Contribution of BDNF/TrkB signalling in the rACC to the development of pain-related aversion via activation of ERK in rats with spared nerve injury

Xu, Wei; Zhang, Le; Zhan, Yufeng; Li, Dengping; Zhang, Yuangui; Wang, Gongming; Zhang, Mengyuan

doi:10.1016/j.brainres.2017.07.010

Cited by 19 publications

(15 citation statements)

References 39 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In contrast, the inhibition of ERK phosphorylation significantly delays axotomy-induced growth cone formation and axon regrowth in denervated muscle fibers [ 90 ]. Similarly, knockdown of the MAPK gene significantly weakens the potential regenerative effects of FGF21 on axonal regeneration, remyelination, and functional recovery following facial nerve injury [ 91 , 92 ]. Therefore, clarifying the roles and actions of GFs interacting with the MAPK/ERK pathway may provide a better understanding of the molecular mechanism underlying the action of GFs in PNI repair.…”

Section: Gf Signaling Mechanisms That Regulate Nerve Regenerationmentioning

confidence: 99%

Growth factors-based therapeutic strategies and their underlying signaling mechanisms for peripheral nerve regeneration

et al. 2020

View full text Add to dashboard Cite

Peripheral nerve injury (PNI), one of the most common concerns following trauma, can result in a significant loss of sensory or motor function. Restoration of the injured nerves requires a complex cellular and molecular response to rebuild the functional axons so that they can accurately connect with their original targets. However, there is no optimized therapy for complete recovery after PNI. Supplementation with exogenous growth factors (GFs) is an emerging and versatile therapeutic strategy for promoting nerve regeneration and functional recovery. GFs activate the downstream targets of various signaling cascades through binding with their corresponding receptors to exert their multiple effects on neurorestoration and tissue regeneration. However, the simple administration of GFs is insufficient for reconstructing PNI due to their short half-life and rapid deactivation in body fluids. To overcome these shortcomings, several nerve conduits derived from biological tissue or synthetic materials have been developed. Their good biocompatibility and biofunctionality made them a suitable vehicle for the delivery of multiple GFs to support peripheral nerve regeneration. After repairing nerve defects, the controlled release of GFs from the conduit structures is able to continuously improve axonal regeneration and functional outcome. Thus, therapies with growth factor (GF) delivery systems have received increasing attention in recent years. Here, we mainly review the therapeutic capacity of GFs and their incorporation into nerve guides for repairing PNI. In addition, the possible receptors and signaling mechanisms of the GF family exerting their biological effects are also emphasized.

show abstract

Section: Gf Signaling Mechanisms That Regulate Nerve Regenerationmentioning

confidence: 99%

Growth factors-based therapeutic strategies and their underlying signaling mechanisms for peripheral nerve regeneration

et al. 2020

View full text Add to dashboard Cite

show abstract

“…However, it is important to emphasize that studies with humans from functional magnetic resonance imaging showed evidence that chronic pain and neuroplasticity are a cognitive maladaptive learning process (Apkarian et al, 2011;Mansour et al, 2014;DosSantos et al, 2017). Whereas studies with animal models investigated the role of one single molecular signaling related to neuroplasticity, such as BDNF/TrkB pathway, for instance (Zhang et al, 2014(Zhang et al, , 2017Wang et al, 2017). This controversy associating neuroplasticity to chronic pain facilitation or chronic pain susceptibility prevention, may be explained, in our study, by the early gene expression changes in the NAc caused by HFD employed 6 weeks before the voluntary physical activity period.…”

Section: Biological Processesmentioning

confidence: 99%

Physical Activity Induces Nucleus Accumbens Genes Expression Changes Preventing Chronic Pain Susceptibility Promoted by High-Fat Diet and Sedentary Behavior in Mice

