Many biological functions oscillate over the course of a day, and the precise timing of these rhythms depends on synchronization to the solar cycle. Changes in day length, shift-work, and transmeridian travel, which disrupt exposure to the solar cycle, lead to mood and cognitive function deficits. Sleep deprivation and circadian disruption are known to underlie mood and cognitive disorders associated with irregular light schedules. However, little is known about the ability of light to directly influence mood and cognitive functions. To determine whether light directly influences mood and cognitive functions, we housed mice in an environment that provided exposure to light pulses throughout the circadian cycle without causing circadian arrhythmicity or disrupting sleep. In these mice, we observed increased depression related behaviors and hippocampal learning deficits with corresponding physiological changes such as elevated corticosterone and deficient long-term potentiation. Chronic administration of the antidepressant fluoxetine rescued the increased depression related behavior, elevated corticosterone, and the hippocampal-dependent learning deficit induced by the light exposure. We sought to identify the cells responsible for conveying this light information to the brain to influence these functions. We focused on a specialized ganglion cell population that are intrinsically photosensitive (ipRGCs) due to expression of the photopigment, melanopsin. In addition to their role in regulation of circadian rhythms and sleep, these cells project to limbic regions indicating a possible role in the regulation of mood and cognitive function. Mice lacking ipRGCs were unaffected by exposure to light pulses throughout the circadian cycle showing that these cells are responsible for conveying light information to areas of the brain that control learning and mood. These findings establish that disruptive light conditions can negatively impact cognitive functions and mood and create a new role for ipRGCs.