Role of depolarization and calcium in contractions of canine trachealis from endogenous or exogenous acetylcholine

1991 ◽  
Vol 69 (4) ◽  
pp. 518-525 ◽  
Author(s):  
E. E. Daniel ◽  
J. Jury ◽  
R. Serio ◽  
L. P. Jager
Keyword(s):  
Chloride Channels ◽  
Membrane Resistance ◽  
Ca Channel ◽  
Field Stimulation ◽  
Mechanical Responses ◽  
Excitatory Junction Potential ◽  
Voltage Dependent ◽  
Excitatory Junction Potentials ◽  
Sucrose Gap ◽  
Junction Potential

The relationships of the electrical to the mechanical responses of the canine trachealis muscle during stimulation of its cholinergic nerves or exposure to exogenous acetylcholine were recorded in the single or the double sucrose gap. At 27 °C, the responses to a train of stimuli consisted of a transient depolarization excitatory junction potential of 10–30 mV followed by fading oscillations and contractions. When stimulus parameters were varied in the single sucrose gap, contractions were more closely associated with the occurrence of and varied in duration with the oscillations rather than with the amplitude of the EJP. Acetylcholine superfused at a concentration of 10−6 M for 30 s caused a prolonged depolarization of 10–20 mV, but a much larger contraction than could be elicited by nerve stimulation. None of the responses to acetylcholine was significantly affected by the Ca channel antagonists, nifedipine, nitrendipine, or verapamil in Ca channel blocking concentrations. When tissues were exposed to a Ca-free medium, the excitatory junction potentials and oscillations rapidly disappeared, but the electrical and mechanical responses to acetylcholine persisted and only gradually disappeared with repetitive exposures. Furthermore, in a medium with normal Ca2+ in the double sucrose gap, depolarization by 10–15 mV with an applied current caused no contraction, and repolarization to the normal membrane potential during acetylcholine-induced contraction caused no relaxation. Tetraethylammonium ion (20 mM) depolarized the membrane, increased membrane resistance, and enhanced the secondary oscillations and contractions after field stimulation. No other K+-channel blocker tested (Ba2+, apamin, 4-aminopyridine, glibenclamide, charybdotoxin) had the effect of prolonging secondary oscillations. We concluded that acetylcholine under our conditions acted to release internal Ca2+ and that the depolarization was secondary to that release or an associated event. Moreover, contractile responses to released acetylcholine during field stimulation do not appear to depend significantly on the opening of voltage-dependent Ca channels. The secondary oscillations were closely related to contraction; they seemed to be modulated by the opening of tetraethylammonium-sensitive, possibly Ca2+-activated K+ channels. The physiological functions, if any, of the initial depolarization associated with acetylcholine released (excitatory junction potential) or added remain unclear.Key words: acetylcholine, tracheal smooth muscle, trachea, chloride channels, sucrose gap, potassium channels.

Neurotransmission in the urinary bladder of rabbits and guinea pigs

1991 ◽  
Vol 261 (2) ◽  
pp. C271-C277 ◽  
Author(s):  
K. E. Creed ◽  
Y. Ito ◽  
H. Katsuyama
Keyword(s):  
Smooth Muscle ◽  
Guinea Pigs ◽  
Field Stimulation ◽  
Mechanical Responses ◽  
Rabbit Bladder ◽  
Excitatory Junction Potential ◽  
Release Of Acetylcholine ◽  
Sucrose Gap ◽  
Alpha Beta ◽  
Junction Potential

