BDNF contributes to the neonatal incision-induced facilitation of spinal long-term potentiation and the exacerbation of incisional pain in adult rats

Ding, Xu; Liang, Yixiao; Su, Li; Liao, Fei-Fei; Fang, Dong; Tai, Jun; Xing, Guo-Gang

doi:10.1016/j.neuropharm.2018.04.032

Cited by 16 publications

(8 citation statements)

References 83 publications

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“…For instance, peripheral inflammation in the neonatal period has evoked hyperexcitability in spinal dorsal horn neurons and hyperexcitability has persisted into adulthood [18]. Additionally, hind paw incision at the first post-natal week has enhanced behavioral response following re-injury in adulthood [19]. In agreement with previous studies, this study showed that IFI induced long-lasting enhancement of mechanical hypersensitivity by AFI and that this prolonged hypersensitivity was suppressed by the inhibition of microglial hyperactivation in the Vi/Vc.…”

Section: Discussionsupporting

confidence: 91%

Microglial activation in the trigeminal spinal subnucleus interpolaris/caudalis modulates orofacial incisional mechanical pain hypersensitivity associated with orofacial injury in infancy

et al. 2021

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Infantile tissue injury induces sensory deficits in adulthood. Infantile facial incision (IFI) was reported to cause an enhancement of incision-induced mechanical hypersensitivity in adulthood due to acceleration of the trigeminal ganglion neuronal excitability. However, the effects of IFI on activation of microglia in the spinal trigeminal nucleus and its involvement in facial pain sensitivity is not well known. Methods: A facial skin incision was made in the left whisker pad in infant (IFI) and/or adult rats (AFI). Mechanical head withdrawal threshold and microglial activation in the trigeminal spinal nucleus were analyzed. Results: Mechanical pain hypersensitivity induced by AFI was significantly exacerbated and prolonged by IFI. The number of Iba1-immunoreactive cells in the trigeminal spinal nucleus following AFI was increased by IFI, suggesting that IFI facilitates microglial hyperactivation following AFI. Intraperitoneal administration of minocycline, a microglial activation inhibitor, suppressed the facial incision-induced microglial hyperactivation in the trigeminal spinal nucleus and the exacerbation of the facial mechanical pain hypersensitivity induced by IFI. Conclusion: These results suggest that facial trauma in infants causes hyperactivation of microglia in the trigeminal spinal nucleus following AFI, leading to the prolongation of the facial mechanical pain hypersensitivity.

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Section: Discussionsupporting

confidence: 91%

Microglial activation in the trigeminal spinal subnucleus interpolaris/caudalis modulates orofacial incisional mechanical pain hypersensitivity associated with orofacial injury in infancy

et al. 2021

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“…Early life challenges, including tissue injury, lead to microglial activation that may result in the release of numerous signaling molecules that can have deleterious effects on the pathogenesis of pain, especially in the neonate (161,162). For example, spinal microglial reactivity, measured by immunostaining of microgliaspecific ionized calcium-binding adapter molecule 1 (Iba-1), was enhanced in rats exposed to a noxious insult (e.g., incision, inflammation) as a neonate (16,88,(163)(164)(165).…”

Section: Neuroimmune Plasticitymentioning

confidence: 99%

“…Alone these models are used to evaluate the effects of early life pain on later acute pain (215)(216)(217). Two-hit models provide evidence that single or repetitive noxious stimulation during the early post-natal period can affect subsequent acute pain later in life in regards to mechanical and thermal sensitivity (37,206), learning and memory (61, 200), and microglial activation (16,163). However, the impact that early post-natal injury has on chronically painful conditions during adulthood has not been evaluated in animal models.…”

Section: Models To Study the Effects Of Early Life Pain On Pain Models To Study The Effects Of Early Life Pain On Pain Occurring Later Inmentioning

confidence: 99%

Early Neonatal Pain—A Review of Clinical and Experimental Implications on Painful Conditions Later in Life

2020

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Modern health care has brought our society innumerable benefits but has also introduced the experience of pain very early in life. For example, it is now routine care for newborns to receive various injections or have blood drawn within 24 h of life. For infants who are sick or premature, the pain experiences inherent in the required medical care are frequent and often severe, with neonates requiring intensive care admission encountering approximately fourteen painful procedures daily in the hospital. Given that much of the world has seen a steady increase in preterm births for the last several decades, an evergrowing number of babies experience multiple painful events before even leaving the hospital. These noxious events occur during a critical period of neurodevelopment when the nervous system is very vulnerable due to immaturity and neuroplasticity. Here, we provide a narrative review of the literature pertaining to the idea that early life pain has significant long-term effects on neurosensory, cognition, behavior, pain processing, and health outcomes that persist into childhood and even adulthood. We refer to clinical and pre-clinical studies investigating how early life pain impacts acute pain later in life, focusing on animal model correlates that have been used to better understand this relationship. Current knowledge around the proposed underlying mechanisms responsible for the long-lasting consequences of neonatal pain, its neurobiological and behavioral effects, and its influence on later pain states are discussed. We conclude by highlighting that another important consequence of early life pain may be the impact it has on later chronic pain states-an area of research that has received little attention.

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“…Previously, we have shown that BDNF/TrkB signaling is important in IL6-induced mechanical hypersensitivity and hyperalgesic priming (Asiedu et al, 2011, Melemedjian et al, 2013). IL6 plays an important role in postsurgical pain (Buvanendran et al, 2006) and spinal BDNF/TrkB signaling contributes to incisional-evoked pain (Li et al, 2008, Masaki et al, 2016, Ding et al, 2018, Tian et al, 2018) but its role in hyperalgesic priming caused by incision has not been explored. To address this gap in knowledge we gave adult, male mice plantar incision with an intrathecal injection of the BDNF sequestering agent, TrkB-fc, given at the same time as the incision.…”

Section: Resultsmentioning

confidence: 99%

Temporal and sex differences in the role of BDNF/TrkB signaling in hyperalgesic priming in mice and rats

Moy

Szabo-Pardi

Tillu

et al. 2019

Neurobiology of Pain

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BDNF contributes to the neonatal incision-induced facilitation of spinal long-term potentiation and the exacerbation of incisional pain in adult rats

Cited by 16 publications

References 83 publications

Microglial activation in the trigeminal spinal subnucleus interpolaris/caudalis modulates orofacial incisional mechanical pain hypersensitivity associated with orofacial injury in infancy

Microglial activation in the trigeminal spinal subnucleus interpolaris/caudalis modulates orofacial incisional mechanical pain hypersensitivity associated with orofacial injury in infancy

Early Neonatal Pain—A Review of Clinical and Experimental Implications on Painful Conditions Later in Life

Temporal and sex differences in the role of BDNF/TrkB signaling in hyperalgesic priming in mice and rats

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