Effects of night lighting on avian cognitive function: Mechanisms involving neurodegeneration, metabolic dysregulation and neuroinflammatory responses

The rapid expansion of urbanization has led to widespread exposure of wild birds to intensive light at night (LAN). While previous studies have established LAN-induced cognitive impairment in birds, the underlying neurobiological mechanisms remain poorly understood. We hypothesized that LAN exposure impaired cognitive function of birds potentially through neurodegeneration, metabolic dysregulation and neuroinflammatory responses in the telencephalon. Using Zebra Finches (Taeniopygia guttata) as an avian model, under 16L:8D photoperiods, we compared associative learning and memory abilities and neurobiological parameters between experimental groups exposed to dim light at night (LAN) versus nocturnal darkness (CTR). Compared to the CTR birds, the LAN-exposed birds exhibited significantly lower learning and memory performances, reduced neuron density and simplified dendritic morphology in the telencephalons. The key energy metabolic substrates (cholic acid, CTP, D-mannose-6-phosphate) and neuroprotective agents (trehalose, menaquinone, L-gulono-1,4-lactone) in the telencephalons of LAN-exposed birds showed depletion, while oxidative stress markers (methionine sulfoxide) and inflammatory mediators (cis-gondoic acid) exhibited elevation. The neurotransmitter dopamine and histamine metabolic pathway were disrupted in the LAN-exposed birds. The microglias were activated with pro-inflammatory IL-1β and IL-6 levels increasing and anti-inflammatory IL-10 decreasing in the telencephalons of the LAN-exposed birds. These findings indicate a potential mechanistic pathway whereby dim light exposure at night can induce neuroinflammation through oxidative stress-mediated microglial activation, energy metabolism and neurotransmitter homeostasis disruption, ultimately leading to neurodegeneration in the telencephalons of birds.