Sunlight Damages Memory and New Brain Cells: Animal Studies Show

UV Irradiation Impairs Cognitive Function and Neurogenesis

The study found that after six weeks of UV irradiation, mice exhibited impaired cognitive function in hippocampus-dependent behavioral tasks, such as the Object Place Recognition (OPR), Novel Object Recognition (NOR), and Y-maze tests. These cognitive deficits were accompanied by a significant reduction in long-term potentiation (LTP) in the hippocampal CA3-CA1 region, a neural process critical for learning and memory.

Furthermore, UV irradiation significantly decreased the number of doublecortin (DCX)-positive and Ki-67-positive neurons in the hippocampal dentate gyrus (DG), indicating a reduction in neurogenesis.

UV Exposure Increases Dopamine Levels in Peripheral and Central Nervous Systems

To understand the mechanisms underlying these cognitive and neurogenesis deficits, the researchers analyzed 28 neuropeptides in mouse serum and found that dopamine, a catecholamine, was the most significantly upregulated. The dopamine level was approximately 130–145% greater in the serum of UV-irradiated mice than in that of sham-irradiated mice.

Dopamine levels in the skin and adrenal glands were also significantly higher in UV-irradiated mice compared to control mice. In specific brain regions, dopamine levels in the prefrontal cortex (PFC) and hypothalamus (HT) significantly increased in response to UV exposure.

Systemic Blockade of Dopamine D1 Receptor Counteracts UV-Induced Memory Dysfunction

To determine whether elevated dopamine levels contributed to the observed deficits, the study administered intraperitoneal injections of either SCH23390 (a dopamine D1 receptor antagonist) or raclopride (a dopamine D2 receptor antagonist) to UV- or sham-irradiated mice. The results showed that SCH23390 significantly improved cognitive function and restored hippocampal LTP in UV-irradiated mice, while raclopride had no significant effect.

These findings suggest that the dopamine D1 receptor signaling pathway plays a crucial role in UV-induced cognitive impairment.

Chronic UV Irradiation Induces Transcriptomic Changes Linked to Dopaminergic Neuron Differentiation Pathway

To further elucidate the transcriptomic changes following UV irradiation and SCH23390 treatment, the study conducted RNA sequencing (RNA-Seq) analysis of differentially expressed genes (DEGs). The results showed that the downregulated DEGs in the UV-SCH group were predominantly enriched in dopamine-related pathways, particularly the dopaminergic neuron differentiation pathway.

This suggests that the dopaminergic neuronal differentiation induced by UV irradiation might be reversed by SCH23390 treatment.

Chronic Peripheral Dopamine Injections Impair Hippocampal Memory and Neurogenesis

Finally, the study examined the effects of peripheral dopamine on hippocampal memory and neurogenesis by injecting mice with either saline or dopamine for six weeks. The results showed that dopamine injections significantly increased serum dopamine levels in a concentration-dependent manner and impaired cognitive function and neurogenesis, reproducing some cognitive alterations observed with UV exposure.

Conclusion

The study provides compelling evidence that chronic UV irradiation impairs cognitive function and neurogenesis, and that these effects are mediated by the dopamine D1 receptor signaling pathway. The findings also suggest that systemic blockade of the dopamine D1 receptor can counteract UV-induced memory dysfunction.

However, further research is needed to fully understand the underlying mechanisms and potential therapeutic applications. Additionally, individual responses to UV exposure may vary in humans, and caution should be exercised when translating and applying the findings of animal studies to humans.

Reference

Yoon, K. N., Kim, S. Y., Ji, J., et al. “Chronic ultraviolet irradiation induces memory deficits via dysregulation of the dopamine pathway”. Exp Mol Med (2024).