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PubMed1981

An electropharmacological analyses of the effects of some drugs on neuromuscular transmission in the vas deferens of the guinea-pig.

1 The effects of several drugs upon the excitatory junction potential (e.j.p.) in the guinea-pig vas deferens have been investigated. 2 Amiodarone, a noradrenergic neurone blocker which also blocks both alpha and beta-adrenoreceptors, did not reduce the e.j.p. 3 The alpha-adrenoreceptor antagonists, azapetine, piperoxan and prazosin, only enhanced the e.j.p. irrespective of their relative potencies at alpha 1 and alpha 2-adrenoreceptors. 4 Sotalol, a beta-adrenoreceptor antagonist, was without effect upon the e.j.p. 5 Clonidine and lysergic acid diethylamide, alpha-adrenoreceptor agonists, produced a dose dependent inhibition of the e.j.p. without apparently affecting the frequency or size of spontaneous junction potentials. 6 The effects of clonidine were antagonized by piperoxan in a competitive reversible manner. 7 It is argued that these results confirm the presence of alpha-adrenoreceptors prejunctionally upon the sympathetic excitatory innervation of the vas deferens but that although an endogenous alpha-adrenoreceptor agonist is released by nerve stimulation either the transmitter that is responsible for the e.j.p. is not noradrenaline or that the postjunctional receptors responsible for the generation of the e.j.p. are not adrenoreceptors.

Adrenergic alpha-Agonists↗
PubMed1997

Competition and cooperation among receptor tyrosine phosphatases control motoneuron growth cone guidance in Drosophila.

The neural receptor tyrosine phosphatases DPTP69D, DPTP99A and DLAR are involved in motor axon guidance in the Drosophila embryo. Here we analyze the requirements for these three phosphatases in growth cone guidance decisions along the ISN and SNb motor pathways. Any one of the three suffices for the progression of ISN pioneer growth cones beyond their first intermediate target in the dorsal muscle field. DLAR or DPTP69D can facilitate outgrowth beyond a second intermediate target, and DLAR is uniquely required for formation of a normal terminal arbor. A different pattern of partial redundancy among the three phosphatases is observed for the SNb pathway. Any one of the three suffices to allow SNb axons to leave the common ISN pathway at the exit junction. When DLAR is not expressed, however, SNb axons sometimes bypass their ventrolateral muscle targets after leaving the common pathway, instead growing out as a separate bundle adjacent to the ISN. This abnormal guidance decision can be completely suppressed by also removing DPTP99A, suggesting that DLAR turns off or counteracts a DPTP99A signal that favors the bypass axon trajectory. Our results show that the relationships among the tyrosine phosphatases are complex and dependent on cellular context. At growth cone choice points along one nerve, two phosphatases cooperate, while along another nerve these same phosphatases can act in opposition to one another.

Animals↗
PubMed1986

An electrophysiological analysis of the effect of reactive blue 2, a putative P2-purinoceptor antagonist, on inhibitory junction potentials of rat caecum.

The electrophysiological effects of the putative P2-purinoceptor antagonist reactive blue 2 (RB2) were investigated in strips of circular muscle of rat caecum with the sucrose gap technique. RB2 (0.1-1 mM) antagonized in a concentration-dependent manner, the amplitude, rate of rise and speed of onset of the inhibitory junction potentials elicited either with single pulse or with train of field stimulation at 10 Hz. A fully effective concentration of RB2 (0.5 mM) decreased the membrane response to high strength hyperpolarizing constant current pulses, thus indicating an increase in membrane conductance. At this concentration RB2 inhibited the hyperpolarization induced by the stable ATP analogue alpha,beta-methylene ATP, but did not significantly inhibit noradrenaline-induced hyperpolarization. RB2 (0.5 mM) also abolished the ability of carbachol to elicit spikes, while the carbachol-induced depolarization and the amplitude of accompanying mechanical responses were largely unaffected. The possible mechanisms responsible for the RB2-induced effects are discussed.

Animals↗
PubMed1982

Interactions among the effects of normorphine, calcium and magnesium on transmitter release in the mouse vas deferens.

