Amplitude Of Excitatory Junction Potentials Research Articles

Effects of amosulalol on the electrical responses of guinea-pig vascular smooth muscle to adrenoceptor activation.

The effects of amosulalol, a newly synthesized sulphonamide-substituted phenylethylamine derivative, on electrical responses of smooth muscle cells of the guinea-pig vascular tissues to noradrenaline, isoprenaline and perivascular nerve stimulation were investigated. Amosulalol (10(-10) -10(-5)M) did not alter the resting membrane potential of smooth muscle cells of the mesenteric artery, the mesenteric vein, the main pulmonary artery and the portal vein. In the mesenteric artery, main pulmonary artery and portal vein, but not in the mesenteric vein, membrane depolarizations produced by noradrenaline were antagonized by amosulalol. In the portal vein, membrane hyperpolarizations produced by isoprenaline were antagonized by amosulalol. In the mesenteric artery, amosulalol (over 10(-6)M) enhanced the amplitude of excitatory junction potentials (e.j.ps) produced by perivascular nerve stimulation. Amosulalol antagonized the noradrenaline-induced decrease in the e.j.p. amplitude; this effect was much weaker than that of phentolamine. Amosulalol also antagonized the isoprenaline-induced enhancement of the e.j.p. amplitude. In the mesenteric vein, the slow depolarizations produced by perivascular nerve stimulation were depressed by amosulalol (over 10(-6)M), but the effect was much weaker than that of prazosin, yohimbine or phentolamine. Actions of amosulalol on electrical properties of vascular tissues can be summarized as follows: amosulalol blocks alpha 1- and beta-adrenoceptors. It also blocks alpha 2-adrenoceptors, though weakly.

The dependence of excitatory junction potential amplitude on the external calcium concentration in mouse vas deferens during narcotic withdrawal.

The dependence of neurotransmitter release on calcium was evaluated in adrenergic terminals from mice that were acutely withdrawn from chronic morphine treatment (CMT). A two fold increase in the number of writhes in response to an i.p. injection of acetylcholine was induced in mice by CMT and subsequent withdrawal. A shift to the left in the relationship between the excitatory junction potential (e.j.p.) amplitude and extracellular calcium concentration ([Ca]o) was induced in vasa deferentia from CMT-withdrawn mice. A reduction in the degree of facilitation of transmitter release during a short low-frequency train of impulses and an increase in the amount of transmitter release during a high-frequency train of impulses was induced in vasa deferentia from CMT-withdrawn mice. The adaptive mechanism of the terminals to the sustained presence of morphine may involve an increase in the probability that the release sites will release transmitter either via increase in calcium influx or an increase in the affinity of calcium to the hypothetical X-receptor.

The dependence of excitatory junction potential amplitude on the external calcium concentration in narcotic tolerant mouse vas deferens.

The dependence of neurotransmitter secretion on external calcium ions during development of opiate tolerance in the mouse vas deferens was studied. The writhing response of mice to an i.p. injection of acetylcholine was inhibited by morphine. Reversal of this antinociceptive effect of morphine during chronic treatment signalled the development of tolerance. Tolerance to morphine at the neuromuscular junction was shown as a reversal of the initial shift of the size of the excitatory junction potential (e.j.p.) vs extracellular calcium concentration relationship back towards the control without any change in the power of 2.4. Facilitation in the amplitude of the e.j.p. occurs with low frequency (2 Hz) stimulation. The initial increase in facilitation induced by morphine was reversed by chronic morphine treatment without any change in the plateau e.j.p. amplitude achieved after a long low frequency train of impulses. At high frequencies (10 Hz) the initial increase in e.j.p. amplitude was followed by a depression. Acute morphine administration decreased the size of the e.j.p., this was followed by an increase in facilitation and a decrease in depression. These effects were reversed after chronic morphine treatment. Tolerance to morphine involves a counteradaptive process which restores the normal entry of calcium ions or its actions within the release sites in promoting transmitter release.

Baclofen has a presynaptic action at the crayfish neuromuscular junction

The action of baclofen, a GABA analog, was studied at the crayfish neuromuscular junction (NMJ). Baclofen depressed the amplitude of excitatory junction potentials (ejps) without affecting muscle input resistance and reduced the frequency of spontaneous miniature ejps without affecting their size. Thus, baclofen may mediate presynaptic inhibition by depressing transmitter release from the excitatory nerve. The site of baclofen's effect at the crayfish NMJ may parallel its site of action in the vertebrate nervous system.

