monocular exposures, binocular neuronal input can be induced by the anesthetics which, since lasting for a longer time, can override that of the short periods of monocular exposure to light. An increase in hydrostatic pressure increases the amount of agent required for anesthesia. The molecular basis of this "pressure reversal of anesthesia" is unknown. Recently, in a model system that bears many similarities to that of neuronal cells (chromaffin cells), it has been shown, by studies involving patchclamp techniques, that high pressure does not primarily affect the channels but rather the mechanism of exocytosis: the application of pressure inhibits exocytosis [12]. If the same process occurs in neurons, pressure may possibly compensate for the increase in transmitter release due to anesthetics as discussed above.
Neurons of the reticular formation seem to play a role in altering the state of consciousness and alertness [13]. These neurons have one property in common with the giant neurons in the visual system of the fly and have been shown to be particularly sensitive to anesthetic action: they have large dendritic trees and/or axonal arborizations with many synaptic connections. It may be this property which causes these neurons, too, to become early victims of the anesthetic effect. I thank Dr. Baler-Rogowski, Dr. R. Hengstenberg and A. Schmid for discussion, R. Reitmajer for help with the experiments.