1 Excitatory junction potentials (e. j. ps) were recorded with intracellular electrodes from smooth muscle cells of the mouse vas deferens. 2 The dependence of the e.j.p. amplitude on the extracellular calcium ion concentration was determined in the absence or presence of normorphine (50 nM-1 microM) or magnesium (1.2-4.8 mM). 3 The interaction between normorphine and calcium was non-competitive beyond a dose-ratio of 1.5, whereas the interaction between magnesium and calcium was competitive up to the highest dose-ratio investigated (1.9). 4 It is suggested that inhibition by normorphine occurs at least partly by a mechanism different from that of magnesium.

Animals↗
PubMed1990

Effects of alpha,beta-methylene ATP on the prejunctional purinoceptors of the sympathetic nerves of the rat caudal artery.

The effects of alpha,beta-methylene ATP, an agent known to stimulate and then to desensitize P2-purinoceptors, on the release of endogenous norepinephrine from the electrically stimulated rat caudal artery were determined. Norepinephrine was quantified by high-performance liquid chromatography-electrochemical detection techniques. alpha,beta-Methylene ATP over the concentration range of 1 to 100 microM did not affect the release of norepinephrine evoked by stimulation for 3 min at 1 Hz. In contrast, 2-chloroadenosine, a P1 receptor agonist, and beta,gamma-methylene ATP, a P2 receptor agonist, produced a concentration-related inhibition of the release of norepinephrine presumably by activating prejunctional purinoceptors. The failure of alpha,beta-methylene ATP to inhibit transmitter release was apparently not related to the length of pretreatment with this agent because pretreatments of 0.5 to 15 min yielded similar results. These findings indicate that the ability of alpha,beta-methylene ATP to decrease excitatory junction potentials and vasoconstriction of the caudal artery, as reported by others, is not due to a decrease in the release of transmitter. In spite of not possessing agonistic properties, alpha,beta-methylene ATP does interact with prejunctional purinoceptors as judged by the finding that the inhibitory effects of 2-chloroadenosine and beta,gamma-methylene ATP, but not those of the alpha-2 agonist clonidine, were antagonized by alpha,beta-methylene ATP. alpha,beta-Methylene ATP thus appears to be an antagonist at prejunctional purinoceptors (classified by us previously as P3-purinoceptors). alpha,beta-Methylene ATP also appears to act as an antagonist against endogenously released adenine nucleosides and nucleotides.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Chloroadenosine↗
PubMed1995

Electrical and mechanical responses produced by nerve stimulation in detrusor smooth muscle of the guinea-pig.

In smooth muscles of the guinea-pig bladder, intramural nerve stimulation generated an excitatory junctional potential (e.j.p.), action potential and twitch contraction. Nicardipine inhibited the action potential but not the e.j.p. The e.j.p. amplitude was reduced by suramin, or desensitization of the ATP receptor with receptor agonists. The amplitude of the twitch contraction was reduced by atropine, and the remainder was blocked by nicardipine. In the presence of maximally effective concentrations of atropine, the threshold concentration of acetylcholine required to produce contraction was about 10(-7) M, whereas acetylcholine concentrations greater than 10(-6) M were required to cause depolarization. It is concluded that nerve stimulation releases acetylcholine and ATP, and the former produces contraction without change in the membrane potential, while the latter generates the e.j.p. which triggers an action potential and thus elicits contractions.

Acetylcholine↗
PubMed1985

Effects of diltiazem on electrical responses evoked spontaneously or by electrical stimulation in the antrum smooth muscle cells of the guinea-pig stomach.

