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PubMed1982

Dual effects of catecholamines on pre- and post-junctional membranes in the dog trachea.

1 Effects of noradrenaline or isoprenaline on the membrane and contractile properties of the smooth muscle cell, or on the excitatory neuro-effector transmission in the dog trachea, in vitro, were observed by use of microelectrodes and double sucrose gap methods.2 Noradrenaline (<5 x 10(-6) M) or isoprenaline (<5 x 10(-7) M) modified neither the membrane potential nor the membrane resistance. Increased concentrations of noradrenaline (>5 x 10(-5) M) depolarized and isoprenaline (>5 x 10(-7) M) hyperpolarized the membrane, and these actions were suppressed by phentolamine and propranolol respectively. Both catecholamines reduced the membrane resistance.3 Noradrenaline (5 x 10(-6) M) or isoprenaline (5 x 10(-7) M) reduced the resting tension, raised the mechanical threshold required to produce the contraction and suppressed the amplitude of phasic contractions evoked by electrical depolarization of the membrane.4 The action potential evoked by an outward current pulse in the presence of tetraethylammonium (TEA) was not affected by 5 x 10(-6) M isoprenaline, while the mechanical response was markedly suppressed.5 The excitatory junction potential (e.j.p.) evoked by electrical field stimulation was blocked by atropine. Noradrenaline (5 x 10(-7) M) or isoprenaline (5 x 10(-8) M) suppressed the amplitude of e.j.p. with no change in the membrane potential or input membrane resistance. Depression in the amplitude of e.j.ps produced by noradrenaline or isoprenaline reduced the amplitude of phasic contractions evoked by e.j.ps.6 These inhibitory actions of the catecholamines on mechanical responses and on e.j.ps were suppressed by pretreatment with propranolol (4 x 10(-6) M).7 Dog tracheal smooth muscles are innervated by cholinergic excitatory and adrenergic inhibitory systems. Electrical field stimulation produced excitation of both cholinergic and adrenergic nerve fibres, and propranolol (4 x 10(-6) M) enhanced the amplitude of e.j.p. generated by excitation of cholinergic nerves when repetitive stimulation (10 stimuli at 20 Hz) was used, but not the amplitude of the e.j.p. evoked by a single stimulus.8 5-Hydroxytryptamine (6 x 10(-6) M) produced a tonic contracture of the dog trachea. After pretreatment with atropine (4 x 10(-6) M), field stimulation (50 mus in duration and repetitive stimuli at 20 Hz) induced reversal of the contracture induced by 5-hydroxytryptamine and this was abolished by propranolol (5 x 10(-6) M).9 These results indicate that endogenous or exogenous catecholamines, in relatively low concentrations, predominantly activate beta-adrenoceptors in the pre- and post-junctional membrane in the dog trachea, and induce muscle relaxation.

Animals↗
PubMed1972

An investigation of spontaneous potentials recorded from the smooth-muscle cells of the guinea-pig seminal vesicle.

1. A spontaneous discharge of small potentials from smooth muscle cells of the guinea-pig seminal vesicle has been described. The mean amplitude, frequency and duration of the potentials were 0.9 mV, 12.2/min, and 92 msec, respectively. Occasionally, large potentials of 5-7 mV were recorded.2. The frequency of spontaneous potentials was enhanced by about twofold in 15 mM potassium-Krebs solution. Removal of calcium from the perfusing solution, or adding excess magnesium (12 mM) suppressed the rate of these potentials. Cobalt (2.5 mM) did not affect them but blocked excitatory junction potentials evoked by the hypogastric nerve stimulation.3. The spontaneous potentials were unaffected by atropine. Their rate and amplitude were reversibly reduced in the presence of high concentrations of phentolamine (10(-4) but not by 10(-5) g/ml.). Guanethidine enhanced the frequency initially (5 min), but subsequently the control rate was not appreciably changed, even after 20 min of guanethidine perfusion.4. After post-ganglionic denervation or reserpine treatment, the frequency of discharge of spontaneous potentials was reduced, without any effect on amplitude.5. The properties of the spontaneous potentials recorded from the smooth muscle cells of the seminal vesicle are similar to those reported for the vas deferens. They appear to be due to an interaction between noradrenaline released from sympathetic nerve endings and the smooth-muscle cell membrane. Present experiments cannot completely rule out the possibility that another transmitter in addition to noradrenaline may be released at this neuroaffector junction.

