcholine (ACh) slowed the decay phase of miniature endplate currents (MEPC) recorded in isolated, voltage-clamped and prostigmine-treated frog sartorius muscle. Washout of ACh led to a decrease of the decay time constant of the MEPC to 72 +/- 5% (n = 5) and 51 +/- 3% (n = 6) of initial values, respectively, followed by very slow and incomplete recovery. MEPC amplitude changed slightly and recovered relatively fast. This discrepancy in the recovery rates is suggested to be due to a 'trapping' ability of desensitized receptors which can compete with the free receptors for ACh molecules and prevent repetitive binding. Thus the high affinity of desensitized receptors to ACh may partially compensate the absence of acetylcholinesterase activity.

Acetylcholine↗
PubMed1975

Excitation-contraction coupling: effects of "zero"-Ca2+ medium.

Frog sartorius muscles, exposed for up to 15--20 min to media containing ethylene glycol bis (beta-aminoethyl ether) - N, N'-tetraacetic acid and thus having free Ca2+ concentration less than 10(-8) M, produce isometric contractions with basically normal but speedier latency relaxation and earliest tension development. The excitation-contraction coupling is thus also basically normal, but speedier evidently in respect to release of activator Ca2+ from the sarcoplasmic reticulum.

Animals↗