A study of the actions and inter-actions of hydrostatic pressure and alcohol anaesthetics at the frog neuromuscular junction
Hydrostatic pressures of 1.03 MPa and above significantly depressed the spontaneous quantal release of transmitter. The miniature endplate potential (MEPP) frequency reduction was approximately exponential. Solutions of increased osmolarity or potassium content had no effect on the pressure-MEPP frequency relationship. An increased extracellular calcium concentration significantly reduced the effectiveness of pressure on frequency. Transient changes in MEPP frequency were often observed on decompression and when pressure was maintained for a period of time. The decay phase of miniature endplate currents (MEPCs) was significantly prolonged by pressures of 10.4 MPa-15.55 MPa, and there was a small reduction in MEPC amplitude at these pressures. Pressure had no effect on the MEPC growth phase time course. On addition of alcohols, regardless whether the MEPP frequency was increased (ethanol) or decreased (benzyl alcohol), application of hydrostatic pressure reduced frequency in a manner independent of the presence of these agents. Additionally, pressure applied to ethanol-lengthened MEPCs prolonged the decay phase to a similar extent as in ethanols' absence. In contrast, pressure (3.19 MPa and 5.25 MPa) potentiated the action of octanol and atropine in shortening the MEPC decay. The amplitude of octanol and atropine treated MEPCs was also markedly depressed by this pressure range. The action of octanol on acetylcholine activated end-plate channels was considered to be consistent with a pressure-dependent channel block. Ethanol, butanol and benzyl alcohol reversibly increased the MEPC decay time constant. Their effects on MEPC decay were discussed in relation to the hypothesis that agents which prolong the decay phase, do so by increasing the average dielectric constant of the membrane. Some of the observations were consistent with this model, others were not.