FAILURE OF THE VISUAL PATHWAY DURING ANOXIA

Abstract

In rabbits, potentials were recorded from the different parts of the visual pathway in response to flashes of light into the eye and to electrical stimulation at various levels during suddenly induced anoxia. Inexcitability of the pathway population occurred in th.e following order: (a) cortex, geniculate, (b) retinal ganglion cells, (c) bipolar cells and (d) photoreceptors. The propagation of excitation towards the bipolar cell level induced by a stimulus survived anoxia for about 20 min. as indicated by the appearance of an electronegative retinogram. The measured survival time (inexcitability of all units) of the retinal ganglion cells was about 5 min.; that of the geniculate population and the most resistant cortical units, about 2 min. When strong light stimuli were applied, conduction across the retinal ganglion cell layer was nearly as resistant to anoxia as optic nerve conduction. Similarly, conduction across the geniculate synapses failed only slightly earlier than conduction of the geniculo-cortical fibers. Propagation of excitation along the presynaptic terminals of the optic radiation was approx. as resistant to anoxia as conduction in the fiber tract. However, there was evidence that conduction along the presynaptic geniculate pathway failed earlier than conduction in the optic nerve. The early effect of anoxia on retinal excitation as measured by the optic tract potential and the electroretinogram simulated a transition from a scotopic to a photopic state; this early effect included extinction of the "late-on-activity," unre-sponsiveness to weak illumination, increased manifestation of "off-activity" and rapid initial decline of the b-wave. At the cortical level the following early events were in contrast to the long survival of the cortical potential in response to synchronous afferent impulses: disappearance of spontaneous waves, disappearance of facilitation and inhibition associated with the spontaneous waves, loss of corticofugal activity and extinction of paroxysmal discharges. At the geniculate level the cycle of enhancement and depression in responsiveness following an optic nerve stimulus was not particularly sensitive to anoxia. The results are discussed as to the correlation between sensitivity to anoxia and synaptic organization.