In circular smooth muscle cells of the guinea-pig stomach (antrum), diltiazem (10(-6)-10(-5)M) blocked the overshooting spike potential generated either spontaneously or by electrical stimulation in the presence of 2 mM tetraethylammonium chloride, but did not block the slow wave and the abortive spike potential. The membrane was depolarized by high concentrations of diltiazem (more than 3 X 10(-6)M), and this depolarization was associated with an increase in the membrane resistance. The interval between slow waves was shortened to about 0.90 times the control (14.7s) by 10(-5)M diltiazem. Transmural nerve stimulation evoked an inhibitory junction potential (i.j.p.) and enhanced the subsequently generated slow wave. Tetrodotoxin (3 X 10(-7)M) blocked both responses but atropine (10(-6)M) blocked only the latter. Diltiazem (more than 10(-6)M) increased the amplitude of the i.j.p. and depressed the enhancement of the slow wave produced by transmural nerve stimulation, presumably due to depolarization of the membrane. The latency for the i.j.p. remained the same in the presence of diltiazem (10(-5)M). It is concluded that in the guinea-pig stomach, diltiazem blocks Ca-influx during the generation of the overshooting spike potential, but not the Ca-influx related to generation of the abortive spike potential or the slow wave. The cholinergic excitatory and the non-adrenergic, non-cholinergic inhibitory transmission may not be much affected by diltiazem.

Action Potentials↗
PubMed1980

Comparative study of the effects of 4-aminopyridine and tetraethylammonium on neuro-effector transmission in the guinea-pig vas deferens.

1 Effects of 4-aminopyridine (4-AP) and tetraethylammonium (TEA) on the neuro-effector junction of the guinea-pig vas deferens were investigated by microelectrode and double sucrose gap techniques. 2 4-AP (0.05 to 0.5 mM) or TEA (0.5 to 1 mM) did not alter the membrane potential, or the membrane input resistance of the smooth muscle cell. 3 The amplitude and frequency of the miniature junction potentials (m.e.j.ps) were not modified by treatment with 4-AP (0.05 to 0.5 mM) or TEA (1 mM). 4 4-AP (1 mM) increased the membrane input resistance, enhanced the spike amplitude of the smooth muscle cells and thereby augmented the amplitude of twitch contraction. 5 4-AP (.05 to 0.5 mM) or TEA (1 mM) markedly increased the amplitude of excitatory junction potentials (e.j.ps), but the facilitation phenomena produced by repetitive stimulation were not affected. 6 The duration of the extracellularly recorded action potential from the small nerve bundle was prolonged by 4-AP (0.5 mM). 7 The amplitude of the e.j.p. was dependent on the external concentration of calcium. A straight line was produced when the amplitude of the e.j.p. and [Ca]o was plotted on a double log scale. Application of 4-AP resulted in a parallel shift of this line to the left. 8 These results indicate that 4-AP (0.05 to 0.5 mM) and TEA (0.5 to 1.0 mM) prolonged the action potential generated from the sympathetic nerve terminal thus enhancing the amplitude of the e.j.p. due to an increase in the Ca-influx. However, in the concentrations used, these compounds did not modify the Ca-mobilization in the nerve terminal or the postsynaptic membrane during the resting state.

4-Aminopyridine↗
PubMed1980

Action of morphine on the neuro-effector transmission in the guinea-pig ileum and in the mouse vas deferens.

Effects of morphine on the neuro-effector junction of the guinea-pig ileum or mouse vas deferens were investigated by the micro-electrode and double sucrose gap methods. 1. Morphine (10(-8)-10(-5) M) did not change the membrane potential, membrane resistance and electrical threshold required to produce the action potential of smooth muscle cells of guinea-pig ileum or mouse vas deferens. 2. Morphine (10(-8)-10(-7) M) markedly suppressed the amplitude of excitatory junction potential (e.j.p.) of ileum or that of vas deferens. However the same concentration of morphine did not suppress the inhibitory junction potential recorded from the guinea-pig ileum or the facilitation phenomena observed with repetitive stimulation in the mouse vas deferens. In addition, this opiate (3.5 x 10(-5) M) did not alter the amplitude or the frequency of miniature excitatory junction potential recorded from the mouse vas deferens. 3. Naloxone (3.5 x 10(-7) M), itself, exerted no effect on the membrane potential and amplitude of the e.j.p. After pretreatment with naloxone, however, the inhibitory action of morphine on the e.j.p. was suppressed. 4. The extracellularly recorded action potential from the small nerve bundle innervating the mouse vas deferens was not affected by morphine (3.5 x 10(-5) M). 5. The amplitude of the e.j.p. of the guinea-pig ileum was dependent on the concentration of [Ca]o. When [Ca]o and the relative amplitude of e.j.p. were plotted on a double logarithmic scale, the above relation yielded a straight line with a slope of 1.7. Application of morphine resulted in a reduction in the slope of the straight line to 1.0. 6. These results indicate that morphine probably suppresses the influx of Ca during spike electrogenesis in the nerve terminal, however, there is no modification of the action of Ca in nerve terminals.

