Comprehensive Behavioral Analysis of Opsin 3 (Encephalopsin)-Deficient Mice Identifies Role in Modulation of Acoustic Startle Reflex

Abstract

AbstractOpsin-3 (Opn3, encephalopsin) was the first nonvisual opsin gene discovered in mammals. Since then, severalOpn3functions have been described, and in two cases (adipose tissue, smooth muscle) light sensing activity is implicated. In addition to peripheral tissues,Opn3is robustly expressed within the central nervous system, for which it derives its name. Despite this expression, no studies have investigated developmental or adult CNS consequences ofOpn3loss-of-function. Here, the behavioral consequences of mice deficient inOpn3were investigated.Opn3-deficient mice perform comparably to wild-type mice in measures of motor coordination, socialization, anxiety-like behavior, and various aspects of learning and memory. However,Opn3-deficient mice have an attenuated acoustic startle reflex (ASR) relative to littermates. This deficit is not because of changes in hearing sensitivity, although Opn3 was shown to be expressed in auditory and vestibular structures, including cochlear outer hair cells. Interestingly, the ASR was not acutely light-dependent and did not vary between daytime and nighttime trials, despite known functions ofOpn3in photoreception and circadian gene amplitude. Together, these results demonstrate the first role ofOpn3on behavior, although the role of this opsin in the CNS remains largely elusive.