Modulation of recognition memory performance by light requires both melanopsin and classical photoreceptors

Abstract

Acute light exposure exerts various effects on physiology and behaviour. Although the effects of light on brain network activity in humans are well demonstrated, the effects of light on cognitive performance are inconclusive, with the size, as well as direction, of the effect depending on the nature of the task. Similarly, in nocturnal rodents, bright light can either facilitate or disrupt performance depending on the type of task employed. Crucially, it is unclear whether the effects of light on behavioural performance are mediated via the classical image-forming rods and cones or the melanopsin-expressing photosensitive retinal ganglion cells. Here, we investigate the modulatory effects of light on memory performance in mice using the spontaneous object recognition task. Importantly, we examine which photoreceptors are required to mediate the effects of light on memory performance. By using a cross-over design, we show that object recognition memory is disrupted when the test phase is conducted under a bright light (350 lux), regardless of the light level in the sample phase (10 or 350 lux), demonstrating that exposure to a bright light at the time of test, rather than at the time of encoding, impairs performance. Strikingly, the modulatory effect of light on memory performance is completely abolished in both melanopsin-deficient and rodless–coneless mice. Our findings provide direct evidence that melanopsin-driven and rod/cone-driven photoresponses are integrated in order to mediate the effect of light on memory performance.

Long-term restoration of visual function in end-stage retinal degeneration using subretinal human melanopsin gene therapy

“…In wildtype rodents with no retinal degeneration, a change in visual environment disrupts object recognition, indicating that these animals encode and remember the background visual environment in which an object is encountered (27,28). By contrast, mice with visual deficits are not able to detect the visuospatial context of an object (29), indicating that they cannot encode visual information regarding their environment. Object recognition performance was analyzed to determine visual context recognition: this was determined by the ratio of time spent exploring a novel object relative to a previously encountered object.…”

“…In contrast, control groups were able to perform the object recognition task using nonvisual cues (since recognition ratios in these mice were above chance or 0.5), but performance did not vary according to visual environment. This test has been validated for the assessment of rod/conedependent image-forming visual responses (29). Previous work has also investigated the effect of changes in background irradiance on performance with wild-type mice requiring a substantial change in irradiance (e.g., an increase from 10 to 350 lx) to disrupt object recognition performance (29).…”

“…This test has been validated for the assessment of rod/conedependent image-forming visual responses (29). Previous work has also investigated the effect of changes in background irradiance on performance with wild-type mice requiring a substantial change in irradiance (e.g., an increase from 10 to 350 lx) to disrupt object recognition performance (29). Therefore, context-dependent behavior in treated mice is likely to be caused by the change in visual environment, rather than any changes in background irradiance caused by the different test arenas.…”

Euflammation Attenuates Central and Peripheral Inflammation and Cognitive Consequences of an Immune Challenge after Tumor Development

“…From the existing literature, studies report LPS-induced disruptions in spatial learning in a water maze, novel object recognition, and spontaneous alternation 6 h – 7 d after a single high dose of LPS (600–800 μg/kg) [30,31], impairment of active avoidance after a common dose of LPS (250 μg/kg) [32], and impairment of contextual conditioning in rats [44]. These LPS-induced cognitive impairments appear to be driven by IL-1β [44,45].…”

“…Three hours later, mice were returned to the clean cage, but one familiar object was replaced with a novel object (hockey puck). Relevant to mouse strains prone to retinal degeneration such as C3H, visual input is not required for novel object recognition when objects differ by various sensory modalities (size, shape, color, material, texture) [30] and has been used successfully in this strain [30–32]. Investigative behavior was scored for 5 min.…”