Stimulating PACα Increases Miniature Excitatory Junction Potential Frequency at theDrosophilaNeuromuscular Junction

2009 ◽  
Vol 23 (1-2) ◽  
pp. 220-224 ◽  
Author(s):  
Daniel Bucher ◽  
Erich Buchner
1982 ◽  
Vol 242 (1) ◽  
pp. C59-C64 ◽  
Author(s):  
C. A. Colton ◽  
J. S. Colton

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.


1999 ◽  
Vol 277 (1) ◽  
pp. R24-R30 ◽  
Author(s):  
Timothy Pearson ◽  
David Hyde ◽  
Ken Bowler

The control of the attainment of acclimation in Cancer pagurus has been studied. Homologous (8 or 22°C) and heterologous acclimation [central nervous system (CNS) and periphery of crabs simultaneously held at 8 or 22°C] were used. The dependence of electrophysiological parameters of dactylopodite closer muscles of walking legs on nerve stimulation was determined between 6 and 26°C. Muscle resting potential (RP) hyperpolarized linearly with increasing measurement temperatures and showed a 69% compensation between 8 and 22°C on homologous acclimation. With the CNS temperature constant at 8°C, the leg muscle RP showed a 72% compensation on heterologous acclimation to 8 and 22°C; when CNS temperature was constant at 22°C, leg muscle RP showed a 48% compensation on heterologous acclimation to 8 and 22°C. In homologous acclimation, the shape of the excitatory junction potential vs. temperature relationship was characteristic of acclimation temperature. In heterologous acclimation, the shape of this plot was related to the temperature experienced by the leg and not by the CNS. Thus acclimation was principally dependent on local tissue temperature and was relatively independent of CNS or hormonal influences.


2005 ◽  
Vol 53 (2) ◽  
pp. S357.3-S357
Author(s):  
E. A. Goebel ◽  
Z. H. Dodd ◽  
A. Losiniecki ◽  
D. Hertzler ◽  
R. Hasan ◽  
...  

1988 ◽  
Vol 254 (6) ◽  
pp. H1142-H1148 ◽  
Author(s):  
T. Inoue ◽  
M. S. Kannan

Electrical responses evoked by perivascular nerve stimulation were recorded from rat small intrapulmonary artery with the microelectrode technique. Nerve stimulation with a single pulse produced an excitatory junction potential that was insensitive to phentolamine, propranolol, atropine, ketanserin, mepyramine, and guanethidine but was abolished by tetrodotoxin. Treatment with reserpine in vivo or with 6-hydroxydopamine in vitro had no significant effect on the amplitude of the junction potentials. In the mesenteric arteries from the same rats, these procedures led to the inhibition of the junction potentials, confirming adequate functional sympathectomy. Low concentrations of alpha, beta-methylene ATP attenuated the amplitude of the excitatory junction potential without changing the membrane potential. The membrane depolarization induced by norepinephrine or serotonin were not. It is concluded that the excitatory junction potential in rat pulmonary artery results from the release of a nonadrenergic, noncholinergic neurotransmitter from perivascular nerves that are not sympathetic and that the most likely transmitter is ATP. Such neurotransmission may play a role in the regulation of regional pulmonary blood flow.


1998 ◽  
Vol 76 (6) ◽  
pp. 684-689 ◽  
Author(s):  
R Serio ◽  
F Mulè ◽  
F Bonvissuto ◽  
A Postorino

Using the sucrose-gap technique, we attempted to assess a role for tachykinins (TKs) in mediating noncholinergic excitatory junction potential (EJP) and contraction, in the circular muscle of rat proximal colon. Excitatory responses were evoked by submaximal electrical field stimulation (EFS) in the presence of atropine (1 µM), guanethidine (1 µM), indomethacin (10 µM), and Nomega -nitro-L-arginine methyl ester (L-NAME) (100 µM). The NK1 receptor antagonist, SR 140,333 (up to 3 µM) or the NK2 receptor antagonists, SR 48,968 and MEN 10,627 (up to 5 µM) produced a partial inhibition of the excitatory responses to EFS. The co-administration of the selective NK1 and NK2 receptor antagonists produced additive effects on the responses to EFS. Selective NK1 receptor agonist, [Sar9, Met (O2)11]-substance P, induced depolarization and contraction, antagonized by SR 140,333, but not by NK2 receptor antagonists. NK2 receptor agonist, [ betaAla8]-neurokinin A (4-10), also produced electrical and mechanical excitatory effects that were antagonized by SR 48,968 or MEN 10,627, but not by the NK1 receptor antagonist. Our results provide evidence that, in circular muscle of rat colon, endogenous tachykinins are the main excitatory transmitters for nonadrenergic, noncholinergic (NANC) excitation and their action is mediated by both NK1 and NK2 receptors.Key words: NK1 receptor, NK2 receptor, nonadrenergic, noncholinergic (NANC) excitatory junction potential, intestine.


1989 ◽  
Vol 256 (1) ◽  
pp. G100-G106
Author(s):  
K. Nakao ◽  
K. Kitamura ◽  
H. Kuriyama

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.


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