Brain-derived neurotrophic factor-TrkB signaling in the medial prefrontal cortex plays a role in the anhedonia-like phenotype after spared nerve injury.
Brain-derived neurotrophic factor-TrkB signaling in the medial prefrontal cortex plays a role in the anhedonia-like phenotype after spared nerve injury.
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内侧前额叶皮质中的脑源性神经营养因子-TrkB信号在神经损伤后的快感缺失样表型中发挥作用
DOI:
10.1007/s00406-018-0909-z
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发表时间:
2020-03
影响因子:
4.7
通讯作者:
Luo A
中科院分区:
文献类型:
--
作者:
Fang X;Yang C;Li S;Zhan G;Zhang J;Huang N;Du X;Xu H;Hashimoto K;Luo A
Although depressive symptoms including anhedonia (i.e., loss of pleasure) frequently accompany pain, little is known about the risk factors contributing to individual differences in pain-induced anhedonia. In this study, we examined if signaling of brain-derived neurotrophic factor (BDNF) and its receptor tropomyosin-receptor-kinase B (TrkB) contribute to individual differences in the development of neuropathic pain-induced anhedonia. Rats were randomly subjected to spared nerved ligation (SNI) or sham surgery. The SNI rats were divided into two groups based on the results of a sucrose preference test. Rats with anhedonia-like phenotype displayed lower tissue levels of BDNF in the medial prefrontal cortex (mPFC) compared with rats without anhedonia-like phenotype and sham-operated rats. In contrast, tissue levels of BDNF in the nucleus accumbens (NAc) of rats with an anhedonia-like phenotype were higher compared with those of rats without anhedonia-like phenotype and sham-operated rats. Furthermore, tissue levels of BDNF in the hippocampus, L2–5 spinal cord, muscle, and liver from both rats with or without anhedonia-like phenotype were lower compared with those of sham-operated rats. A single injection of 7,8-dihydroxyflavone (10 mg/kg; TrkB agonist), but not ANA-12 (0.5 mg/kg; TrkB antagonist), ameliorated reduced sucrose preference and reduced BDNF-TrkB signaling in the mPFC in the rats with anhedonia-like phenotype. These findings suggest that reduced BDNF-TrkB signaling in the mPFC might contribute to neuropathic pain-induced anhedonia, and that TrkB agonists could be potential therapeutic drugs for pain-induced anhedonia.
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影响因子:
4.8
作者:
Hurtado E;Cilleros V;Nadal L;Simó A;Obis T;Garcia N;Santafé MM;Tomàs M;Halievski K;Jordan CL;Lanuza MA;Tomàs J
通讯作者:
Tomàs J
影响因子:
4.6
作者:
Ma M;Ren Q;Yang C;Zhang JC;Yao W;Dong C;Ohgi Y;Futamura T;Hashimoto K
通讯作者:
Hashimoto K
DOI:
10.1093/ijnp/pyw089
发表时间:
2017-03-01
期刊:
The international journal of neuropsychopharmacology
影响因子:
--
作者:
Dong C;Zhang JC;Yao W;Ren Q;Ma M;Yang C;Chaki S;Hashimoto K
通讯作者:
Hashimoto K
DOI:
10.1016/j.jaac.2012.01.011
发表时间:
2012-04
影响因子:
13.3
作者:
McMakin DL;Olino TM;Porta G;Dietz LJ;Emslie G;Clarke G;Wagner KD;Asarnow JR;Ryan ND;Birmaher B;Shamseddeen W;Mayes T;Kennard B;Spirito A;Keller M;Lynch FL;Dickerson JF;Brent DA
通讯作者:
Brent DA
影响因子:
3.4
作者:
Ma M;Ren Q;Yang C;Zhang JC;Yao W;Dong C;Ohgi Y;Futamura T;Hashimoto K
通讯作者:
Hashimoto K