Motor organization in pharynx of Helix pomatia.

Identified motor neurons in the buccal ganglia of Helix pomatia and pharynx muscles innervated by them were studied with intracellular recording and cobalt staining. Retrograde cobalt staining via the buccal nerves indicated that neurons occupy relatively constant positions within the ganglia. With intracellular cobalt staining it was shown that the shape of a representative motor neuron (B4) is similar in different preparations. In some cases, however, deviations from the normal pattern of axon distribution were found. Presumed motor endings of neuron B4 in the muscle were also visualized with intracellular staining. Recordings from individual motor neurons show typical phase relationships of spontaneous spike activity. Most motor neurons are active in the retraction phase of the radula. Only excitatory motor neurons were found. Most neurons directly supply more than one muscle. Amplitude of excitatory junction potentials (EJP) and plasticity at neuromuscular junctions from one neuron are similar in different muscles. Single muscle fibers receive polyneuronal innervation. Activity of single motor neurons already leads to muscle contraction even without spiking of the muscle cells. Muscle tension depends on integrated EJP size. Most motor neurons supply typical combinations of a set of muscles. Thus, several muscles can be activated synchronously by activity of a single motor neuron. In this way muscle combinations are predetermined morphologically by the peripheral branching patterns of the respective neurons.

Differential effects of halothane on airway nerves and muscle.

Effects of halothane on the excitation-contraction coupling or neuro-effector transmission in the dog tracheal muscle were observed in vitro in an attempt to clarify the cellular mechanisms involved in anesthetic-induced bronchodilation. Double sucrose gap, microelectrode, and tension recording methods were used. Application of halothane evoked an initial induction of phasic contraction with no alteration in the electrical membrane properties, and secondarily a reduction in muscle tone with membrane hyperpolarization. Halothane suppressed the amplitude of the twitch contractions evoked by indirect (nerve mediated) or direct muscle stimulation, the degree of suppression being greater with the former stimulation. The threshold membrane depolarization required for the generation of tension development was increased. In the presence or absence of TEA, halothane completely suppressed the generation of an action potential or a local response in the muscle membrane, following stimulation by outward current pulses. Therefore, halothane has complex actions on Ca++ economy in the tracheal smooth muscle cell, i.e., initial release of Ca++ from the store sites followed by inactivation or a reduction in free calcium ions in the cytoplasm, and/or suppression of the influx of Ca++ across the cell membrane. Low concentrations of halothane (less than or equal to 1%) suppressed the amplitude of excitatory junction potential (EJP) without altering the membrane potential, membrane resistance, or muscle sensitivity to acetylcholine. Therefore, this anesthetic probably suppresses the release of transmitter from the nerve terminals. Halothane also suppressed the facilitation phenomena of EJP during repetitive nerve stimulation. These direct inhibitory effects of halothane on smooth muscle cells and excitatory neuro-effector transmission could account for the potent bronchodilator action of this anesthetic.

Effects of a New Alphai-Adrenoceptor Blocking Agent, 3-[2-[4-(2-Methoxyphenyl)-1-Piperazinyl]Ethyl]-(1H,3H)-Quinazoline-2,4-Dione Monohydrochloride (SGB1534), on Electrical and Mechanical Properties of Guinea-pig Mesenteric Artery

Effects of a newly synthesized alpha-adrenoceptor blocking agent, 3-[2-[4-(2-methoxyphenyl)-1 - pi perazi nyl] ethyl]-(1H, 3H)-quinazoline-2, 4-dione monochloride (SGB1534), on the electrical and mechanical properties of smooth muscles of guinea-pig mesenteric artery and on the electrical properties of smooth muscles of rat tail artery were investigated. SGB1534 (10−10 M–10−5 M) did not modify the membrane potential and ionic conductance of the membrane in guinea-pig mesenteric artery, but this agent did inhibit depolarizations induced by noradrenaline, phenylephrine, or histamine with similar potencies. This agent inhibited serotonin-induced depolarization, but with a weak potency. In rat tail artery, the noradrenaline-induced depolarization (10−5 M) was inhibited by yohimbine (5×10−7 M), but not by SGB1534 (10−6 M). SGB1534 (10−6 M) did not modify the amplitude of excitatory junction potentials (e.j.ps), the facilitation process or spike potential evoked by perivascular nerve stimulation in the mesenteric artery. Noradrenaline, phenylephrine or histamine evoked the contraction in guinea-pig mesenteric artery, and this contraction was inhibited by SGB1534 (over 10−10 M). The serotonin-induced contraction was inhibited by higher concentrations of SGB1534 (over 10−6 M). The concentration of SGB1534 required to inhibit the contractions evoked by these amines was much higher than that required to inhibit the depolarizations. SGB1534 (<10−6 M) had no effect on the excess K-induced depolarization and contraction. These results indicate that SGB1534 possesses the property of an alpha1-but not alpha2-adrenoceptor blocking agent. In addition, this agent possesses a histaminergic receptor blocking action and a weak serotonergic receptor blocking action.