Action Potentials↗
PubMed1981

Gap junctions on CA3 pyramidal cells of guinea pig hippocampus shown by freeze-fracture.

In freeze-fracture replicas of the hippocampus of guinea pig, gap junctions were found on membranes identified as belonging to the apical dendrites or somata of the CA3 pyramidal cells. The junctions were not part of mixed synapses. It is concluded that adjacent pyramidal cells, which in places lacked an interposed glial sheath are electrically coupled.

Animals↗
PubMed1980

Pharmacology of ORG NC 45 compared with other non-depolarizing neuromuscular blocking drugs.

From results of pharmacological tests on the neuromuscular and autonomic blocking actions of a series of pancuronium analogues, Org NC 45, the C16 monoquaternary analogue of pancuronium, was selected for detailed study. Org NC 45 has a non-depolarizing mechanism of action, is more rapid in onset and shorter in duration of action than pancuronium. It shows less cumulation than pancuronium or tubocurarine, and is easily antagonized by anticholinesterases and aminopyridines. Org NC 45 exhibits a low propensity to release histamine. Its ability to inhibit cholinesterases is not likely to be important at neuromuscular blocking doses. Org NC 45 possesses negligible ganglion-blocking activity and there is a wide margin between neuromuscular and vagal blocking doses. Thus cardiovascular side-effects are unlikely to occur with the use of Org NC 45. It will hydrolyse mainly to its 3-hydroxy analogue which, like Org NC 45, possesses a wide margin between neuromuscular and vagal blocking doses. Org NC 45 has a high selectivity for the neuromuscular junction and represents a potentially useful addition to the armamentarium of clinically useful muscle relaxants.

Aminopyridines↗
PubMed1986

Junctional transmission in renin-containing and smooth muscle cells of the afferent arteriole.

Intracellular recordings were done in renin-containing juxtaglomerular (JG) and vascular smooth muscle (VSM) cells of the mouse kidney afferent arteriole. Both cell types exhibited a membrane potential around -75 mV and spontaneous depolarizing transients resembling spontaneous excitatory junction potentials (SEJPs) in the arterioles of other organs. The amplitude distribution of these randomly occurring transients was skewed in both cell types with a modal value of 1.2-1.9 mV. Activation of presumably postjunctional alpha 1-, P2-, ANG II- and AVP-receptors depolarized JG and VSM cells. Application of the P1-purinoceptor agonist 2-chloroadenosine strongly increased frequency and amplitude of the SEJP-like events, whereas these transients were abolished by the P1-purinoceptor antagonist 8-phenyltheophylline, both substances presumably acting on prejunctional receptors. The SEJP-like events were completely depressed by reserpine treatment, but not abolished by alpha 1-, alpha 2-, and P2-antagonists. At present, it cannot be decided, whether norepinephrine is the sole transmitter in the afferent arteriole, acting on specialized junctional adrenoceptors with the P2-purinoceptors being irrelevant for junctional transmission, or whether both substances are co-transmitters. Except norepinephrine and ATP, all other transmitter candidates tested were ruled out for various reasons.

Animals↗
PubMed1981

Freeze-fracture study of the crayfish stretch receptor.

The crayfish slow-adapting stretch receptor was fixed under relaxed or stretched conditions (twice the relaxed length) and then processed for freeze-fracture study. The sensory neuron membrane had evenly distributed intramembrane particles mostly on its P face. The density of these particles was higher in the cell body than in the dendritic tips, which are the terminal portions of the dendrites. The dendritic tips were cylindrical under the relaxed condition and showed deformations with stretch stimuli. When they were fixed under the stretched condition with 1.6% glutaraldehyde in 0.12 M phosphate buffer (the total osmolarity of this fixative is isosmotic with the physiological solution), the dendritic tips showed regional swelling and shrinkage. The intramembrane particle density of the swollen parts decreased and there were particle-free patches of membrane, whereas the particle density of the shrunken parts increased. On the other hand when the receptor was fixed with 1.6% glutaraldehyde in 0.2 M phosphate buffer (the total osmolarity is hyperosmotic but buffer osmolarity is isosmotic), the diameter of the dendritic tips became smaller, and their membrane particle densities were almost the same as that under the relaxed condition. The sheath cells covering the sensory neuron were characterized by their sheet-like profiles, gap junctions, and crater-like protrusions. The receptor muscle membrane had longitudinal foldings, occasional invaginations, peripheral couplings, string-shaped particle aggregates, and band-shaped particle aggregates.

