Abstract
The neuropathic pain phenotype is the consequence of functional and morphological reorganization of the PNS and CNS. This reorganization includes DRGs and the spinal cord, and extends to multiple supraspinal areas including the limbic and reward systems. Several recent papers show that acute manipulation of cortical and subcortical brain areas causally correlates with the cognitive, emotional and sensory components of neuropathic pain, yet mechanisms responsible for pain chronification remain largely unknown. Here we show that nucleus accumbens expression of ΔFos-B, a transcription factor that plays a critical role in addiction and in the brain response to stress, is reduced long term following peripheral neuropathic injury. Conversely, boosting ΔFos-B expression in the nucleus accumbens by viral transfection causes a significant and long-lasting improvement of the neuropathic allodynia. We suggest that ΔFos-B in the nucleus accumbens is a key modulator of long term gene expression leading to pain chronification.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 77-83 |
| Number of pages | 7 |
| Journal | Neuroscience Letters |
| Volume | 702 |
| DOIs | |
| State | Published - May 29 2019 |
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Keywords
- Chronic pain
- Gene expression
- Immediate early genes
- Limbic system
ASJC Scopus subject areas
- Neuroscience(all)
Cite this
}
Reduced ΔFosB expression in the rat nucleus accumbens has causal role in the neuropathic pain phenotype. / Pollema-Mays, Sarah L.; Centeno, Maria Virginia; Chang, Zheng; Apkarian, Apkar; Martina, Marco.
In: Neuroscience Letters, Vol. 702, 29.05.2019, p. 77-83.Research output: Contribution to journal › Article
TY - JOUR
T1 - Reduced ΔFosB expression in the rat nucleus accumbens has causal role in the neuropathic pain phenotype
AU - Pollema-Mays, Sarah L.
AU - Centeno, Maria Virginia
AU - Chang, Zheng
AU - Apkarian, Apkar
AU - Martina, Marco
PY - 2019/5/29
Y1 - 2019/5/29
N2 - The neuropathic pain phenotype is the consequence of functional and morphological reorganization of the PNS and CNS. This reorganization includes DRGs and the spinal cord, and extends to multiple supraspinal areas including the limbic and reward systems. Several recent papers show that acute manipulation of cortical and subcortical brain areas causally correlates with the cognitive, emotional and sensory components of neuropathic pain, yet mechanisms responsible for pain chronification remain largely unknown. Here we show that nucleus accumbens expression of ΔFos-B, a transcription factor that plays a critical role in addiction and in the brain response to stress, is reduced long term following peripheral neuropathic injury. Conversely, boosting ΔFos-B expression in the nucleus accumbens by viral transfection causes a significant and long-lasting improvement of the neuropathic allodynia. We suggest that ΔFos-B in the nucleus accumbens is a key modulator of long term gene expression leading to pain chronification.
AB - The neuropathic pain phenotype is the consequence of functional and morphological reorganization of the PNS and CNS. This reorganization includes DRGs and the spinal cord, and extends to multiple supraspinal areas including the limbic and reward systems. Several recent papers show that acute manipulation of cortical and subcortical brain areas causally correlates with the cognitive, emotional and sensory components of neuropathic pain, yet mechanisms responsible for pain chronification remain largely unknown. Here we show that nucleus accumbens expression of ΔFos-B, a transcription factor that plays a critical role in addiction and in the brain response to stress, is reduced long term following peripheral neuropathic injury. Conversely, boosting ΔFos-B expression in the nucleus accumbens by viral transfection causes a significant and long-lasting improvement of the neuropathic allodynia. We suggest that ΔFos-B in the nucleus accumbens is a key modulator of long term gene expression leading to pain chronification.
KW - Chronic pain
KW - Gene expression
KW - Immediate early genes
KW - Limbic system
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UR - http://www.scopus.com/inward/citedby.url?scp=85057442104&partnerID=8YFLogxK
U2 - 10.1016/j.neulet.2018.11.036
DO - 10.1016/j.neulet.2018.11.036
M3 - Article
VL - 702
SP - 77
EP - 83
JO - Neuroscience Letters
JF - Neuroscience Letters
SN - 0304-3940
ER -