Pupillary dilation in response to the absence of light occurs due to the reduction or absence of constriction signals which otherwise oppose tonic sympathetic pupillary dilation (1). Since the iris sphincter is stronger than the dilator muscle, pupil dilation does not readily occur until the sphincter muscle relaxes (2). Relaxation of the iris sphincter is accomplished by inhibition of the Edinger–Westphal nucleus (via α2-adrenergic receptor activation) at a central nervous system level, most notably from the reticular activating formation (3).

The sympathetic circuit which activates the dilator muscle originates in the ventrolateral hypothalamus, sending a projection through the brainstem on each side into the lateral column of the spinal cord, where it synapses at the cervicothoracic level of C7–T2. The
subsequent preganglionic neuron projects over the apical pleura of the lung and into
the spinal rami to synapse at the superior cervical ganglion at the level of the carotid artery bifurcation on the right and left side of the neck. From here, a postganglionic
neuron follows a long course along the internal carotid artery into the head and orbit, reaching the iris dilator muscle via the long ciliary nerves. Sympathetic axons release norepinephrine within the muscle, which acts on excitatory alpha 1A adrenergic receptors to contract the (3).

1. Mason, P. (2011). Medical Neurobiology; Oxford, UK/New York, NY: Oxford University Press, 199.

2. Smith, P. G. (n.d.). Neural Regulation of the Pupil. Encyclopedia of Neuroscience, 2597–2601.

3. Levin, L. A., and Kaufman, P. L. (2011). Adler’s Physiology of the Eye: Clinical Application. Edinburgh; New York, NY: Saunders/Elsevier.