c-fos modulates brain-derived neurotrophic factor mRNA expression in mouse hippocampal CA3 and dentate gyrus neurons

Dong, Mei; Wu, Yongfei; Fan, Yunxia; Xu, Ming; Zhang, Jianhua

doi:10.1016/j.neulet.2006.02.063

Cited by 43 publications

(20 citation statements)

References 22 publications

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“…Our hypothesis of reduced BDNF release is in line with the concept that increased BDNF levels augment neurogenesis (111,112); thus, conversely, attenuated BDNF release/signaling should reduce neurogenesis in the dentate subgranular layer, as noted in our model. This is also consistent with our finding of decreased c-Fos expression, as c-Fos and BDNF are known to be coregulated (113)(114)(115), as well as with our previous data demonstrating impaired long-term potentiation 24 h after tibial surgery (110), tentatively indicating a transient effect of surgery on neuronal hyperexcitability. However, alternative explanations should be considered, such as posttranslational regulation of BDNF synthesis (116), and synthesis by already-existing BDNF mRNA cannot be excluded.…”

Section: Discussionsupporting

confidence: 93%

Orthopedic surgery modulates neuropeptides and BDNF expression at the spinal and hippocampal levels

Zhang

Barde

Yang

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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Pain is a critical component hindering recovery and regaining of function after surgery, particularly in the elderly. Understanding the role of pain signaling after surgery may lead to novel interventions for common complications such as delirium and postoperative cognitive dysfunction. Using a model of tibial fracture with intramedullary pinning in male mice, associated with cognitive deficits, we characterized the effects on the primary somatosensory system. Here we show that tibial fracture with pinning triggers cold allodynia and up-regulates nerve injury and inflammatory markers in dorsal root ganglia (DRGs) and spinal cord up to 2 wk after intervention. At 72 h after surgery, there is an increase in activating transcription factor 3 (ATF3), the neuropeptides galanin and neuropeptide Y (NPY), brain-derived neurotrophic factor (BDNF), as well as neuroinflammatory markers including ionized calcium-binding adaptor molecule 1 (Iba1), glial fibrillary acidic protein (GFAP), and the fractalkine receptor CX3CR1 in DRGs. Using an established model of complete transection of the sciatic nerve for comparison, we observed similar but more pronounced changes in these markers. However, protein levels of BDNF remained elevated for a longer period after fracture. In the hippocampus, BDNF protein levels were increased, yet there were no changes in Bdnf mRNA in the parent granule cell bodies. Further, c-Fos was down-regulated in the hippocampus, together with a reduction in neurogenesis in the subgranular zone. Taken together, our results suggest that attenuated BDNF release and signaling in the dentate gyrus may account for cognitive and mental deficits sometimes observed after surgery.postoperative pain | nerve injury | memory | delirium | neurogenesis

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Section: Discussionsupporting

confidence: 93%

Orthopedic surgery modulates neuropeptides and BDNF expression at the spinal and hippocampal levels

Zhang

Barde

Yang

et al. 2016

Proc. Natl. Acad. Sci. U.S.A.

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“…In addition, the KA-induced increase in activation of Akt and mTOR may serve to negatively regulate the induction of autophagy, as evidenced by the decrease in the ratio of LC3-II/I by 8-16h after KA treatment. Previous studies in our laboratory have found a KA-induced, c-fosregulated increase in BDNF [32], which may induce the activation of Akt [33]. A previous study of intrastriatal KA administration in the rat showed a transient decrease in Akt phosphorylation measured 24-48h following KA [34], but differences in species, route of administration and time course may explain this apparent discrepancy with the results of our study.…”

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confidence: 99%

Kainic acid induces early and transient autophagic stress in mouse hippocampus

Shacka

Lü

Xie

et al. 2007

Neuroscience Letters

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105

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Kainic acid (KA) treatment is a well-established model of hippocampal neuron death mediated in large part by KA receptor-induced excitotoxicity. KA-induced, delayed neuron death has been shown previously to follow the induction of seizures and exhibit characteristics of both apoptosis and necrosis. Growing evidence supports a role of autophagic stress-induced death of neurons in several in vitro and in vivo models of neuron death and neurodegeneration. However, whether autophagic stress also plays a role in KA-induced excitotoxicity has not been previously investigated. To examine whether KA alters the levels of proteins associated with or known to regulate the formation of autophagic vacuoles, we isolated hippocampal extracts from control mice and in mice following 2-16h KA injection. KA induced a significant increase in the amount of LC3-II, a specific marker of autophagic vacuoles, at 4-6h following KA, which indicates a transient induction of autophagic stress. Levels of autophagy-associated proteins including ATG5 (conjugated to ATG12), ATG6 and ATG7 did not change significantly after treatment with KA. However, ratios of phospho-mTOR/ mTOR were elevated from 6-16h, and ratios of phospho-Akt/Akt were elevated at 16h following KA treatment, suggesting a potential negative feedback loop to inhibit further stimulation of autophagic stress. Together these data indicate the transient induction of autophagic stress by KA which may serve to regulate excitotoxic death in mouse hippocampus. Keywords kainic acid; hippocampus; autophagy; ATG5; ATG7; Akt; mTOR; LC3The excitatory amino acid neurotransmitter glutamate is known to play an important role in a vast array of neuronal activities as well as in the induction of excitotoxic neurodegeneration through massive activation of its receptors [1;2]. Kainic acid (KA) is a potent glutamate receptor agonist with selectivity towards non-N-methyl-D-aspartate (NMDA)-type glutamate receptors [3;4]. KA is well known for its ability to induce seizures within minutes of its administration and is followed by a delayed excitotoxic neuron death in the hippocampus several hours later, in part through an increase in intracellular calcium and activation of calcium-dependent neuron death pathways [5][6][7]. Both apoptotic and necrotic death of neurons Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Autophagic stress results from alterations in autophagy, a lysosomal degradation pathway that is responsible for the homeostatically regulated turnover of macronutrients and organelles [10]. Macroautophagy, the most prominent form of autophagy ...

