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The central nervous system is shown to be involved in (a) normal spontaneous flashing, both single and multiple, (b) some types of post-stimulatory flashing and scintillation, (c) comatose behavior and refractoriness to stimulation. 2. Two and probably three latencies in response to head and anterior cord stimulation exist. At present it is not possible to distinguish between cord pathways (conducting at ca. 15 and 50 cm./sec.) and central delay as possible causes of these latency differences. 3. From posterior cord and from lantern surface it is possible to record small and characteristic volleys of action potentials associated 1:1 with spontaneous flashing and involving latencies comparable with those previously found for electrical stimulation. Multiple volleys may invoke multiple flashes. Flash intensity increases with both volley frequency and spike frequency but there is apparently not a close relation between volley structure and flash contour. 4. Electrical stimulation in the eye can either inhibit or enhance flashing, depending on relative intensities of brain and eye stimulation. 5. In preparations including ganglia the anti-cholinesterase eserine can induce both asynchronous activation of small units and a recurrent alternating large scale activation and block of luminescence.
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Case et al. (1963) studied this question.
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