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

2001 ◽  
Vol 85 (1) ◽  
pp. 98-104 ◽  
Author(s):  
Hao Li ◽  
Doug Harrison ◽  
Grace Jones ◽  
Davy Jones ◽  
Robin L. Cooper

We investigated behavior, physiology, sensitivity to exogenous application of ecdysone, and nerve terminal structure for differences between the reduced ecdysone genotype, ecd 1 /ecd 1, and wild-type control ecd 1 /TM6Banimals during the early and late third instars when raised at 25°C. The ecd 1 mutants were able to survive through larval development and form pupae. However, the results demonstrate that the time to pupation is lengthened by about 50 h for the ecd 1 /ecd 1 as compared with the wild-type control siblings. In addition to the lengthened larval cycle in the mutant, ecd 1 /ecd 1animals, they also display behavioral differences as compared with controls. The rate of body wall contraction and mouth hook movements are reduced in the early third instar of ecd 1 /ecd 1 as compared with controls. The physiological measure of excitatory junction potential amplitude for the combined Is and Ib terminals did not reveal any differences among the two genotypes during the early third instar but the synaptic strength is reduced in the late third instars for controls. Application of exogenous ecdysone is still effective during the late third instar for the ecd 1 /ecd 1 but not the controls. This suggests that endogenous production of ecdysone have already taken place in the wild-type but not the ecd 1 /ecd 1larvae, thus the rapid nongenomic responses could still be observed in the late third ecd 1 /ecd 1larvae. Structurally the number of varicosities and the terminal length showed significant differences between ecd 1 /ecd 1 and the wild-type ecd 1 /TM6B genotype in the late third instars.


2000 ◽  
Vol 203 (5) ◽  
pp. 941-950 ◽  
Author(s):  
J.W. Barclay ◽  
R.M. Robertson

Functional neuromuscular connections are critical for appropriate behavioural responses, but can be negatively affected by increases in temperature. We investigated the effects of heat shock on the thermosensitivity of a neuromuscular pathway to the hindleg tibial extensor muscle of Locusta migratoria. We found that exposure to heat shock induced thermoprotection of both neuromuscular transmission and extensor muscle contraction by (i) increasing the upper temperature limit for failure, (ii) improving recovery following heat-induced failure and (iii) stabilizing excitatory junction potential amplitude and duration and extensor muscle contraction force at high temperatures. Furthermore, the heat-shock-induced thermoprotection of extensor muscle contraction was not attributable to a protective effect on intrinsic components of muscle contraction. Finally, the use of jumping as a locomotor strategy to avoid capture, a behavioural response dependent upon functionally competent neuromuscular connections at the hindleg tibial extensor muscle, became less sensitive to temperature following heat shock. We conclude that the natural stress response of the locust stabilizes neuromuscular signalling during temperature stress, and that this can underlie a thermoprotection of muscle contraction force and thus alter the thermosensitivity of an escape behaviour critical for survival.


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.


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.


1995 ◽  
Vol 347 (1320) ◽  
pp. 187-204 ◽  

A bidomain model of the smooth muscle syncytium has been used to analyse the sources of transmitter secretion that give rise to the excitatory junction potential (EJP) in the guinea-pig vas deferens. The timecourse of the spontaneous excitatory junction potential (SEJP) has been taken to be the same as the time course of action of a quantum of transmitter. The amplitude of the SEJP is dependent on both the size of the quantum secreted and the distance away of the source of the quantum from the muscle cells. Two such sources are considered, one identified as the close-contact varicosities (ccvs) about 50 nm from the muscle and the other as loose-contact varicosities (LCVS) at greater distances. It is shown that in order for the syncytium to reach equipotential by the time the EJP has declined to about 80% of its peak, each muscle cell must receive a quantum of transmitter. The relatively low density of innervation of muscle cells by ccvs so far reported, together with the extremely low probability for secretion from these, indicates that many LCVS surrounding each muscle cell contribute to the EJP . The rising phase of the EJP contains components that indicate the sources of the transmitter responsible for its generation, and these components have been made explicit by differentiating the EJP to give the DEJP. This always has a smooth and relatively slow component that lasts for about 80 to 100 ms and occasionally has fast components superimposed on it. These latter are shown to be almost certainly due to secretion of quanta from the ccvs. It is known that there is a distribution of action potential velocities in the sympathetic nerves to the vas deferens. To account for this, the secretion of quanta from different ccvs on a set of muscle cells in the syncytium were given different delays so that the DEJP consisted of a slow wave form that extended over 80 ms, composed of clearly discernible components arising from the ccvs. This wave form could be smoothed by allowing each cell in the syncytium to receive a quantum of transmitter from a ccv, a condition that did not then allow for the appearance of fast components in the DEJP. A model that generated both the non-interm ittent slow component of the DEJP and the interm ittent fast component consisted of each cell in the syncytium receiving an innervation from a single ccv as well as from a large number of LCVS. In this case, all the varicosities could secrete a quantum of transm itter with a particular probability after a delay characteristic for that varicosity. The size of the quanta were drawn from distributions with means that were graded according to the distance of the varicosities from the muscle cells. It is shown that under these conditions the model can account for the observed combinations of fast and slow components of the DEJP . Also accounted for are the effects of stimulating the intram ural sympathetic nerves compared with stimulating the hypogastric nerve, as well as the effects of increasing the number of nerves stimulated and increasing the calcium concentration. The suggestion is made that the EJP is due to the LCVS in this preparation with the occasional secretion from a ccv modifying the rate of rise of the EJP .


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