Alpha, beta-Methyleneadenosine 5'-triphosphate (alpha, beta-mATP) produced transient contraction of strips of bladder taken from rabbits or guinea pigs, and mechanical responses to field stimulation at 5-100 Hz were reduced by this drug by 5-20%. Atropine reduced responses by approximately 50%, and both drugs together by 80-95%. In double sucrose gap experiments on the rabbit bladder, alpha, beta-mATP selectively reduced but did not abolish an initial excitatory junction potential (ejp), and atropine selectively abolished a late depolarization. In the guinea pig, a single ejp was partially inhibited by either alpha,beta-mATP or atropine. Residual responses were further reduced by tetrodotoxin in both species. The initial ejp and late depolarization in the rabbit were reduced in parallel by hemicholinium over 2 h, suggesting that release of acetylcholine (ACh) and the second transmitter by nerves may be coupled. ACh but not ATP produced an increase in intracellular concentration of inositol trisphosphate in dispersed smooth muscle cells from the rabbit bladder; ATP but not carbachol produced a small transient current across the cell membrane in this species. It is concluded that ACh mobilizes intracellular Ca2+ for contraction, whereas the effect of ATP is dependent on extracellular Ca2+.

Chloride and depolarization by acetylcholine in canine airway smooth muscle

1993 ◽  
Vol 71 (3-4) ◽  
pp. 284-292 ◽  
Author(s):  
E. E. Daniel ◽  
J. Jury ◽  
J.-P. Bourreau ◽  
L. Jager
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Chloride Channels ◽  
Reversal Potential ◽  
Chloride Ion ◽  
Resting Potential ◽  
Mechanical Responses ◽  
Intracellular Ca ◽  
Excitatory Junction Potentials ◽  
Sucrose Gap

The role of chloride channels has been examined in canine tracheal smooth muscle by recording mechanical responses to field stimulation and to acetylcholine (ACh) and by sucrose gap recording of excitatory junction potentials and ACh-induced electrical changes. The results of substitution studies using isethionate for chloride provided evidence that a chloride conductance contributes to the resting potential. The extrapolated reversal potential for ACh-induced depolarization was positive to the resting potential. Isethionate substitution inhibited ACh-induced depolarization, consistent with a contribution from increased Cl− conductance to the depolarization induced by ACh. However, closure of K+ channels and opening of a nonspecific cation channel could also contribute to depolarization. Further study of the effects of isethionate substitution during prolonged tissue exposure to chloride-free medium showed that retention or the accumulation of Ca2+ in intracellular stores was impaired. We conclude that effects of chloride deprivation on responses to ACh may reflect an early increase in Cl− conductance, but longer term changes reflect the requirement for this anion to maintain internal Ca2+ stores.Key words: chloride ion, airway smooth muscle, ion channels, release of intracellular Ca2+.

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

1982 ◽  
Vol 242 (3) ◽  
pp. H325-H336 ◽  
Author(s):  
H. Suzuki ◽  
T. Itoh ◽  
H. Kuriyama
Keyword(s):  
Mesenteric Artery ◽  
Channel Blocker ◽  
Surface Membrane ◽  
Smooth Muscles ◽  
Membrane Resistance ◽  
Membrane Properties ◽  
Ca Channel ◽  
Mechanical Responses ◽  
Ca Antagonist ◽  
Excitatory Junction Potentials

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.

K+-channel blockers do not decrease acetylcholine depolarizations in canine trachealis

1992 ◽  
Vol 70 (1) ◽  
pp. 43-52 ◽  
Author(s):  
E. E. Daniel ◽  
J. Jury ◽  
R. Serio ◽  
L. P. Jager
Keyword(s):  
Chloride Channels ◽  
Reversal Potential ◽  
Membrane Conductance ◽  
Membrane Resistance ◽  
Resting Potential ◽  
K Channel ◽  
Channel Blockers ◽  
Membrane Effects ◽  
Sucrose Gap ◽  
Time Courses