Animals↗
PubMed1984

Presynaptic, muscarinic inhibition of non-adrenergic, non-cholinergic neuromuscular transmission in the chicken rectum.

Cholinergic inhibition of the non-adrenergic, non-cholinergic ( NANC ) transmission was investigated in the chicken isolated rectum with Remak's nerve attached. Stimulation of Remak's nerve (RT stimulation) at frequencies higher than 5 Hz elicited a late, slow contraction of the rectum in addition to an initial, fast NANC contraction. The late, slow contraction was blocked by atropine (0.25 microgram ml-1), potentiated by physostigmine (50 ng ml-1) and accompanied by an overflow of acetylcholine into the vascular perfusate, indicating the existence of cholinergic innervation to the rectum via Remak's nerve. RT stimulation (10 pulses at 0.5-1.0 Hz) elicited NANC -mediated excitatory junction potentials (e.j.ps). The e.j.p. amplitude declined at the second stimulus and then increased to reach a plateau. Atropine, by abolishing this decrease in amplitude, increased the mean amplitude of the e.j.ps during trains of stimuli but atropine did not affect the amplitude of the first e.j.p. Physostigmine reduced the mean e.j.p. amplitude, and this action was readily antagonized by atropine. A single intramural nerve stimulation delivered 2s or less before RT stimulation with trains of stimuli, suppressed the amplitude of the first e.j.p. of the train. This effect was abolished by atropine. Atropine in concentrations high enough to affect the e.j.p. amplitude had no effect on the resting membrane potential, the threshold for generating an action potential, or membrane resistance of the smooth muscle. It is concluded that RT stimulation at low frequencies causes the release of acetylcholine simultaneously with the NANC transmitter. The released acetylcholine acts mainly on prejunctional muscarinic receptors and mediates an inhibitory effect on the release of the NANC transmitter.

Acetylcholine↗
PubMed1983

Effects of adrenoceptor agonists and antagonists on smooth muscle cells and neuromuscular transmission in the guinea-pig renal artery and vein.

In the guinea-pig renal artery and vein, the membrane potential was -66.8 mV and -46.8 mV, the length constant 0.54 mm and 0.43 mm, and the time constant 240 ms and 98 ms, respectively. The maximum slope of the depolarization produced by a 10 fold increase [K]o was 46 mV in the renal artery and 39 mV in the renal vein. Noradrenaline (NA over 5 X 10(-7)M in the artery and over 10(-7)M in the vein) depolarized the membrane and slightly reduced the membrane resistance, assessed from relative changes in the amplitude of electrotonic potential. The action of NA was suppressed by prazosin in the artery but by yohimbine in the vein, i.e. the alpha 1-adrenoceptor is present in the extrajunctional muscle membrane in the renal artery while the alpha 2-adrenoceptor is present in the renal vein. Dopamine and isoprenaline did not modify the membrane properties. In the renal artery, repetitive perivascular nerve stimulation (0.1 ms, 50 Hz, 5 shocks) evoked excitatory junction potential (e.j.p.). Applications of guanethidine (10(-6) M) or tetrodotoxin (3 X 10(-7) M) abolished the generation of the e.j.p.. Low concentrations of phentolamine (5 X 10(-7) M), prazosin (10(-7) M) and yohimbine (5 X 10(-7) M) enhanced the e.j.p. amplitude, while high concentrations of phentolamine (10(-5) M) and prazosin (greater than 10(-5) M) reduced the amplitude of e.j.p.s. NA, dopamine and clonidine consistently suppressed the amplitude of e.j.ps, at any given concentration over 10(-7) M. Spontaneous generated miniature e.j.ps (m.e.j.ps) were recorded on rare occasions. Phentolamine and yohimbine both at 5 x 10(-7) M and prazosin 10(-7) M increased the appearance of m.e.j.ps. 5 In the renal vein, repetitive nerve stimulation failed to generate the e.j.p. Sympathetic innervation to this tissue seems to be sparse. 6 Specificity of innervation and adrenoceptors present on smooth muscle cells in both the renal artery and vein are discussed, and the presynaptic regulation ofNA release is compared with findings in other vascular tissues.

