Spontaneous Pain Disrupts Ventral Hippocampal CA1-Infralimbic Cortex Connectivity and Modulates Pain Progression in Rats with Peripheral Inflammation | Zendy

Longyu Ma | Zendy; Lupeng Yue | Zendy; Yuqi Zhang | Zendy; Yue Wang | Zendy; Bingxuan Han | Zendy; Shuang Cui | Zendy; FengYuan Liu | Zendy; You Wan | Zendy; Ming Yi | Zendy

Open Access

Spontaneous Pain Disrupts Ventral Hippocampal CA1-Infralimbic Cortex Connectivity and Modulates Pain Progression in Rats with Peripheral Inflammation

Author(s) -

Longyu Ma,

Lupeng Yue,

Yuqi Zhang,

Yue Wang,

Bingxuan Han,

Shuang Cui,

FengYuan Liu,

You Wan,

Ming Yi

Publication year - 2019

Publication title -

cell reports

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 6.264

H-Index - 154

eISSN - 2639-1856

pISSN - 2211-1247

DOI - 10.1016/j.celrep.2019.10.002

Subject(s) - infralimbic cortex , hippocampal formation , neuroscience , inflammation , peripheral , hyperalgesia , cortex (anatomy) , medicine , psychology , prefrontal cortex , nociception , cognition , receptor

Pain involves an intrinsically dynamic connectome characterized by fluctuating spontaneous brain activity and continuous neuroplastic changes of relevant circuits. Activity in the hippocampus-medial prefrontal cortex (mPFC) pathway has been suggested to correlate with spontaneous pain and pain chronicity, but causal evidence is lacking. Here we combine longitudinal in vivo electrophysiological recording with behavioral testing and show that persistent spontaneous pain disrupts ventral hippocampal CA1-infralimbic cortex (vCA1-IL) connectivity and hippocampal modulation of IL neuronal activity in rats with peripheral inflammation. Chemo- and optogenetic rescue of vCA1-IL dysfunction relieves spontaneous pain. Circuit-specific overexpression of brain-derived neurotrophic factor (BDNF) in vCA1-IL reverses electrophysiological changes, relieves spontaneous pain, and accelerates overall recovery from inflammatory pain. Our work identifies a neural pathway that specifically correlates with spontaneous pain and supports the significance of using a circuit dynamics-based strategy for more comprehensive understanding of circuitry mechanisms underlying chronic pain.

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