Relationship between interblink interval and dopamine

Abstract

We thank Lemon and Shah for their insightful comments. The finding that dopamine mediates spontaneous blink through the caudal nucleus provides the mechanism behind altered blink states in diseases such as Parkinson’s disease and schizophrenia. Fatigue has also been linked to impaired dopaminergic transmission,1,2 and it is fascinating to speculate that the changes observed in blinking could be in part centrally mediated. A local role of dopamine might also be proposed. The finding of dopaminergic nerves adjacent to goblet cells suggests a role in the regulation of these mucin-secreting cells which are critical to a stable tear film.3 Dopamine receptors have also been isolated from bovine cornea.4 Our field of study is at a crossroads between local, ocular, and central stimuli, as we challenge subjects both by desiccation of the ocular surface and by visual task to assess effects on blinking. The suggestion by Lemon and Shah to assess subjects under fixed-stare conditions is well taken. In fact, we intend to study alterations in blink patterns under various conditions of task and nontask, trying to tease out changes due to ocular dryness and those due to discomfort. It is quite possible that sympathetic dopaminergic stimulation from the stressed cornea and conjunctiva results in blinking, demonstrating its fundamental role in both central and local control of this critical function.