Tags

Type your tag names separated by a space and hit enter

Interleukin-1β overproduction is a common cause for neuropathic pain, memory deficit, and depression following peripheral nerve injury in rodents.
Mol Pain. 2016; 12MP

Abstract

BACKGROUND

Chronic pain is often accompanied by short-term memory deficit and depression. Currently, it is believed that short-term memory deficit and depression are consequences of chronic pain. Here, we test the hypothesis that the symptoms might be caused by overproduction of interleukin-1beta (IL-1β) in the injured nerve independent of neuropathic pain following spared nerve injury in rats and mice.

RESULTS

Mechanical allodynia, a behavioral sign of neuropathic pain, was not correlated with short-term memory deficit and depressive behavior in spared nerve injury rats. Spared nerve injury upregulated IL-1β in the injured sciatic nerve, plasma, and the regions in central nervous system closely associated with pain, memory and emotion, including spinal dorsal horn, hippocampus, prefrontal cortex, nucleus accumbens, and amygdala. Importantly, the spared nerve injury-induced memory deficits, depressive, and pain behaviors were substantially prevented by peri-sciatic administration of IL-1β neutralizing antibody in rats or deletion of IL-1 receptor type 1 in mice. Furthermore, the behavioral abnormalities induced by spared nerve injury were mimicked in naïve rats by repetitive intravenous injection of re combinant rat IL-1β (rrIL-1β) at a pathological concentration as determined from spared nerve injury rats. In addition, microglia were activated by both spared nerve injury and intravenous injection of rrIL-1β and the effect of spared nerve injury was substantially reversed by peri-sciatic administration of anti-IL-1β.

CONCLUSIONS

Neuropathic pain was not necessary for the development of cognitive and emotional disorders, while the overproduction of IL-1β in the injured sciatic nerve following peripheral nerve injury may be a common mechanism underlying the generation of neuropathic pain, memory deficit, and depression.

Authors+Show Affiliations

Department of Physiology and Pain Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China Guangdong Province Key Laboratory of Brain Function and Disease, Guangzhou, China.Department of Physiology and Pain Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China Guangdong Province Key Laboratory of Brain Function and Disease, Guangzhou, China.Department of Physiology and Pain Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China Guangdong Province Key Laboratory of Brain Function and Disease, Guangzhou, China.Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ, USA.Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ, USA.Department of Physiology and Pain Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China Guangdong Province Key Laboratory of Brain Function and Disease, Guangzhou, China.Department of Physiology and Pain Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China Guangdong Province Key Laboratory of Brain Function and Disease, Guangzhou, China Department of Cell Biology and Neuroscience, Rutgers University, Piscataway, NJ, USA.Department of Physiology and Pain Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China Guangdong Province Key Laboratory of Brain Function and Disease, Guangzhou, China liuxg@mail.sysu.edu.cn zhou.lijun@yahoo.com.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

27175012

Citation

Gui, Wen-Shan, et al. "Interleukin-1β Overproduction Is a Common Cause for Neuropathic Pain, Memory Deficit, and Depression Following Peripheral Nerve Injury in Rodents." Molecular Pain, vol. 12, 2016.
Gui WS, Wei X, Mai CL, et al. Interleukin-1β overproduction is a common cause for neuropathic pain, memory deficit, and depression following peripheral nerve injury in rodents. Mol Pain. 2016;12.
Gui, W. S., Wei, X., Mai, C. L., Murugan, M., Wu, L. J., Xin, W. J., Zhou, L. J., & Liu, X. G. (2016). Interleukin-1β overproduction is a common cause for neuropathic pain, memory deficit, and depression following peripheral nerve injury in rodents. Molecular Pain, 12. https://doi.org/10.1177/1744806916646784
Gui WS, et al. Interleukin-1β Overproduction Is a Common Cause for Neuropathic Pain, Memory Deficit, and Depression Following Peripheral Nerve Injury in Rodents. Mol Pain. 2016;12 PubMed PMID: 27175012.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Interleukin-1β overproduction is a common cause for neuropathic pain, memory deficit, and depression following peripheral nerve injury in rodents. AU - Gui,Wen-Shan, AU - Wei,Xiao, AU - Mai,Chun-Lin, AU - Murugan,Madhuvika, AU - Wu,Long-Jun, AU - Xin,Wen-Jun, AU - Zhou,Li-Jun, AU - Liu,Xian-Guo, Y1 - 2016/05/12/ PY - 2016/01/10/received PY - 2016/04/04/accepted PY - 2016/5/14/entrez PY - 2016/5/14/pubmed PY - 2016/12/27/medline KW - Neuropathic pain KW - depression KW - interleukin-1β KW - microglia KW - peripheral nerve injury KW - short-term memory deficit JF - Molecular pain JO - Mol Pain VL - 12 N2 - BACKGROUND: Chronic pain is often accompanied by short-term memory deficit and depression. Currently, it is believed that short-term memory deficit and depression are consequences of chronic pain. Here, we test the hypothesis that the symptoms might be caused by overproduction of interleukin-1beta (IL-1β) in the injured nerve independent of neuropathic pain following spared nerve injury in rats and mice. RESULTS: Mechanical allodynia, a behavioral sign of neuropathic pain, was not correlated with short-term memory deficit and depressive behavior in spared nerve injury rats. Spared nerve injury upregulated IL-1β in the injured sciatic nerve, plasma, and the regions in central nervous system closely associated with pain, memory and emotion, including spinal dorsal horn, hippocampus, prefrontal cortex, nucleus accumbens, and amygdala. Importantly, the spared nerve injury-induced memory deficits, depressive, and pain behaviors were substantially prevented by peri-sciatic administration of IL-1β neutralizing antibody in rats or deletion of IL-1 receptor type 1 in mice. Furthermore, the behavioral abnormalities induced by spared nerve injury were mimicked in naïve rats by repetitive intravenous injection of re combinant rat IL-1β (rrIL-1β) at a pathological concentration as determined from spared nerve injury rats. In addition, microglia were activated by both spared nerve injury and intravenous injection of rrIL-1β and the effect of spared nerve injury was substantially reversed by peri-sciatic administration of anti-IL-1β. CONCLUSIONS: Neuropathic pain was not necessary for the development of cognitive and emotional disorders, while the overproduction of IL-1β in the injured sciatic nerve following peripheral nerve injury may be a common mechanism underlying the generation of neuropathic pain, memory deficit, and depression. SN - 1744-8069 UR - https://www.unboundmedicine.com/medline/citation/27175012/Interleukin_1β_overproduction_is_a_common_cause_for_neuropathic_pain_memory_deficit_and_depression_following_peripheral_nerve_injury_in_rodents_ L2 - https://journals.sagepub.com/doi/10.1177/1744806916646784?url_ver=Z39.88-2003&rfr_id=ori:rid:crossref.org&rfr_dat=cr_pub=pubmed DB - PRIME DP - Unbound Medicine ER -