Pupil dilatation in response to vagal afferent electrical stimulation is mediated by inhibition of parasympathetic outflow in the rat.

Pupil dilatation (PD) was produced by vaginocervical mechanical stimulation (VCMS) in intact rats, and in rats with spinal cord (SC) transection at level T7 (i.e., above the level of entry into SC of all genitospinal nerves). After transection of SC, bilateral vagotomy abolished PD in response to VCMS, providing evidence that the vagus nerve conveys VCMS directly from the genitalia to the brain. In the present study, unilateral electrical stimulation of the central stump of the vagus nerve (ESV) transected at the spinal cervical level produced PD in otherwise intact rats, and in rats that had undergone bilateral cervical sympathectomy (CSX). Unilateral ESV produced bilaterally symmetrical PD. By contrast, unilateral electrical stimulation of the cervical sympathetic chain produced PD only ipsilateral to stimulation. These results provide evidence that activation of sympathetic outflow, although sufficient to produce PD, does not, by itself, mediate PD in response to ESV. After bilateral CSX, transection of the brain stem at the mid-pontine level abolished PD in response to unilateral ESV, while preserving the pupillary light reflex. Since CSX eliminates all sympathetic control of the pupil, and transection of the brain stem at the mid-pontine level blocks access of vagus-induced activity that ascends to the oculomotor nucleus in the midbrain, we conclude that ESV produces PD, at least in part, via inhibition of output from the (parasympathetic) oculomotor nucleus.