Animals↗
PubMed2000

An immunocytochemical study of intrapancreatic ganglia, nerve fibres and neuroglandular junctions in Brockmann bodies of the tompot blenny (Blennius gattoruggine), a marine teleost.

The innervation of the Brockmann bodies in the teleost fish, Blennius gattoruggine, was studied using immunocytochemical techniques at both the light and electron microscopy levels. Islet innervation consisted of intrapancreatic ganglia, generally localized inside the rim of the exocrine tissue of the Brockmann bodies, in proximity to the islet, nerve fibres and nerve terminals with synaptic complexes. The intrapancreatic ganglia were of variable size, with different numbers of ganglionic cells, that appeared unipolar in section. The cell bodies showed immunoreactivity to galanin, oxytocin, peptide tyrosine tyrosine and glucagon. The extrinsic and intrinsic nerve fibres passed through the exocrine parenchyma and crossed the connectival septa and islet connectival sheath, penetrating into the islets, where they became increasingly thinner. They terminated on the endocrine cells with dilated nerve terminals. At least three types of terminals were detected, depending on the different vesicle content: peptidergic, cholinergic or adrenergic. They presented specialized synaptic structures, the neuroglandular junctions, some of which contained neurosecretory granules immunogold labelled by galanin antiserum. This new finding confirms the role of galanin as a neurotransmitter. This rich supply of innervation may be important in the regulation and integration of islet secretion.

Animals↗
PubMed1986

Pharmacological studies on the role of cholinergic nerves in the neuromuscular transmission in the circular smooth muscle of guinea-pig vas deferens.

Effects of various drugs were examined on the mechanical responses of the circular smooth muscle of guinea-pig vas deferens evoked by field stimulation and ACh. During field stimulation (0.1 msec, 3-80 Hz) a contraction consisting of two (initial and second) phases occurred. In addition, another contraction (after-response) occurred after the cessation of the stimulation particularly at higher frequencies (40-80 Hz). Guanethidine (2-20 microM) suppressed both the initial and second phases of the field stimulation-evoked responses. Prazosin (0.1-1 microM) suppressed the second phase but minimally affected the initial phase. Both phases were suppressed by atropine (0.1-1 microM) and potentiated by physostigmine (5 microM). dTC (0.5-20 microM) did not suppress either phase but potentiated the second phase. ACh (0.28-280 microM) produced a contraction, which was reduced by atropine but was little affected by either dTC or TTX. These results suggest that at the postsynaptic site of the neuromuscular junction in this tissue the sympathetic process activates the smooth muscle through two different types of receptor; one is non-noradrenergic and the other is an alpha-adrenoreceptor. In addition, a cholinergic process also activates the smooth muscle through muscarinic receptors.

Acetylcholine↗
PubMed1982

The effects of substance P on smooth muscle cells and on neuro-effector transmission in the guinea-pig ileum.

1 The effects of substance P (SP) on the membrane and contractile properties of the smooth muscle cell, or on neuro-effector transmission in the guinea-pig ileum were observed by means of microelectrodes, double sucrose gap and tension recording.2 SP (10(-13)-10(-10)M) induced a phasic contraction of longitudinal muscle strips, but did not change the muscle tone of circular muscle strips, in concentrations up to 10(-8)M.3 SP (10(-10)-10(-8)M) evoked three different membrane responses in longitudinal muscle cells: (i) bursts of spike discharges with no significant change in the membrane potential and input membrane resistance; (ii) bursts of spike discharges with a small but clear depolarization of the membrane and increase in the input membrane resistance; (iii) slow waves with no change in the membrane potential.4 In the circular muscle cells, low concentrations of SP (<10(-8)M) did not affect the membrane potential or the spikes, but SP (10(-7)M) increased the spike discharges with no significant change in the membrane potential.5 SP (10(-10)M) reduced the threshold depolarization required for the generation of action potentials with no change in membrane potential of the longitudinal muscle cells.6 Pretreatment with atropine (5 x 10(-6)M), tetrodotoxin (TTX 10(-6)M) or baclofen (4.7 x 10(-6)M) had no effect on the excitatory actions of SP on the smooth muscle cells of longitudinal and circular muscle strips.7 Excitatory actions of SP on the membrane potential or spike activities of longitudinal muscle cells were preserved in NaCl but not in Ca-deficient solution.8 SP (10(-10)-10(-9)M) enhanced the amplitude of the excitatory junction potentials (e.j.ps) evoked by electrical field stimulation in longitudinal muscle cells with no change in the membrane potential and input resistance. SP (10(-10)-10(-9)M), however, did not change the amplitude of inhibitory junction potentials (i.j.ps) recorded from the circular muscle cells.9 These results indicate that SP in relatively low concentrations acts on both smooth muscle cells and on excitatory neuro-effector transmission in the longitudinal muscle; the main site of the action of SP is probably the muscle membrane.