Animals↗
PubMed1986

Neuromuscular transmission in an insect visceral muscle.

The electrical properties of the muscles of locust oviduct have been examined using intracellular recordings. The muscle cells are both dye and electrically coupled. They possess a wide array of spontaneous electrical activity ranging from slow oscillations of membrane potential to action potentials. In addition to possessing spontaneous electrical activity, certain regions of the oviduct are under motor control. The amplitude of evoked excitatory junction potentials (EJPs) increased step wise revealing innervation from a maximum of three motor units. These EJPs underwent summation and facilitation, and reached a critical threshold at which point the membrane revealed an active response. Bath applied glutamate, aspartate, proctolin, and octopamine were tested for their ability to alter resting potential and EJPs. L-glutamate (1.6 X 10(-5) M and above) produced a dose-dependent depolarization of membrane potential accompanied by a reduction in amplitude of EJPs. Although L-aspartate resulted in similar effects, the concentrations required were higher than those for glutamate. Proctolin (6.3 X 10(-11) M-6.0 X 10(-9) M) resulted in a dose-dependent depolarization but had little or no effect on amplitude of EJPs. Application of D, L-octopamine (3.2 X 10(-5) M-1.7 X 10(-4) M) induced a small hyperpolarization and a reduction in amplitude of EJP. It is suggested that contractions of locust oviduct appear to be regulated by a combination of a classical neurotransmitter such as glutamate, along with the neuromodulators octopamine and proctolin.

Animals↗
PubMed1986

Possible interaction of cholinergic nerves with two different (pre and post) sites of the neuromuscular junction in guinea-pig vas deferens.

Effects of various drugs on the mechanical responses of the longitudinal smooth muscle of guinea-pig vas deferens evoked by ACh and field nerve stimulation were examined. ACh (28-280 microM) produced a contraction consisting of two phases. The first phase of the contraction was suppressed by guanethidine and by nicotinic antagonists. The second phase was suppressed only by atropine. Both phases were unaffected by TTX or prazosin. Field stimulation (0.1 msec, 40 Hz) evoked contractions which also consisted of two (early and late) phases. Guanethidine (0.1-1 microM) suppressed both phases whilst prazosin (1 microM) suppressed only the late phase. Atropine (0.1 microM) suppressed both phases whilst physostigmine (5 microM) potentiated both phases of field stimulation-evoked contractions. Pentolinium suppressed both phases of field stimulation-evoked contractions at low concentrations (2-10 microM), but potentiated them at a higher concentration (100 microM). dTC at a low concentration (0.5 microM) suppressed the early phase, but slightly enhanced the late phase of field stimulation responses. At a higher concentration (20 microM), dTC potentiated both phases of the response. Pentolinium and dTC did not affect the contractions induced by 90 mM-K ions, ATP or NA. These results suggest that cholinergic nerves possess an excitatory action not only directly at the smooth muscle but also at the noradrenergic nerve terminals. The role of each receptor is discussed further.

Adrenergic Fibers↗
PubMed1995

Electrical activity in rat tail artery during asynchronous activation of postganglionic nerve terminals by ciguatoxin-1.