Effects of a new alpha-adrenoceptor blocking agent, ethyl-7-[4-(2-methoxyphenyl)-1-piperazinyl] heptanoate dihydrochloride (SGB-483), on smooth muscle and neuromuscular transmission in guinea-pig mesenteric artery.

The effects of ethyl-7-[4-(2-methoxyphenyl)-1-piperazinyl] heptanoate dihydrochloride (SGB-483) on the smooth muscle of the guinea-pig mesenteric artery were investigated using microelectrodes. The resting membrane potential was -70.3 +/- 2.1 mV.SGB-483 (10(-8)M - 10(-4)M) did not modify the membrane potential or membrane resistance, as estimated from measurement of current-voltage relationships. Noradrenaline (NA; above 10(-5)M) depolarized the membrane. After pretreatment with SBG-483 10(-5)M or prazosin 10(-6)M, the NA-induced depolarization of the membrane was inhibited; yohimbine (10(-5)M) was ineffective. Phenylephrine and NA (greater than 3 X 10(-7)M) but not clonidine (10(-6)M) contracted the artery. These contractions were inhibited by SGB-483. Following repetitive perivascular nerve stimulation, the amplitude of excitatory junction potentials (e.j.ps) increased to a certain steady state value (e.j.p.(s]. The amplitude of e.j.p.(s) was frequency-dependent. Application of SGB-483 (over 10(-8)M) enhanced the amplitude of e.j.p.(s), dose-dependently with no change in the amplitude of the first e.j.p. (e.j.p.(f] evoked by the first stimulus. After pretreatment with NA, the amplitudes of both e.j.p.(f) and e.j.p.(s) were inhibited, dose-dependently. Following pretreatment with SGB-483 (10(-6) - 10(-5)M), the NA-induced reduction in the amplitude of both e.j.p.(f) and e.j.p.(s) were reversed and the control values restored. Clonidine (10(-7)M) inhibited the amplitude of e.j.p.(f) and e.j.p.(s), and SGB-483 (10(-7)M) partially restored the amplitude of both. Yohimbine (10(-7)M) and phentolamine (10(-7)M) enlarged the amplitude of e.j.p.(s); the amplitude of e.j.p.(f) was inhibited by yohimbine and enlarged by phentolamine. Prazosin (10(-6)M) had no effect on the amplitude of either e.j.p.(f) or e.j.p.(s), at any given stimulus frequency. SBG-483 (10(-7)M) did not enhance the amplitudes of either e.j.p.(f) or e.j.p.(s) following pretreatment with phentolamine (10(-7)M) or yohimbine (10(-7)M) but did enhance the amplitude following pretreatment with prazosin (10(-7)M). SGB-483 possesses the property of an alpha 1- and alpha 2-adrenoceptor antagonist. The alpha-antagonistic action was apparent on post-junctional smooth muscle cells. The alpha 2-antagonistic action on neuromuscular transmission was mediated at pre-junctional nerve terminals to enhance the release of NA. The prejunctional actions of SGB-483 were more selective than those of yohimbine or phentolamine.

Effects of dopamine of neuromuscular transmission in the guinea-pig mesenteric artery

The effects of dopamine on neuromuscular transmission in the guinea-pig mesenteric artery were investigated using a microelectrode method. Dopamine did not modify the membrane potential or the membrane resistance of the smooth muscle, but did reduce the amplitude of excitatory junction potentials (e.j.p.) and enhance the facilitation of e.j.p. produced by repetitive stimulation. Phentolamine (10 −7 M) enhanced the amplitude and the facilitation of the e.j.p. and with the addition of dopamine (10 −6 M) there was a reduction in the amplitude of e.j.p. but not in the facilitation. Haloperidol and sulpiride (> 10 −6 M) increased the amplitude of e.j.p. without altering the postjunctional membrane properties. Holoperidol and sulpiride did not increase the facilitation of e.j.p. produced by repetitive stimulation. In the presence of haloperidol or sulpiride (10 −5 M), dopamine (10 −6 M) did not suppress the amplitude of the e.j.p. These results indicate that in the guinea-pig mesenteric artery, dopamine inhibits the release of transmitter at the presynaptic membrane.

