scholarly journals Quantal evoked depolarizations underlying the excitatory junction potential of the guinea-pig isolated vas deferens

1999 ◽  
Vol 520 (2) ◽  
pp. 527-537 ◽  
Author(s):  
Rohit Manchanda ◽  
K. Venkateswarlu
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 .


1987 ◽  
Vol 65 (9) ◽  
pp. 1988-1990 ◽  
Author(s):  
M. J. MacKay ◽  
D. W. Cheung

In the guinea-pig saphenous artery, stimulation of perivascular nerves elicited contraction and two types of synaptic potentials: the excitatory junction potential and the slow depolarization. The synaptic potentials were inhibited by atriopeptin II but not by sodium nitroprusside. Exogenous noradrenaline induced membrane depolarization and contraction, and both sodium nitroprusside and atriopeptin II inhibited the contraction but not the depolarization. These results suggest that atriopeptin II has an inhibitory effect both presynaptically at the nerve terminals and postsynaptically on the vascular smooth muscle cells.


1990 ◽  
Vol 179 (1-2) ◽  
pp. 129-139 ◽  
Author(s):  
Frank Porreca ◽  
Diane LoPresti ◽  
Susan J. Ward

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