1. The effects of ciguatoxin-1 (CTX-1) on the membrane potential of smooth muscle cells have been examined in rat proximal tail arteries isolated in vitro. 2. CTX-1 (> or = 10 pM) increased the frequency of spontaneous excitatory junction potentials (s.e.j.ps). At 100-400 pM, there was also a marked and maintained depolarization (19.7 +/- 1.4 mV, n = 14, at 400 pM). 3. In 20-400 pM CTX-1, perivascular stimuli evoked excitatory junction potentials (e.j.ps) which were prolonged in time course relative to control. 4. Although threshold and latency of the e.j.p. were not affected by CTX-1 (< or = 400 pM), propagated impulses were blocked at > or = 100 pM. 5. The spontaneous activity and the depolarization produced by CTX-1 were reduced in the presence of Ca2+ (0.1 mM)/Mg2+ (25 mM), omega-conotoxin (0.1 microM) or Cd2+ (50-100 microM). 6. All effects of CTX-1 were abolished by tetrodotoxin (0.3 microM). 7. Raised Ca2+ (6 mM) reduced the depolarization and spontaneous activity produced by CTX-1. 8. In 400 pM CTX-1, the membrane repolarized (17 +/- 3.2 mV, n = 4) following the addition of phentolamine (1 microM). S.e.j.ps and e.j.ps were selectively abolished by suramin (1 mM), and the membrane repolarized by 1.3 +/- 1.6 mV (n = 4). 9. We conclude that CTX-1 releases noradrenaline and ATP by initiating asynchronous discharge of postganglionic perivascular axons. In 100-400 pM CTX-1, the smooth muscle was depolarized to levels resembling those recorded in this artery during ongoing vasoconstrictor discharge in vivo.

Animals↗
PubMed1982

Effects of divalent cations and normorphine on spontaneous excitatory junction potentials in the mouse vas deferens.

1 Excitatory junction potentials (e.j.ps) occurring spontaneously or evoked by nerve stimulation were recorded intracellularly from smooth muscle cells of the mouse isolated vas deferens. 2 The amplitude of the evoked e.j.ps and the amplitude and frequency of spontaneous e.j.ps were measured before and during application of normorphine or solutions which might be expected change the influx of calcium ions into the nerve terminals. 3 Spontaneous e.j.ps could be recorded even in solutins which contained tetrodotoxin (1 microM), no added calcium an EGTA (1mM). A four fold increase in calcium concentration from 1.25 to 5 mM greatly increased the amplitude of the evoked e.j.ps but had no effect on the amplitude or frequency of the spontaneous e.j.ps. 4 Magnesium (12mM) and cobalt (4mM) both greatly reduced the evoked e.j.ps and also reduced the frequency of spontaneous e.j.ps. 5 Normorphine (2 microM) reduced the amplitude of the evoked e.j.p by 70% but had no effect on the amplitude or frequency of spontaneous e.j.ps. 6 It is suggested that normorphine inhibits noradrenaline secretion from nerve varicosities by a mechanism different from that of magnesium and cobalt. One possibility is a block of action potential propagation along varicose fibers.

Action Potentials↗
PubMed1985

Actions of ATP and alpha, beta-methylene ATP on neuromuscular transmission and smooth muscle membrane of the rabbit and guinea-pig mesenteric arteries.