Animals↗
PubMed1988

Electrophysiological analysis of the inactivation of sympathetic transmitter in the guinea-pig vas deferens.

1. The properties of junction potentials evoked by nerve stimulation and by local application of drugs, and currents evoked by nerve stimulation, in the smooth muscle cells of the guinea-pig vas deferens have been investigated. The effects of temperature on these responses have been studied using intracellular and extracellular recording. 2. Local, brief (5-15 ms) application of 10(-4) M-adenosine-5'-triphosphate (ATP) from glass micropipettes onto the surface of the vas deferens, using pressure pulses (103-206 kPa), elicited a depolarization of the smooth muscle cell membranes which closely resembled the nerve stimulation-evoked excitatory junction potential (EJP). 3. Local application of 10(-4) M-noradrenaline (NA) failed to produce any detectable membrane potential response. Junction potentials elicited by a mixture of 10(-4) M-ATP and 10(-4) M-NA (ratio by volume 1:50) in the drug ejection micropipette were similar in shape to those evoked by ATP alone. 4. Cooling the tissue from 35 to 25 degrees C did not significantly alter resting membrane potentials but resulted in a significant prolongation of the rising and decaying phases of the EJPs. Fifty per cent decay times for EJPs at 35 and 25 degrees C were (mean +/- S.D.) 236 +/- 20 and 434 +/- 30 ms respectively (P less than 0.01). 5. Extracellularly recorded excitatory junction currents (EJCs) elicited by nerve stimulation, believed to reflect the transmembrane current underlying the EJPs, were prolonged in parallel at low temperatures (50% decay times of EJCs at 35 and 25 degrees C: 11.73 +/- 3.94 and 26.15 +/- 8.4 ms, respectively, P less than 0.01). 6. Junction potentials evoked by locally applied, exogenous ATP were also significantly prolonged by cooling (50% decay times: 663 +/- 88 ms at 35 degrees C and 1955 +/- 79 ms at 25 degrees C, P less than 0.01). 7. Bath application of 10(-6) M-alpha,beta-methylene ATP, the enzymatically stable, desensitizing analogue of ATP, reversibly abolished nerve-evoked EJPs. Local application of 10(-6) M-alpha,beta-methylene ATP led to a prolonged depolarization of the smooth muscle cells lasting between 20 and 60 s. 8. Junction potentials elicited by locally applied alpha,beta-methylene ATP were not prolonged or otherwise significantly altered on cooling. The durations of the depolarizations were 46.0 +/- 12.1 s at 35 degrees C and 43.4 +/- 10.6 s at 25 degrees C (P greater than 0.1).(ABSTRACT TRUNCATED AT 400 WORDS)

Adenosine Triphosphate↗
PubMed1987

Characteristic features of transmitter release from sympathetic nerve terminals.

