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<p>Artificial light at night (ALAN) is a growing environmental pollutant with significant risks to brain health in both animals and humans. This study assessed the ALAN-induced negative impact and examined potential mitigative strategies on neurobehavioural traits and associated neural pathways in diurnal Indian house crows subjected to dim light at night (dLAN, 6&#xa0;lx) in a 12-hour:12-hour light-dark cycle. The 12-hour dLAN period was either interrupted midway by a 2-hour dark period (controls in 0&#xa0;lx dark night; experiment 1) or preceded by a 50&#xa0;µg day⁻¹ crow⁻¹ melatonin pre-treatment 30&#xa0;min before the dLAN onset (controls received vehicle; experiment 2). dLAN exposure reduced nocturnal melatonin levels, and negatively impacted the circadian behaviour, sleep, mood and cognitive performance as well as the mRNA expression of genes associated with neurogenesis (<i>bdnf</i>,<i> dcx</i>,<i> nr4a2</i>), neuroinflammation (<i>tnfα</i> and <i>tnfr1</i>), and epigenetic regulation (<i>hat1</i>,<i> hdac2</i>,<i> hdac4</i>) in hippocampus and nidopallium caudolaterale brain regions. The midnight 2-hour dark period partially restored, but the evening melatonin pre-treatment completely restored the dLAN-induced disrupted neurobehaviours and associated gene expressions. These results provide mechanistic insights into night-light pollution effects, and suggest a pivotal role of melatonin in preserving the sleep integrity and cognitive functions in animals, perhaps also in humans.</p>

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Midnight darkness and evening melatonin pre-treatment reverse night-light-induced neurobehavioural disruptions in a diurnal corvid

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月25日

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  • Amaan Buniyaadi,
  • Abhilash Prabhat,
  • Sanjay Kumar Bhardwaj,
  • Vinod Kumar

摘要

Artificial light at night (ALAN) is a growing environmental pollutant with significant risks to brain health in both animals and humans. This study assessed the ALAN-induced negative impact and examined potential mitigative strategies on neurobehavioural traits and associated neural pathways in diurnal Indian house crows subjected to dim light at night (dLAN, 6 lx) in a 12-hour:12-hour light-dark cycle. The 12-hour dLAN period was either interrupted midway by a 2-hour dark period (controls in 0 lx dark night; experiment 1) or preceded by a 50 µg day⁻¹ crow⁻¹ melatonin pre-treatment 30 min before the dLAN onset (controls received vehicle; experiment 2). dLAN exposure reduced nocturnal melatonin levels, and negatively impacted the circadian behaviour, sleep, mood and cognitive performance as well as the mRNA expression of genes associated with neurogenesis (bdnf, dcx, nr4a2), neuroinflammation (tnfα and tnfr1), and epigenetic regulation (hat1, hdac2, hdac4) in hippocampus and nidopallium caudolaterale brain regions. The midnight 2-hour dark period partially restored, but the evening melatonin pre-treatment completely restored the dLAN-induced disrupted neurobehaviours and associated gene expressions. These results provide mechanistic insights into night-light pollution effects, and suggest a pivotal role of melatonin in preserving the sleep integrity and cognitive functions in animals, perhaps also in humans.