Effect of Quaternary Ammonium Ions on Electrical Activity of Spinal Ganglion Cells in Frogs

1983

British J Pharmacology

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1 The effect of substance P on the sensitivity of nicotinic acetylcholine (ACh) receptors of bullfrog sympathetic ganglion cells and frog skeletal muscle endplate was examined electrophysiologically. 2 The amplitude of ACh-induced postsynaptic potential (ACh potential) and current (ACh current) were reversibly and dose-dependently reduced by substance P at low concentrations (0.42-42 AM).3 The mean amplitude of the miniature endplate potential (m.e.p.p.) was also reduced by substance P (4.2 pM).4 Substance P (4.2 tM) shifted the S-shaped dose-response curve of the ACh current downward. A Lineweaver-Burk plot constructed from the dose-response curve revealed that substance P depressed the maximum response ( V,,,) without changing the apparent affinity (Km) of ACh for the receptor.5 Substance P (0.42-42 1M) did not alter the reversal potential of the ACh current of the endplate. The half-decay time of endplate current (e.p.c.) and its voltage-dependency were not altered by substance P in these concentrations. 6 The depression of the ACh current by substance P may not be due to a blockade of the opened channel which has been activated by the preceding combination of ACh with the receptor. 7 These results suggest that substance P suppresses the sensitivity of nicotinic ACh-receptors of the sympathetic ganglion cell and skeletal muscle endplate, acting on a certain allosteric site but not the recognition site of ACh in the receptor-ionic channel complex.

Section: Methodsmentioning

confidence: 99%

Substance P modulates the sensitivity of the nicotinic receptor in amphibian cholinergic transmission

Akasu

Kojima

1983

British J Pharmacology

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“…In order to examine the effect of adrenaline on the membrane resistance The effects of adrenaline on the TEA-potential of spinal ganglion cells were also examined.It has been known that spinal ganglion cells are capable of producing action potentials(TEA-potential)when these cells are stimulated directly in the TEA solution (KOKETSU et al,1959).These TEA-potentials appear to be generated by an inward Ca2+movement across the cell membrane,as in the case of sympathetic ganglion cells,since these TEA-potentials are resistant to TTX.Unlike the case of sympathetic ganglion cells,however,adrenaline showed no effects on these TEA-potential(four experiments) (Fig.9).This result suggests that adrenaline does not interact with Ca2+ conductance during the generation of TEA-potential.…”

Section: Effect Of Adrenaline On the Membrane Resistancementioning

confidence: 99%

Effects of Adrenaline on the Action Potential of Sympathetic Ganglion Cells in Bullfrogs

Minota

1977

Jpn.J.Physiol

“…In any case, in order to estimate fixed membrane potential, the action potential of ganglion cell was recorded immediately before the P-potential and slow IPSP were elicited. Results obtained from the experiment using two microelectrodes were essentially similar to those obtained using the bridge-circuit (KoKETSU et al, 1959). Two microelectrodes voltage-clamp technique (AKASU and KoKETSU, 1981) was used to analyse the conductance changes and the reversal potential of slow inhibitory postsynaptic current (slow IPSC).…”

mentioning

confidence: 58%

Electrogenesis of the slow inhibitory postsynaptic potential in bullfrog sympathetic ganglia.

Akasu

1983

Jpn.J.Physiol

The ionic mechanisms of the slow surface positive (P)-potential and the slow inhibitory postsynaptic potential (IPSP), an intracellularly recorded P-potential in sympathetic ganglia, were analysed by means of sucrose-gap, intracellular microelectrode techniques, and voltage clamp technique. Both the P-potential and the slow IPSP consist of two different potential components, namely the ouabain-sensitive and the ouabain-insensitive components. The ouabain-sensitive component was enhanced by a moderate conditioning hyperpolarization. This component was most reasonably explained as a potential change generated by an activation of the elctrogenic Na+ pump. The ouabaininsensitive potential component of the P-potential and the slow IPSP decreased in the amplitude and finally reversed its polarity by conditioning hyperpolarization. The reversal potential of ouabain-insensitive component of slow IPSP and slow inhibitory postsynaptic current (IPSO) was close to the Ex. The amplitude of ouabain-insensitive component of P-potential and slow IPSP was markedly decreased by an elevation of external K+ concentration. The reversal potential of ouabain-insensitive component shifted to a more positive potential level in high K+ Ringer's solution. On the other hand, it was augmented in K+-free Ringer's solution. A reduction of the membrane resistance was observed during the generation of the slow IPSP, when the membrane potential of ganglion cells was held at a membrane potential level more negative than -60 mV. The slow IPSC recorded by voltage-clamp method was associated with an increase in membrane conductance. It was concluded that the ouabain-insensitive component was generated by an activarion of K+ conductance.