TRPC5 Channel Is the Mediator of Neurotrophin-3 in Regulating Dendritic Growth via CaMKII  in Rat Hippocampal Neurons

He, