A STUDY OF THE EFFECTS OF ANAESTHESIA AND ASPHYXIA ON THE MONO-SYNAPTIC PATHWAY THROUGH THE SPINAL CORD

Abstract

The anesthetic nembutal, though depressing the activity of all components of the monosynaptic pathway, produces a block in transmission essentially by stabilizing the motoneur-one membrane so that the synaptic potential no longer initiates the discharge of impulses. Asphyxia produces a brief depression which is quickly followed by a period of hyper-excitability attributable to depolarization of the membranes of the afferent nerve fibres and the m.otoneurone somas. With continued asphyxia, the depolarization progresses so that eventually there is failure of impulse propagation. This first becomes evident with orthodromic impulses in the pre-synaptic fibres and later with the antidromic propagation from axon to soma. Presumably variations in O2 require-ment determine this order of failure of the components of the pathway. O2 lack has the same effect as asphyxia except for the absence of an early transient depression of activity which precedes the phase of hyperexcitability. Sudden readmission of O2 during the period of asphyxial or anoxic hyperexcitability results in a depression. CO2 excess produces pure depression of the monosynaptic pathway. The accumulation of CO2 explains the early depression in asphyxia, and, together with less diffusible products of anoxial metabolism, it accounts for the depression on sudden readmission of O2. During the period of hyperexcitability, this depressant action would be submerged by the preponderating excitatory action of the partial depolarization.