Using the double sucrose gap, we have examined the role of K+ channels in the cholinergic depolarizations in response to field stimulation and acetylcholine (Ach) in canine trachealis. Acetylcholine-like depolarization per se decreased electrotonic potentials from hyperpolarizing currents. The net effect of acetylcholine (10−6 M) depolarization on membrane conductance was a small increase after the depolarization was compensated by current clamp. Reversal potentials for acetylcholine depolarization and for the excitatory junction potential (EJP) were determined by extrapolation to be 20–30 mV positive to the resting potential, previously shown to be approximately −55 mV. They were shifted positively by tetraethylammonium ion (TEA) at 20 mM or Ba2+ at 1 mM. TEA or Ba2+ initially depolarized the membrane and increased membrane resistance. Repolarization of the membrane restored any reductions in EJP amplitudes associated with depolarization. After 15 min, the membrane potential partially repolarized, and acetylcholine-induced depolarization and contractions were then increased by TEA. 4-Aminopyridine depolarized the membrane but decreased membrane resistance. Apamin (10−6 M), charybdotoxin (10−7 M), and glybenclamide (10−5 M) each failed to significantly depolarize membranes, increase membrane resistance, or reduce EJP amplitudes or depolarization to 10−6 M Ach. Glybenclamide reduced depolarizations to added acetylcholine slightly. TEA occasionally reduced the EJP markedly, but this was shown to be most likely a prejunctional effect mediated by norepinephrine release. TEA alone among K+-channel blockers slowed the onset and the time courses of the EJP as well as the acetylcholine-induced depolarization. K+-channel closure cannot be a complete explanation of acetylcholine-induced membrane effects on this tissue. Acetylcholine must have increased the conductance of an ion with a reversal potential positive to the resting potential in addition to any effect to close K+ channels.Key words: acetylcholine, tracheal smooth muscle, trachea, chloride channels, sucrose gap, potassium channels, tetraethylammonium, Ba2+.

Effects of endogenous and exogenous prostaglandin in neurotransmission in canine trachea

1987 ◽  
Vol 65 (7) ◽  
pp. 1433-1441 ◽  
Author(s):  
E. E. Daniel ◽  
C. Davis ◽  
V. Sharma
Keyword(s):  
Nerve Stimulation ◽  
Potent Inhibitor ◽  
Dose Range ◽  
Low Frequency ◽  
Organ Bath ◽  
Field Stimulation ◽  
Frequency Responses ◽  
Amplitude Maximum ◽  
Excitatory Junction Potentials ◽  
Sucrose Gap

The effect of PGE2 on neurotransmission in the canine tracheal strip dissected free of epithelium was studied in the single sucrose gap and organ bath. PGE2 was a potent inhibitor of the initiation of excitatory junction potentials (ejps) by just submaximal nerve stimulation. In a concentration of 10−9 or 10−8 M PGE2 nearly or completely abolished them. Contractile responses to field stimulation in the sucrose gap at 27 °C or in muscle baths at 37 °C were also reduced or abolished by PGE2 in the same dose range; reductions were greater at low frequency. Responses to acetylcholine were also depressed but significantly less than to field stimulation. These are consistent with major presynaptic as well as some postsynaptic inhibitory actions of PGE2. No evidence was obtained that endogenous PGE2 affected excitatory junction potentials and contractions; i.e. they were stable for hours and unaffected by indomethacin 10−6 and 10−5 M under our conditions. Post-stimulus potentiation of ejps amplitude, maximum at 10 s, was observed and became more marked after the first ejp had been markedly reduced or abolished by PGE2. This potentiation was unaffected by indomethacin. It was suggested that a presynaptic process inhibited by PGE2 might participate in this potentiation. The canine trachea is a useful preparation when studied under the experimental condition used here for study of effects of products of arachidonate on neurotransmission.

Thromboxane effects on canine trachealis neuromuscular function

1988 ◽  
Vol 64 (5) ◽  
pp. 1979-1988 ◽  
Author(s):  
R. Serio ◽  
E. E. Daniel
Keyword(s):  
Platelet Activating Factor ◽  
Neuromuscular Control ◽  
Direct Effects ◽  
Potential Oscillations ◽  
Mechanical Responses ◽  
Excitatory Junction Potentials ◽  
Sucrose Gap ◽  
Secondary Membrane ◽  
Trachealis Muscle

