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Research Shows Sound-Induced Stress Can Intensify and Extend Pain in Mice

Research Shows Sound-Induced Stress Can Intensify and Extend Pain in Mice

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New research from Tokyo University of Science uncovers how sound stress alone can heighten and extend pain in mice, highlighting the role of environment in pain perception and inflammation.

2 min read

Recent studies have revealed that exposure to sound stress alone can significantly increase and prolong pain sensations in mice. Conducted by researchers from Tokyo University of Science, this research emphasizes the impact of auditory environmental factors on pain and inflammation processes. The findings demonstrate that high-pitched ultrasonic vocalizations emitted by mice under stress can induce emotional transmission and heightened pain sensitivity in other mice, even in the absence of physical injury.

Pain, a vital physiological response, can originate from tissue damage or psychological stressors, leading to both sensory and emotional discomfort. Existing literature suggests that emotional or psychological stress can amplify pain responses, and in social settings, animals exposed to conspecifics experiencing inflammation often show increased pain sensitivity — a phenomenon known as hyperalgesia. However, the mechanisms behind social or emotional pain transfer remain largely unclear.

In this study, researchers recorded ultrasonic vocalizations from mice experiencing pain and exposed naive mice to these sounds in isolated conditions, without any physical stimuli or external stressors. The experiments showed that sound stress exposure reduced paw withdrawal thresholds, confirming the development of hyperalgesia. Molecular analysis indicated that sound stress modulated gene expression in the brain related to inflammation, specifically upregulating genes like prostaglandin-endoperoxidase synthase 2 and C-X-C motif chemokine ligand 1, and activating pathways associated with inflammatory responses.

Furthermore, treatment with anti-inflammatory drugs effectively suppressed the pain responses caused by sound stress. This suggests a link between sound-induced neuroinflammation and increased pain sensation. Notably, the findings highlight that social transfer of pain can occur solely through sound exposure, without any other sensory inputs like sight or smell.

The implications of this research extend to understanding how environmental and social factors influence chronic pain and stress-related disorders. It also opens avenues for exploring ultrasound’s role in neuroinflammatory mechanisms and pain modulation. Asst. Prof. Kasai emphasizes the importance of creating stress-free medical environments and suggests that this research could aid in developing novel pain management strategies that consider emotional and environmental influences.

This groundbreaking study underscores the importance of auditory environment considerations in pain management and provides new insights into the neurobiological basis of stress-induced hyperalgesia, with potential applications in both clinical and research settings.

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