Post-tetanic decay of evoked and spontaneous transmitter release and a residual-calcium model of synaptic facilitation at crayfish neuromuscular junctions.

The post-tetanic decay in miniature excitatory junction potential (MEJP) frequency and in facilitation of excitatory junction potentials (EJPs) was measured at crayfish neuromuscular junctions. A 2-s tetanus at 20 Hz caused the MEJP frequency to increase an average of 40 times and the EJP amplitude to increase an average of 13 times. Both MEJP frequency and EJP facilitation decayed with two time constants. The fast component of MEJP frequency decay was 47 ms, and that of EJP facilitation was 130 ms. The slow component of MEJP frequency decay was 0.57 s, and that of EJP facilitation was approximately 1 s. These results were consistent with the predictions of a residual calcium model, with a nonlinear relationship between presynaptic calcium concentration and transmitter release.

An electrophysiological study of presynaptic alpha-adrenoceptors in the vas deferens of the mouse.

1--Effects of clonidine and alpha-adrenoceptor antagonists were studied on sympathetic neuroeffector transmission in the mouse vas deferens. The amplitude of excitatory junction potentials (e.j.ps) was taken as a measure of transmitter release per impulse. 2--At a concentration of 0.5 microM, prazosin abolished depolarizations evoked by iontophoretically applied noradrenaline, but changed neither spontaneous nor nerve stimulation-evoked e.j.ps. 3--Yohimbine 0.1 and 1 microM, rauwolscine 1 microM and corynanthine 1 microM di not change the e.j.p. amplitudes elicited by the first 2-3 pulses in trains of 15 pulses at 3 Hz, but increased the e.j.ps elicited by the subsequent pulses. Corynanthine 1 microM was much less effective than yohimbine 1 microM or rauwolscine 1 microM, and corynanthine 0.1 microM had no effect. 4--Clonidine 0.01 microM reduced the e.j.p. amplitudes evoked by single pulses and its effect was counteracted by yohimbine 1 microM. 5--In vasa deferentia from reserpine-treated mice the e.j.p. trains were changed in much the same way as by yohimbine and rauwolscine. Yohimbine 1 microM did not further increase the e.j.p. amplitudes in these organs, whereas clonidine 0.01 microM caused a marked inhibition. 6--It is concluded that the release of the motor transmitter in the mouse vas deferens is inhibited by activation of presynaptic alpha-adrenoceptors, and that these receptors are normally activated by neurally released noradrenaline.

Effects of nifedipine on smooth muscle cells of the rabbit mesenteric artery.

The effects of nifedipine on electrical and mechanical responses of smooth muscle cells of the rabbit mesenteric artery were investigated using the microelectrode and isometric tension recording methods for intact cells and saponin-treated skinned muscles. Nifedipine inhibited the Ca-spike evoked by outward current pulses in the presence of tetraethylammonium (TEA) and that by perivascular nerve stimulation without affecting the amplitude of excitatory junction potentials (EJPs). Nifedipine(<3×10−7M) modified neither the amplitude of EJPs nor the facilitation process. This drug inhibited the contraction evoked by direct muscle stimulation under conditions of treatment with guanethidine and tetrodotoxin(TTX), excess concentrations of [K]o exogenously applied norepinephrine(NE) and perivascular nerve stimulation. The K-induced contraction was markedly inhibited by nifedipine (>3×10−9M), and the potencies of inhibitory action of nifedipine appeared in the following order: direct muscle stimulation>perivascular nerve stimulation>exoge-nously applied NE. Nifedipine inhibited the NE-induced oscillatory contractions more than the NE-induced tonic and phasic contractions. In the Na-free solution, the tissue generated a small tonic contraction after 20-30 min superfusion. This contraction ceased with application of nifedipine. In the saponin treated muscles (50μg/ml for 20min), Ca accumulation into and Ca release from the store sites, as well as the contractile proteins including calmodulin, were not affected by nifedipine (1×10−7M). These results indicate that nifedipine acts only on the myoplasmic membrane of smooth muscles of the mesenteric artery. The nifedipine-induced relaxation appears to be due to inhibition of the voltage dependent Ca channel.

Direct and indirect effects of histamine on the smooth muscle cells of the guinea-pig main pulmonary artery.