Recently, using intracellular recording techniques, it has been shown that transmitter release from individual varicosities in sympathetic nerves occurs intermittently, and that only a single quantum of transmitter is secreted when the release process of a varicosity is activated by the nerve action potential. Here we discuss results obtained using a novel method of extracellular recording which allows simultaneous measurement of both the nerve action potential and transmitter release from postganglionic sympathetic nerve terminals. We have confirmed that release is intermittent, but the importance of this new approach is that the relationship between the nerve terminal action potential and transmitter release can be studied unambiguously for the first time. Thus, we are able to show unequivocally that: (1) intermittence is caused by a low probability of transmitter release in the invaded varicosity; (2) frequency-dependent facilitation of release is determined by the rate of arrival of the action potential and not by detectable changes in its configuration; (3) the current underlying the exciitatory junction potential (EJP) is brief compared to the total duration of the EJP, and (4) clonidine may inhibit transmitter release by modifying the nerve terminal action potential. These results provide important new insights into the fundamental mechanisms involved in the physiological and pharmacological control of transmitter release from sympathetic nerves.

Action Potentials↗
PubMed1985

Pre- and post-junctional actions of prostaglandin I2, carbocyclic thromboxane A2 and leukotriene C4 in dog tracheal tissue.

Effects of carbocyclic thromboxane A2 (cTxA2), prostacyclin (PGI2) or leukotriene C4 (LTC4) on the membrane and contractile properties of the smooth muscle cells and on the excitatory neuro-effector transmission in the dog trachea were observed by means of the microelectrode, double sucrose gap and tension recording methods. cTxA2, PGI2 or LTC4 at a concentration of 10(-7)M had no effect on the membrane potential of smooth muscle cells of the dog trachea. At 10(-6)M, cTxA2 and LTC4 slightly depolarized, and PGI2 hyperpolarized the membrane. cTxA2 (greater than 2.7 X 10(-10)M) evoked a sustained contraction, while the amplitude of the twitch contractions evoked by field stimulation in the presence of indomethacin (10(-6)M) and propranolol (10(-6)M) was inhibited, dose-dependently. PGI2 (greater than or equal to 2.7 X 10(-7)M) reduced the muscle tone and the amplitude of twitch contractions evoked by field stimulations. cTxA2 or PGI2 (10(-10)-10(-7)M) reduced the amplitude of the excitatory junction potentials (e.j.ps) evoked by field stimulation with no change in the membrane potential, input membrane resistance or the sensitivity of the muscle cells to acetylcholine (ACh). LTC4 (1.6 X 10(-8)M) evoked a sustained contraction of the dog trachea; however, this agent did not affect either the amplitude of the twitch contractions or the e.j.ps evoked by field stimulation. The amplitude of the e.j.p. was dependent on the external concentration of Ca2+, and the inhibitory actions of cTxA2 on e.j.ps were partly overcome by increasing the concentrations of [Ca]o. When the amplitudes of e.j.ps were plotted against [Ca]o on a double log scale, the above relation yielded a straight line with a slope of 1.7 or 1.0, in the absence or presence of cTxA2, respectively. After treatment with Ca2+-free 2 mM EGTA-containing solution, cTxA2 or LTC4 did not evoke a contraction in the dog trachea, whereas ACh (10(-7)-10(-6)M) did. These results indicate that cTxA2 and PGI2 have dual actions on pre- and post-junctional membranes of the dog tracheal tissue, i.e. both agents inhibit the excitatory neuro-effector transmission in the dog trachea, presumably by inhibiting the release of ACh from the vagal nerve terminal. cTxA2 and LTC4 or PGI2 evoke contraction or relaxation of the muscle tissue, respectively, apparently through direct actions on the smooth muscle cells.

Animals↗
PubMed1982

Local regulation of transmitter release from rodent sympathetic nerve terminals?

1. Electrophysiological techniques were used to observe the release of transmitter from single release sites in the sympathetic neuro-effector junction of the rodent vas deferens. Transmitter release produces transient peaks in the rate of depolarization of the smooth muscle cells, known as 'discrete events'. 2. The amplitude distributions of stimulus-evoked discrete events in both mouse and guinea-pig vas are multi-modal. In the mouse, the distribution fits a Poisson with a 'quantal content' of about two. There are too many zeros in the amplitude distributions of guinea-pig discrete events to fit a Poisson distribution, and it is likely that in this species there is a mechanism preceding the transmitter release process which may occasionally prevent it operating. 3. alpha-adrenoreceptor agonists and antagonists produce, respectively, left and right shifts in the amplitude distributions of discrete events at a single latency, with no change in the amplitudes at the modes. 4. There is, however, no evidence of any inhibitory relationship between either discrete events evoked by successive stimuli, or early and late discrete events following a given stimulus. 5. Transmitter release at this junction is therefore packeted, with few quanta released by each stimulus. Release from single sites is affected in ways compatible with the 'alpha-feed-back' hypothesis by alpha-adrenoreceptor agonists and antagonists, but in the absence of drugs we can find no evidence of any local feed-back inhibition of transmitter release.

