Beyond visual perception, light plays a vital role in influencing the brain and behavior. The non-image-forming effects of light on mammals include regulating peripheral physiological processes, entraining circadian rhythms, managing pupillary reflexes, elevating arousal or alertness, and altering mood and cognitive functions [1,2]. The most consistent, dependable, and predictable natural cue for the entrainment of the circadian rhythm is the daily cycle of light and dark [3]. It establishes daily rhythms in biological functions and ensures that the activities of different tissues and organs are in sync with the day/night or light and dark cycles [4]. Studies suggest that inadequate exposure to daylight has an adverse effect on emotion and cognition. This is evident in individuals with seasonal affective disorder (SAD), which is characterized by symptoms of depression, anxiety, poor motivation, and cognitive impairment [5]. The seasonal variation in the amount of sunlight that individuals experience is connected with the onset and remission of symptoms in the autumn and spring, respectively.

Bright light therapy can reduce SAD symptoms prior to full remission in the spring, adding support to the theory that a lack of light causes SAD. In addition to variations in ambient light, diminished photoreception can be caused by eye illnesses such as glaucoma or age-related macular degeneration, both of which have been linked to cognitive impairments [6,7]. Compared to low daylight light illumination, bright daylight promotes arousal and improves attention. [8,9], activates digestive activity [10,11], suppresses the levels of plasma cortisol [12], and also increases the level of melatonin at night [13]. Furthermore, patients who had just undergone spinal surgery reported less pain and a decreased need for analgesics when hospital rooms had more sunlight [14]. Heart attack patients in sunny hospital rooms had shorter hospital stays and higher survival rates [15]. Apart from its influence on health, the amount of daylight positively relates to superior cognitive function in many organisms [16]. However, the underlying mechanism for this effect of light illumination remains unclear.

In higher vertebrate brains, the hippocampus, thalamus, and cortex regions are known for their involvement in learning, memory, and cognitive functions. The hippocampus plays a critical role in episodic memory and shows significant flexibility in adulthood, including producing new neurons [17]. Damage in the hippocampal region leads to spatial learning deficits [18]. Cortical areas are associated with the organization of cognition and emotion [19]. Information is transmitted from the sensory periphery to the cerebral end-station through the thalamus [20]. Memory and cognitive processes have been linked to the expression of brain-derived neurotrophic factor (BDNF) [21]. Reduced BDNF expression negatively affects learning and memory [22]. GSK3β regulates immune system signaling pathways, and its dysregulation is involved in several cellular processes that cause neurodegenerative disorders [23]. In addition, increased GSK-3β expression has been linked with hyperactivity and mania, whereas deletion of GSK-3β in the developing nervous system causes neuronal progenitor hyperproliferation and neurogenesis suppression [24].

The persistent expression of growth-associated protein (Gap-43) mRNA in adult neurons shows the plasticity of such cells throughout life by retaining the ability to grow axons and form synapses [25]. Neurogranin (Ng) participates in numerous postsynaptic signal transduction pathways. Being involved in learning and memory, Ng expression is higher in the hippocampus, striatum, and cortex [26]. High-affinity BDNF receptor function depends on signal-transducing receptors called protein-tyrosine kinases (TrkB) [27]. TrkB-encoded protein causes tyrosine phosphorylation in neuronal cells and directly affects BDNF biological activity [28]. A highly conserved miRNA called MicroRNA-132 (miR-132), activated by the neurotrophin BDNF by CREB, promotes dendritic outgrowth [29].

Pro-inflammatory cytokine TNF-α is typically produced by immune cells, although brain neurons and glia also express it. It inhibits hippocampal adult neurogenesis, while anti-TNFα therapy increases neurogenesis [30]. It was linked with memory development and consolidation [31]. During memory formation, BDNF and TNF-α are known to interact with one another. Since these are the potential indicators for modulating postsynaptic signal transduction pathways and neurogenesis, it is critical to investigate their expression patterns after exposure to various light illumination treatments.

Although light entrains or resets circadian rhythms in nocturnal and diurnal mammals, including humans, the circadian-independent direct effects of light on the brain and behavior differ significantly [[32], [33], [34], [35]]. Light stimulates physical activity and wakefulness in diurnal mammals; it inhibits activity and promotes sleep in nocturnal mammals [36]. Most studies used diurnal mammals to understand the effect of exposure to daytime light illumination on mood disorders. A study on nocturnal mice reveals that single-day exposure to bright light (400 vs. 50 lx) alters the mice's memory. However, no such effects are revealed after four weeks [37]. Further, nocturnal rats have shown that brief exposure to bright light induces increased anxiety in the Elevated Plus Test [38]. Nevertheless, it is still unclear how bright light will influence learning, memory, and cognition in nocturnal rodents. No studies have examined exposure to differential light illumination during the light phase and its effects on learning, memory, and cognition in nocturnal rats. We hypothesized that exposure to bright light during the day or being raised under bright light conditions affects learning, memory, cognition, and the ensuing expression of transcripts in the brain's higher learning center in nocturnal rats. To study the effect of bright light exposure on learning, memory, and cognition in nocturnal rats, we first investigated the changes in learning, memory, and cognition in rats after 30 days of different light illuminance. Then, we also detected the alterations in the expression of transcripts of critical molecules that play dominant roles in synaptic plasticity, including Bdnf, Trk, miR132, Ng, Gap-43, Crebp, and Gsk3β in key learning centers.