Electrophysiological studies of the effects of histamine on the smooth muscles in the guinea-pig main pulmonary artery revealed that this amine produced muscle contraction with an associated depolarization of the membrane. Application of cimetidine potentiated and that of mepyramine suppressed these histamine-induced responses. In the presence of mepyramine, histamine produced membrane hyperpolarization. Contractions produced by perivascular nerve stimulation were potentiated by histamine, and additional application of cimetidine further potentiated while addition of mepyramine suppressed the histamine-induced enhancement. The amplitude of excitatory junction potentials was increased by application of histamine plus cimetidine and was decreased by histamine plus mepyramine. Excitatory effects of histamine on the electrical and mechanical responses were reduced by application of tetrodotoxin, prazosin, phentolamine or guanethidine. In the presence of these drugs, histamine produced depolarization with an associated increase in membrane resistance and, in high concentrations, produced spike potentials. Electrical and mechanical responses of the smooth muscles to exogenously applied noradrenaline were potentiated by pretreatment with histamine and cimetidine, and were suppressed by histamine and mepyramine. These observations indicate that the guinea-pig main pulmonary artery possesses two types of histamine receptor, H1- and H2-receptors, in the smooth muscles and in the perivascular adrenergic nerves. Stimulation of H1 or H2-receptor produces excitatory or inhibitory effects, respectively, on the smooth muscles and on the adrenergic nerves. Contraction of the muscle tissues produced by histamine is brought about by a direct effect on the smooth muscles and by increased release of transmitters, as a result of excitation of perivascular nerves.

Sub-miniature junction potentials in excitatory neuromuscular synapses of the locust

By recording miniature excitatory junction potentials (mejps) intracellularly at two points from a multiterminally innervated muscle fibre it is possible to select mejps whose amplitudes are not substantially affected by electrotonic decay. Many amplitude histograms of such selected mejps from untreated locust jumping muscle show a bimodal distribution with a high proportion of small-amplitude mejps (sub-mejps). Most amplitudes of excitatory junction potentials (ejps) resulting from the release of a single transmitter quantum correspond to the large-mode mejps. Tetanic nerve stimulation, in high [Mg 2+] o without Ca 2+, greatly reduces the proportion of sub-mejps. It is concluded that there are two modes of spontaneous transmitter release from the motor nerve endings.

Thermal acclimation in a crustacean neuromuscular system.

1. Effects of temperature on the muscle fibre membrane and synapses of stretcher muscle preparations made from autotomized limbs of the Pacific shore crab (Pachygrapsus crassipes) were investigated. 2. Acclimation of the crabs to different temperatures modified properties of both muscle fibre membrane and synapses. 3. Increased temperature produced an increase in membrane potential of the muscle fibres. A semi-log plot of these data revealed two linear phases of the membrane potential-temperature relationship, with a change in slope near the acclimation temperature. 4. Maximum values for excitatory junction potential (EJP) amplitude and time constant of EJP decay, and minimum values for facilitation were obtained at temperatures close to the acclimation temperature. It is suggested that the decline in EJP amplitude and time constant of decay produced by deviations in temperature from the acclimation temperature is compensated for by an increase in the amount of facilitation. In this way, maximum tension can be produced by the stretcher muscle in a range of at least 8 degrees C around the acclimation temperature.

Effects of diltiazem on smooth muscles and neuromuscular junction in the mesenteric artery.

Effects of diltiazem on membrane properties, neuromuscular transmissions, and mechanical responses were investigated in intact and skinned muscles of the guinea pig mesenteric artery. Diltiazem (greater than 10(-6) M) depolarized the membrane, increased the membrane resistance, and suppressed the spike evoked by either electrical depolarization or summation of excitatory junction potentials (EJPs). This drug also suppressed the facilitation process of amplitudes of EJPs produced by repetitive perivascular nerve stimulations. These suppressions of EJPs were not caused by a reduced number of active nerves contributing to the generation of EJP but but rather to a reduction in the release of chemical transmitters. Norepinephrine (NE)-induced and K-induced contractions were suppressed by diltiazem noncompetitively, but the contraction evoked in Na-deficient solution was not suppressed, i.e., diltiazem is not a nonselective inhibitor of the Ca influx. In the saponin-treated skinned muscles diltiazem did not suppress the release from or the accumulation into the Ca store site, nor did it suppress activation of the Ca receptor in contractile proteins. These results indicate that diltiazem acts on the surface membrane and nerve terminal as a Ca antagonist or Ca-channel blocker.

Effects of a thioreactive agent, diamide, on neuromuscular transmission in lobster.

