Hydrostatic Pressure Does Not Antagonize Halothane Effects on Single Neurons of Aplysia californica

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Abstract
The ability of high pressures to antagonize the effects of halothane on a well-defined function of neural tissue was studied. Giant neurons of the marine gastropod Aplysia were selected as a model system as the biophysical properties of their membranes may be accurately monitored to a level of resolution exceeding that of vertebrate central neurons, yet the adaptation response of these cells is an integrative mechanism which these neurons have in common with sensory and central neurons of more complex nervous systems. Individual cells were exposed to 0.17 mM halothane in sea water for 60 min and then compressed in 150 atm. The halothane caused a gradual hyperpolarization of the membrane, and reduced the membrane responsiveness, as measured by the number of action potentials generated during a test stimulation, to 56.9% of control values (SE = 3.5%) without affecting the development of the slow outward current which controls adaptation in these cells. Compression without halothane exposure caused a reduction in the number of action potentials produced, but this effect was due to an enhancement of the outward current. Simultaneous exposure to halothane and 150 atm pressure caused an additive, not an antagonistic, effect on the adaptation response (total reduction to < 5% of control). The fact that simultaneous compression and exposure to halothane had additive effects on the adaptation response by affecting 2 different mechanisms that control membrane permeability in these cells does not support the hypothesis that pressure reversal, as described to occur in whole animals, is due to direct interaction of pressure and an anesthetic at 1 site in the cell membrane.