In the rabbit mesenteric artery, adenosine triphosphate (ATP), showed two actions on the membrane potential of muscle cells: low concentrations (1-10 microM) hyperpolarized and high concentrations (greater than or equal to 50 microM) depolarized the membrane. Both changes in the potential were accompanied by increases in ionic conductance. In the rabbit mesenteric artery, alpha, beta-methylene ATP (MeATP), (greater than or equal to 30 nM) depolarized the muscle membrane at a lower concentration than ATP (greater than or equal to 50 microM), and increased the ionic conductance of the membrane. The depolarization induced by ATP was prevented by low concentrations of MeATP, but the hyperpolarization was retained. Furthermore, the hyperpolarization was not affected by theophylline (10 microM). In the guinea-pig mesenteric artery, ATP and MeATP depolarized and increased the ionic conductance of muscle membrane, but to depolarize the membrane, higher concentrations of both agents were required, compared to those in the rabbit mesenteric artery. In the mesenteric arteries from both species, perivascular nerve stimulation evoked excitatory junction potentials (e.j.ps). In both tissues, MeATP inhibited the amplitude of e.j.ps at lower concentrations than did ATP, and both agents had more potent inhibitory actions on rabbit than on guinea-pig. The inhibition of e.j.p. induced by low concentrations of these agents showed no relationship to depolarization, but the inhibition induced by high concentrations was paralleled by depolarization and increase in ionic conductance of the membrane. In the rabbit mesenteric artery, overflow of noradrenaline (NA) and its metabolite (3,4-dihydroxyphenylglycol; DOPEG) produced by perivascular nerve stimulation was examined. ATP (0.1 mM) but not MeATP (0.1 microM) reduced the overflow of NA, whereas both agents had no effect on the overflow of DOPEG. Exogenously applied high concentrations of NA (greater than or equal to 3 microM) depolarized the muscle membrane in both species. These NA-induced depolarizations were not affected by treatment with ATP or MeATP. It is concluded that, in the rabbit mesenteric artery, ATP is more likely to be involved in generation of e.j.ps than is NA. A similar interpretation in the guinea-pig mesenteric artery is complicated by the depolarization produced by high concentrations of ATP or MeATP.

Adenosine Triphosphate↗
PubMed1982

Some characteristics of transmission from non-adrenergic, non-cholinergic excitatory nerves to the smooth muscle of the chicken.

Non-adrenergic, non-cholinergic excitatory junction potentials (e.j.p.s) were recorded from the longitudinal muscle cells of the chicken rectum following stimulation of the nerve of Remak and field stimulation of intramural nerves. The amplitude of e.j.p.s was a direct function of the stimulus intensity. When peak depolarization of an e.j.p. reached threshold, a muscle action potential was evoked. When the extrinsic nerve was stimulated with a given stimulus intensity, the e.j.p.s recorded from different cells showed little change in amplitude and time-course, reached their peaks in 74 ms and declined to half their amplitudes in 230 ms. These corresponding values for the e.j.p.s in response to field stimulation were 51 ms and 159 ms respectively, but became larger as the microelectrode was moved away from the stimulating site. The amplitude became smaller also and the distance at which the e.j.p. declined to half its control amplitude was 4.3 mm. The time constant for the exponential decay phase of the e.j.p. was the same as the time constant for the muscle membrane. Facilitation of e.j.p. amplitude occurred during repetitive nerve stimulation; however, the facilitation was accompanied frequently by an initial depression phase during extrinsic nerve stimulation.

Adrenergic Fibers↗
PubMed1986

Dual excitatory actions of acetylcholine at the neuromuscular junction in the guinea-pig vas deferens.

The action of acetylcholine (ACh) on the smooth muscle of guinea-pig vas deferens was studied using the sucrose-gap method. ACh, when applied at a concentration of 10(-6) M, evoked a depolarization of the smooth muscle membrane which was slow in time course (slow depolarization). When ACh was applied at higher concentrations, another depolarization which was fast in time course (fast depolarization) occurred, overlapping the early part of the slow depolarization. The magnitudes of both depolarizations were concentration-dependent on ACh. TTX and adrenergic receptor antagonists had little effect on either depolarizations, while guanethidine and nicotinic receptor antagonists mainly suppressed the fast depolarization. In contrast, atropine suppressed the slow depolarization. The membrane conductance observed by current application, was reduced during the slow depolarization, and the reversal potential of the depolarization was 18.3 mV negative to the resting membrane potential. Whereas, the reversal potential of the fast depolarization was 27.6 mV positive to the resting membrane potential. This reversal potential was quite similar to that of the adenosine triphosphate (ATP)-induced depolarization, previously observed in the same tissue. From these observations, it is suggested that in the guinea-pig vas deferens, ACh acts on nicotinic receptors at the sympathetic postganglionic nerve terminal, causing the release mostly of a non-adrenergic transmitter, probably ATP. In addition, ACh also acts on muscarinic receptors on the smooth muscle membrane, inducing membrane depolarization resulting from a reduction of the membrane conductance to potassium ions.

Acetylcholine↗