Diamide[diazine-dicarboxylic acid-bis(dimethylamide)], a thiol-oxidizing agent, has both pre- and postsynaptic actions on the glutaminergic neuromuscular junction of the lobster walking leg. Postsynaptically, diamide produced an increase in the response to exogenously applied glutamate, whereas the effect of diamide on presynaptic transmitter release involved two major changes: 1) a decrease in excitatory junction potential amplitude and 2) an increase in miniature junction potential frequency. Short-term facilitation also decreased. Equilibration with 1,4-dithiothreitol (a sulfhydryl-reducing agent) reversed the decline in excitatory junction potential frequency, and the fall in short-term facilitation. The miniature junction potential frequency increase induced by diamide was independent of external Ca2+, as diamide in a Ca2+-free solution produced a similar response to that in a Ca2+-containing solution. We propose that the action of diamide on transmitter release is similar to the action of polyvalent cations, i.e., diamide has two sites of action, a blockade of inward Ca2+ flux and an increased release of Ca2+ inside the terminal.

Increased effectiveness of a motorneuron after partial denervation of its target muscle in the cricket Telegryllus oceanicus.

Fibers of the metathoracic extensor tibia muscle of the cricket Teleogryllus oceanicus are innervated by a slow excitatory axon (slow fibers), a fast excitatory axon (fast fibers), or by both slow and fast axons (dual fibers). Sectioning metathoracic nerve 5 removes the fast axon input to the muscle but not that of the slow axon. Following such partial denervation, the mechanical responses initiated by the slow axon increase progressively for at least 30 days; twitch tensions reach 5-10 times those of control muscles and tetanic tensions 10-30 times control values. After sectioning nerve 5, resting membrane potentials decrease in those fibers which originally received fast axon input and the input resistance of all fiber types increases, including that of slow fibers which are not innervated through nerve 5. Excitatory junctional potentials (EJPs) initiated by the slow axon become larger following partial denervation, accounting in part for the larger contraction amplitudes. The increased input resistance is adequate to account for the larger EJPs in slow fibers but not for the proportionally greater increase in EJP amplitude in fibers which were formerly dually innervated. The change in EJP amplitude is abrupt in slow fibers and gradual in formerly dual fibers.

Ionic dependence of electrical activity in small mesenteric arteries of guinea-pigs.

The regulation of blood vessel diameter is under the control of the autonomic nervous system (as well as hormones and metabolites), sympathetic nerve stimulation evoking depolarizing post-synaptic potentials. Excitatory junction potentials (EJPs) were recorded from vascular smooth muscle cells of guinea-pig small mesenteric arteries (pressurized) following nerve stimulation. Repetitive stimulation (greater than 5Hz) led to summation of EJPs, which evoked spikes and vasoconstriction. Replacing extracellular Na+ with choline (plus atropine) resulted in a decrease in EJP amplitude, but spike amplitude and maximum rate of rise (+Vmax) were unaffected. Decreasing the Ca2+ concentration produced decreases in EJP amplitude and spike +Vmax. Verapamil and bepridil, agents that depress Ca2+ influx in vascular and visceral smooth muscle, depolarized the membrane and depressed EJPs and spikes at higher concentrations (10(-5) M and 5 X 10(-6) M, respectively). The data indicate that EJPs are dependent on external Na+ and Ca2+ ions, and that spikes are dependent on Ca2+. Thus, neuromuscular transmission in this muscle is similar to that in non-vascular smooth muscles, such as intestinal muscles and vas deferens.

The Modulatory Action of Dopamine On Crustacean Foregut Neuromuscular Preparations

ABSTRACT Effects of dopamine (DA) on contractile and electrical properties of decapod foregut neuromuscular preparations were examined. Dopamine produced dramatic increases in nerve-evoked contractions and, in particular muscles, contractures and spontaneous contractions. These effects were observed at concentrations as low as 5 × 10−9 M-DA. The DA-produced enhancement of nerve-evoked contractions was associated with an increase in amplitude of excitatory junctional potentials (EJPs). The increase in EJPs resulted in part from an increase in muscle fibre membrane resistance that was particularly prominent over depolarized membrane potentials. A presynaptic action of dopamine cannot be as yet excluded. In fibres from the muscle in which dopamine produced a contracture, dopamine also produced a depolarization. In fibres from the muscle in which dopamine activated spontaneous contractions, dopamine also produced spontaneous rhythmic action potentials. Dopamine also accelerated the half-time of muscle relaxation following muscle contraction