The objective of this study is to determine which inflammatory mediators had direct effects on canine trachealis muscle neuromuscular control to identify candidate mediators of the hyperresponsiveness observed in vitro after O3 exposure. Studies were carried out in the sucrose gap at 29 degrees C and in the muscle bath at 37 degrees C. Leukotriene (LT) B4, LTD4, and prostaglandin (PG) D2 had neither direct nor significant effects on the excitatory junction potentials (EJP's), the secondary membrane potential oscillations, or the associated contractions that followed field stimulation of cholinergic nerves. U 46619, a stable analogue of thromboxane (Tx) A2, enhanced (10(-10)-10(-7) M) the duration and the amplitude of secondary oscillations and associated contractions without affecting the EJP's. In the muscle bath, U 46619 enhanced field-stimulated contractions; this was antagonized competitively by SQ 29548. In both the sucrose gap and the muscle bath, higher concentrations (10(-9) M and higher) caused direct effects, small depolarizations, and contractions. These effects of U 46619 were unaffected by indomethacin or guanethidine but were abolished by SQ 29548, an antagonist selective at TxA2-PGH2 receptors. U 46619 at 10(-9) M did not affect electrical or mechanical responses to acetylcholine and at 10(-9) M did not increase the sensitivity to acetylcholine. Platelet-activating factor (PAF) was inactive in all muscle-bath and most sucrose-gap experiments. In 7 of 20 of the latter, it caused effects qualitatively like those of U 46619, but whether it acted through release of TxA2 could not be tested because of the rapid tachyphylaxis to PAF. We conclude that TxA2 may mediate the hyperresponsiveness found in vitro after O3 treatment.

Prostaglandins augment muscarinic responses in the rabbit cecum

1989 ◽  
Vol 256 (1) ◽  
pp. G100-G106
Author(s):  
K. Nakao ◽  
K. Kitamura ◽  
H. Kuriyama
Keyword(s):  
Electrical Stimulation ◽  
Membrane Potential ◽  
Prostaglandin E2 ◽  
Muscle Tone ◽  
Thromboxane A2 ◽  
Twitch Contraction ◽  
Mechanical Responses ◽  
Excitatory Junction Potential ◽  
Junction Potential

Effects of prostaglandin E2, F2 alpha, and synthetic thromboxane A2 (PGE2, PGF2 alpha, and STA2, respectively) on electrical and mechanical responses of the rabbit cecum were investigated. Transmural electrical stimulation evoked an excitatory junction potential (EJP) and contraction, events that were inhibited by 1 microM atropine or 0.3 microM tetrodotoxin. Indomethacin (up to 30 microM) modified neither the membrane potential nor the muscle tone but did inhibit amplitudes of the EJP and the twitch contraction. In the presence of 30 microM indomethacin, PGE2 (below 1 nM) had no effect on the membrane potential or muscle tone, while PGE2 (above 10 nM) contracted the cecal tissues, without depolarization. PGE2 enhanced the twitch contraction and restored the EJP in the presence of 30 microM indomethacin. Acetylcholine (0.1-3 microM) depolarized the membrane, but in the presence of 30 microM indomethacin, this depolarization was inhibited. PGE2 (0.1-100 nM) prevented these inhibitory actions of indomethacin. PGF2 alpha (0.1-100 nM) had weaker actions than PGE2 while STA2 (0.1-100 nM) had no effect on muscarinic responses. Thus muscarinic responses are augmented by primary prostaglandins.

scholarly journals Reversible control of synaptic transmission in a single gene mutant of Drosophila melanogaster.

