Microglial phagocytosis mediates long-term restructuring of spinal GABAergic circuits following early life injury

Xu, Yajing; Moulding, Dale A.; Jin, Wenanlan; Beggs, Simon

doi:10.1016/j.bbi.2023.04.001

Cited by 3 publications

(2 citation statements)

References 62 publications

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“… 32 , 59 After neonatal injury, the inhibitory circuits and microglial activity of the spinal cord dorsal horn are dysregulated, leading to hyperactivity. 60 – 65 Moriarty et al found that a peripheral nerve block was sufficient to prevent neonatal nociceptive priming while systemic morphine injection was not. 13 We previously demonstrated that growth hormone, which is a vital player in neonatal nociceptive development, 66 can be used to prevent neonatal nociceptive priming.…”

Section: Discussionmentioning

confidence: 99%

Macrophage memories of early-life injury drive neonatal nociceptive priming

Dourson,

Fadaka,

Warshak

et al. 2024

Cell Reports

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Section: Discussionmentioning

confidence: 99%

Macrophage memories of early-life injury drive neonatal nociceptive priming

Dourson,

Fadaka,

Warshak

et al. 2024

Cell Reports

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“…Previous work has evaluated the vulnerable periods that exist in the somatosensory and immune systems 5,38,52–57 as well as genetic risk factors in children following surgery 32,58 . After neonatal injury, the inhibitory circuits and microglial activity of the spinal cord dorsal horn (SCDH) are dysregulated leading to hyperactivity of spinal output 59–64 . Moriarty et al found that a peripheral nerve block was sufficient to prevent neonatal nociceptive priming, while systemic morphine injection was not 13 .…”

Section: Discussionmentioning

confidence: 99%

Macrophage epigenetic memories of early life injury drive neonatal nociceptive priming

Dourson

Fadaka

Warshak

et al. 2023

Preprint

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These systems are vulnerable to effects of early life injury which can influence outcomes related to nociception following subsequent injury later in life (i.e. neonatal nociceptive priming). The underpinnings of this phenomenon are largely unknown, although macrophages can be epigenetically trained by injury. We found that macrophages are both necessary and partially sufficient to drive neonatal nociceptive priming possibly due to a long-lasting epigenetic remodeling of peripheral macrophages. The p75 neurotrophic factor receptor (NTR) was observed to be an important effector in regulating neonatal nociceptive priming. p75NTR modulates the inflammatory profile and responses of rodent and human macrophages. This pain memory was able to be transferred to a naive host to alter sex-specific pain-related behaviors. This study reveals a novel mechanism by which acute post-surgical pain may transition to chronic pain in children.

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Injured sensory neurons-derived galectin-3 contributes to neuropathic pain via programming microglia in the spinal dorsal horn

Shan,

Xu,

et al. 2024

Brain, Behavior, and Immunity

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Microglial phagocytosis mediates long-term restructuring of spinal GABAergic circuits following early life injury

Cited by 3 publications

References 62 publications

Macrophage memories of early-life injury drive neonatal nociceptive priming

Macrophage memories of early-life injury drive neonatal nociceptive priming

Macrophage epigenetic memories of early life injury drive neonatal nociceptive priming

Injured sensory neurons-derived galectin-3 contributes to neuropathic pain via programming microglia in the spinal dorsal horn

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