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“…For example, we found that METH caused differential c-fos expression in a manner that parallels the changes in BDNF expression among the experimental groups. Members of the AP-1 family of transcription factors, especially c-fos, are induced in several models of neuronal injuries [105], [106]. BDNF is often induced in the same models of brain injury [105], [106], with BDNF and c-fos being, oftentimes, co-induced in neurons after excitotoxic damage [105].…”

Section: Discussionmentioning

confidence: 99%

“…Members of the AP-1 family of transcription factors, especially c-fos, are induced in several models of neuronal injuries [105], [106]. BDNF is often induced in the same models of brain injury [105], [106], with BDNF and c-fos being, oftentimes, co-induced in neurons after excitotoxic damage [105]. Moreover, c-fos mutant knockout mice show altered responses in BDNF expression after injections of the excitotoxin, kainic acid [105], [106].…”

Section: Discussionmentioning

confidence: 99%

“…BDNF is often induced in the same models of brain injury [105], [106], with BDNF and c-fos being, oftentimes, co-induced in neurons after excitotoxic damage [105]. Moreover, c-fos mutant knockout mice show altered responses in BDNF expression after injections of the excitotoxin, kainic acid [105], [106]. Also of interest is the demonstration that BDNF can induce c-fos expression in midbrain dopaminergic neurons [107].…”

Section: Discussionmentioning

confidence: 99%

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Methamphetamine Preconditioning Alters Midbrain Transcriptional Responses to Methamphetamine-Induced Injury in the Rat Striatum

et al. 2009

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Methamphetamine (METH) is an illicit drug which is neurotoxic to the mammalian brain. Numerous studies have revealed significant decreases in dopamine and serotonin levels in the brains of animals exposed to moderate-to-large METH doses given within short intervals of time. In contrast, repeated injections of small nontoxic doses of the drug followed by a challenge with toxic METH doses afford significant protection against monoamine depletion. The present study was undertaken to test the possibility that repeated injections of the drug might be accompanied by transcriptional changes involved in rendering the nigrostriatal dopaminergic system refractory to METH toxicity. Our results confirm that METH preconditioning can provide significant protection against METH-induced striatal dopamine depletion. In addition, the presence and absence of METH preconditioning were associated with substantial differences in the identity of the genes whose expression was affected by a toxic METH challenge. Quantitative PCR confirmed METH-induced changes in genes of interest and identified additional genes that were differentially impacted by the toxic METH challenge in the presence of METH preconditioning. These genes include small heat shock 27 kD 27 protein 2 (HspB2), thyrotropin-releasing hormone (TRH), brain derived neurotrophic factor (BDNF), c-fos, and some encoding antioxidant proteins including CuZn superoxide dismutase (CuZnSOD), glutathione peroxidase (GPx)-1, and heme oxygenase-1 (Hmox-1). These observations are consistent, in part, with the transcriptional alterations reported in models of lethal ischemic injuries which are preceded by ischemic or pharmacological preconditioning. Our findings suggest that multiple molecular pathways might work in tandem to protect the nigrostriatal dopaminergic pathway against the deleterious effects of the toxic psychostimulant. Further analysis of the molecular and cellular pathways regulated by these genes should help to provide some insight into the neuroadaptive potentials of the brain when repeatedly exposed to drugs of abuse.

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c-fos modulates brain-derived neurotrophic factor mRNA expression in mouse hippocampal CA3 and dentate gyrus neurons

Cited by 43 publications

References 22 publications

Orthopedic surgery modulates neuropeptides and BDNF expression at the spinal and hippocampal levels

Orthopedic surgery modulates neuropeptides and BDNF expression at the spinal and hippocampal levels

Kainic acid induces early and transient autophagic stress in mouse hippocampus

Methamphetamine Preconditioning Alters Midbrain Transcriptional Responses to Methamphetamine-Induced Injury in the Rat Striatum

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