Marked miosis caused by deafferenting the oculomotor nuclear complex in the cat

Animals show highly constricted pupils in certain conditions (e.g., coma). To know the anatomical basis for this miosis, mechanical separation of the oculomotor nuclear complex was done using four transections of the brain. Two frontal transections were placed rostral and caudal to the oculomotor nuclear complex. Two bilateral oblique transections were performed by aiming through the dorsal edge of the Edinger–Westphal nucleus at an angle of 50° from the horizontal plane and vertical to the frontal plane. After the transections, we examined pupillary size for up to 2 weeks to exclude acute effects of deafferentiation. The transections were histologically examined. If the bilateral pupils were highly constricted after the transections, those pupils remained in the miotic state during the survival periods (4–14 days). The deafferented midbrain of the animals, which showed marked miosis, contained the intact oculomotor nuclear complex and nerves with the whole part of the midbrain ventral to them, but with only a small region dorsolateral to them. Given the previous finding that electrical microstimulation of the area ventral to the oculomotor nuclear complex and nerves has failed to elicit pupil constriction, our results suggest that the oculomotor nuclear complex itself could work as a generator for the strong activity of preganglionic pupilloconstrictor neurons.