et al. 2020

View full text Add to dashboard Cite

Recent findings from rodent studies suggest that high-fat diet (HFD) increases hyperalgesia independent of obesity status. Furthermore, weight loss interventions such as voluntary physical activity (PA) for adults with obesity or overweight was reported to promote pain reduction in humans with chronic pain. However, regardless of obesity status, it is not known whether HFD intake and sedentary (SED) behavior is underlies chronic pain susceptibility. Moreover, differential gene expression in the nucleus accumbens (NAc) plays a crucial role in chronic pain susceptibility. Thus, the present study used an adapted model of the inflammatory prostaglandin E2 (PGE2)induced persistent hyperalgesia short-term (PH-ST) protocol for mice, an HFD, and a voluntary PA paradigm to test these hypotheses. Therefore, we performed an analysis of differential gene expression using a transcriptome approach of the NAc. We also applied a gene ontology enrichment tools to identify biological processes associated with chronic pain susceptibility and to investigate the interaction between the factors studied: diet (standard diet vs. HFD), physical activity behavior (SED vs. PA) and PH-ST (PGE vs. saline). Our results demonstrated that HFD intake and sedentary behavior promoted chronic pain susceptibility, which in turn was prevented by voluntary physical activity, even when the animals were fed an HFD. The transcriptome of the NAc found 2,204 differential expression genes and gene ontology enrichment analysis revealed 41 biologic processes implicated in chronic pain susceptibility. Taking these biological processes together, our results suggest that genes related to metabolic and mitochondria stress were up-regulated in the chronic pain susceptibility group (SED-HFD-PGE), whereas genes related to neuroplasticity were up-regulated in the non-chronic pain susceptibility group (PA-HFD-PGE). These findings provide pieces of evidence that HFD intake and sedentary behavior provoked gene expression changes in the NAc related to promotion of chronic pain susceptibility, whereas voluntary physical activity provoked gene expression changes in the NAc related to prevention of chronic

show abstract

“…Given that a definite property of LTM is its sensitivity to protein synthesis inhibitors around training (Davis and Squire, 1984 ; Medina et al, 2008 ) and that ERK1/2 plays a crucial role in several forms of synaptic plasticity (English and Sweatt, 1997 ; Rosenblum et al, 2002 ), it is reasonable to think that ERK1/2 might be involved in many cellular processes including LTM formation (Atkins et al, 1998 ). After this seminal work demonstrating that contextual fear LTM depends on the activation of ERK1/2 in the dorsal hippocampus, several studies confirmed that this signaling cascade is required in selected brain regions in a variety of learning tasks, including Pavlovian fear conditioning (Schafe et al, 2000 ), step-down inhibitory avoidance (Walz et al, 1999 ), learning a novel taste (Swank and Sweatt, 2001 ), recognition memory (Kelly et al, 2003 ), spatial Morris water maze (Kelleher et al, 2004 ), cocaine-induced conditioned place preference (Pan et al, 2011 ) and conditioned place avoidance (Wang et al, 2017 ). Most of these studies have also shown that learning was associated with specific changes in the phosphorylation state of ERK1/2.…”

Section: Role Of Erk1/2 In Long-term Memory Formationmentioning

confidence: 99%

ERK1/2: A Key Cellular Component for the Formation, Retrieval, Reconsolidation and Persistence of Memory

Medina

Viola

2018

Front. Mol. Neurosci.

View full text Add to dashboard Cite

Extracellular regulated kinase 1/2 (ERK1/2) has been strongly implicated in several cellular processes. In the brain ERK1/2 activity has been primarily involved in long-term memory (LTM) formation and expression. Here, we review earlier evidence and describe recent developments of ERK1/2 signaling in memory processing focusing the attention on the role of ERK1/2 in memory retrieval and reconsolidation, and in the maintenance of the memory trace including mechanisms involving the protection of labile memories. In addition, relearning requires ERK1/2 activity in selected brain regions. Its involvement in distinct memory stages points at ERK1/2 as a core element in memory processing and as one likely target to treat memory impairments associated with neurological disorders.

show abstract

Contribution of BDNF/TrkB signalling in the rACC to the development of pain-related aversion via activation of ERK in rats with spared nerve injury

Cited by 19 publications

References 39 publications

Growth factors-based therapeutic strategies and their underlying signaling mechanisms for peripheral nerve regeneration

Growth factors-based therapeutic strategies and their underlying signaling mechanisms for peripheral nerve regeneration

Physical Activity Induces Nucleus Accumbens Genes Expression Changes Preventing Chronic Pain Susceptibility Promoted by High-Fat Diet and Sedentary Behavior in Mice

ERK1/2: A Key Cellular Component for the Formation, Retrieval, Reconsolidation and Persistence of Memory

Contact Info

Product

Resources

About