Dysfunction of the paraventricular thalamus–prelimbic cortex circuit underlies maternal separation–induced deficits in contagious pain

Contagious pain is considered one of the most common forms of emotional contagion observed in animal models. Nevertheless, little is known about the precise neural mechanisms governing the regulation of contagious pain in response to diverse environmental stressors. Here, we report that early life maternal separation (MS) precipitates impairments in the pain contagion between familiar partners. Specifically, we identify the indispensable role of glutamatergic projections from the paraventricular thalamus (PVT) to the prelimbic cortex (PrL) for the development of vicarious pain hypersensitivity. MS dampens activation of the PVT → PrL pathway during social interactions between observer and painful demonstrator. Augmenting the excitability or activity of the PVT → PrL circuit through chemogenetic interventions or tactile stimulation resembling social touch significantly ameliorates the MS-evoked contagious pain deficits. Collectively, our findings delineate a neural circuitry substrate underlying the loss of contagious pain stemming from MS and propose a potential therapeutic avenue for mitigating empathic impairments associated with early life adversity.

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Publication Details

Journal
Science Advances
Published
2025-10-08
DOI
https://doi.org/10.1126/sciadv.ady1944
Primary Topic
Neuroendocrine regulation and behavior
Type
article
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article

Dysfunction of the paraventricular thalamus–prelimbic cortex circuit underlies maternal separation–induced deficits in contagious pain

Xiaoping Tong, Fan Jiang, Yu Gong, Rui Du et al.
Science Advances
Neuroendocrine regulation and behavior
article

Dysfunction of the paraventricular thalamus–prelimbic cortex circuit underlies maternal separation–induced deficits in contagious pain

Xiaoping Tong, Fan Jiang, Yu Gong, Rui Du, Zhong-Yong Zhang, Ming-Gang Liu, Xin-Yu Su, Tian‐Le Xu, Yujiao Deng, Guanghai Wang, Xing-Lei Song, Yujin Jian, Jun Chen, Chun-Li Li, Ying Li, Yan Wang, Qin Jiang
article en

Abstract

Contagious pain is considered one of the most common forms of emotional contagion observed in animal models. Nevertheless, little is known about the precise neural mechanisms governing the regulation of contagious pain in response to diverse environmental stressors. Here, we report that early life maternal separation (MS) precipitates impairments in the pain contagion between familiar partners. Specifically, we identify the indispensable role of glutamatergic projections from the paraventricular thalamus (PVT) to the prelimbic cortex (PrL) for the development of vicarious pain hypersensitivity. MS dampens activation of the PVT → PrL pathway during social interactions between observer and painful demonstrator. Augmenting the excitability or activity of the PVT → PrL circuit through chemogenetic interventions or tactile stimulation resembling social touch significantly ameliorates the MS-evoked contagious pain deficits. Collectively, our findings delineate a neural circuitry substrate underlying the loss of contagious pain stemming from MS and propose a potential therapeutic avenue for mitigating empathic impairments associated with early life adversity.

Science AdvancesVol. 11(41)
Northwestern Polytechnical University (CN), Shanghai Jiao Tong University (CN), XinHua Hospital (CN), Shanghai Children's Medical Center (CN), Zhejiang Lab (CN), Songjiang District Central Hospital (CN), Tang Du Hospital (CN), Air Force Medical University (CN), Northwestern Polytechnic University (US)
Openalex Percentile: Top 68%
Neuroendocrine regulation and behavior
DOIOpen Access PDFOpenAlex
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