1983 ◽  
Vol 96 (6) ◽  
pp. 1517-1522 ◽  
Author(s):  
J H Koenig ◽  
K Saito ◽  
K Ikeda
Keyword(s):  
Drosophila Melanogaster ◽  
Elevated Temperature ◽  
Synaptic Transmission ◽  
Transmitter Release ◽  
Flight Muscle ◽  
Single Gene ◽  
Gene Mutant ◽  
Excitatory Junction Potential ◽  
Excitatory Junction Potentials ◽  
Junction Potential

Synaptic transmission of the single gene mutant, shibirets1 (shi), of Drosophila melanogaster is reversibly blocked by elevated temperature. The presynaptic mechanism of transmission was studied in the neuromuscular junction of the dorsal longitudinal flight muscle of this mutant. It was observed that when the temperature was raised to 29 degrees C in shi flies, the amplitude of the excitatory junction potential (EJP) greatly diminished, the frequency of spontaneously released miniature excitatory junction potentials (MEJP's) was greatly reduced, and almost complete vesicle depletion was observed. These conditions were reversible if the temperature was lowered to 19 degrees C. These data suggest that the block in transmission is a result of vesicle depletion. It is suggested that depletion occurs not as a result of excessive release of transmitter but rather as a result of a block in the recycling of vesicles, which causes depletion as exocytosis (transmitter release) proceeds normally.

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

1983 ◽  
Vol 81 (3) ◽  
pp. 355-372 ◽  
Author(s):  
R S Zucker ◽  
L O Lara-Estrella
Keyword(s):  
Transmitter Release ◽  
Calcium Concentration ◽  
Neuromuscular Junctions ◽  
Slow Component ◽  
Nonlinear Relationship ◽  
Time Constants ◽  
Excitatory Junction Potential ◽  
Excitatory Junction Potentials ◽  
Presynaptic Calcium ◽  
Junction Potential

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.

Electrical and Mechanical Properties of the Red and White Muscles in the Silver Carp

1972 ◽  
Vol 57 (2) ◽  
pp. 551-567
Author(s):  
T. YAMAMOTO
Keyword(s):  
Mechanical Properties ◽  
White Muscle ◽  
Silver Carp ◽  
Membrane Resistance ◽  
Resting Potential ◽  
Resting Membrane Potential ◽  
Mechanical Responses ◽  
Red Muscle ◽  
Red And White Muscles ◽  
Specific Membrane

1. Electrical and mechanical properties of the red muscle (M. levator pinnae pectoralis) and white muscle (M. levator pinnae lateralis abdominis) in the silver carp (Carassius auratus Linné) were investigated by using caffeine and thymol. 2. A complete tetanus could be produced in the red muscle. But in the white muscle no tetanus was produced and there was a gradual decrease in tension during continuous stimulation, even at a frequency of 1 c/s or less. 3. Caffeine (0.5-1 mM) and thymol (0.25-0.5 mM) potentiated the twitch tension in both muscles without an increase in the resting tension; they produced a contracture in both muscles when the concentration was increased further. 4. The falling phase of the active state of contraction was nearly the same in both muscles and was prolonged by caffeine (0.5 mmM) and by thymol (0.25 mM). 5. The resting membrane potential of the red muscle was scarcely affected by caffeine (0.5-5 mM), whereas in the white muscles a depolarization of 10 mV was observed with caffeine of more than 2 mM. The resting potential of both muscles was little changed by o.25 mm thymol. However, at a concentration of more than 0.5mM thymol depolarized the membrane in both muscles to the same extent. 6. In caffeine (2-3 mM) solution the mean specific membrane resistance was reduced from 8.8 kΩ cm2 to 6.0 kΩ cm2 in the red muscle, and from 5.0 kΩ cm2 to 2.7 kΩ cm2 in the white muscle. In thymol (0.5-1 mM) solution it was reduced from 11.2 kΩcm2 to 6.5 kΩ cm2 in the red muscle, and from 5.4kΩ cm2 to 3.1 kΩ) cm2 in the white muscle. The specific membrane capacitance, calculated from the time constant and the membrane resistance, remained more or less the same in both muscles after a treatment with these agents. 7. Electrical properties of the muscles and the effects of caffeine and thymol on mechanical responses suggest that there are no fundamental differences between red and white muscles except for the excitation-contraction coupling. A lack of summation of twitch, a successive decline of twitch, and inability to produce potassium contracture in the white muscle may be due to the fact that the Ca-releasing mechanism is easily inactivated by depolarization of the membrane.

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