Animals↗
PubMed1983

[Effects of temperature on postsynaptic potentials at the cyto-neural junctions of the frog semicircular canal].

An analysis of the EPSPs recorded intracellularly from single fibres of the VIII nerve revealed that the resting release of chemical transmitter at the cyto-neural junctions in the sensory organ of frog semicircular canals displays a rather low temperature dependence. This provides evidence that, in labyrinthine receptors, the resting activity is actually "evoked" in nature. A comparison between the discharge of EPSPs and propagated spikes in the VIII nerve fibres has shown that the "encoders" of primary vestibular neurones are highly sensitive to temperature changes and irreversibly damaged at temperatures exceeding 28 degrees C.

Animals↗
PubMed1998

Mechanism of neuromuscular blockade induced by phenthonium, a quaternary derivative of (-)-hyoscyamine, in skeletal muscles.

1. The mechanisms underlying the postjunctional blockade induced by phenthonium [N-(4-phenyl) phenacyl 1-hyoscyamine] were investigated in mammalian and amphibian muscles. This muscarinic antagonist was previously shown to enhance specifically the spontaneous acetylcholine (ACh) release at concentrations that blocked neuromuscular transmission. 2. In both rat diaphragm and frog sartorius muscles, phenthonium (Phen, 1-100 microM) depressed the muscle twitches elicited by nerve stimulation (IC50: 23 microM and 5 microM, respectively), and blocked the nerve-evoked muscle action potential. The neuromuscular blockade was not reversed after incubation with neostigmine. 3. Equal concentrations of Phen decreased the rate of rise and prolonged the falling phase of the directly elicited action potential in frog sartorius muscle fibres, indicating that the drug also affects the sodium and potassium conductance. 4. Phen (50 and 100 microM) protected the ACh receptor against alpha-bungarotoxin (BUTX) blockade in the mouse diaphragm allowing recording of endplate potentials and action potentials after 5 h wash with physiological salt solution. 5. Phen (10-100 microM) produced a concentration- and voltage-dependent decrease of the endplate current (e.p.c.), and induced nonlinearity of the current-voltage relationship. At high concentrations Phen also shortened the decay time constant of e.p.c (tau(e.p.c.)) and reduced its voltage sensitivity. 6. At the same range of concentrations, Phen also reduced the initial rate of [125I]-BUTX binding to junctional ACh receptors of the rat diaphragm (apparent dissociation constant = 24 microM), the relationship between the degree of inhibition and antagonist concentration being that expected for a competitive mechanism. 7. It is concluded that Phen affects the electrical excitability of the muscle fibre membrane, and blocks neuromuscular transmission through a mechanism that affects the agonist binding to its recognition site and ionic channel conductance of the nicotinic ACh receptor.

Animals↗
PubMed1983

An inhibitory effect of ethanol on adrenergic neuromuscular transmission in the guinea-pig vas deferens.

Effects of ethanol on adrenergic neuromuscular transmission were investigated in the isolated vas deferens of the guinea-pig. The contractile responses to adrenergic nerve stimulation were depressed by ethanol in a concentration-dependent, reversible manner at a concentration range between 25 and 500 mM. Ethanol also depressed the contractions induced by exogenous noradrenaline. The resting membrane potentials recorded intracellularly from the smooth muscle cells were not affected by the alcohol. The excitatory junction potentials (EJPs) evoked by nerve stimulation decreased in amplitude, but the facilitation phenomena observed with repetitive stimulation remained unaltered. Ethanol slightly increased the frequency of the spontaneous EJPs, but decreased their amplitude. The extracellularly recorded action potentials from the small sympathetic nerve bundles innervating the vas deferens were suppressed by high concentrations of ethanol (more than 200 mM). These results indicate that ethanol inhibits adrenergic neuromuscular transmission in the vas deferens probably through depressing the sensitivity of the postsynaptic membrane to the transmitter and a block of axonal conduction in the presynaptic nerve terminals.

Acetylcholine↗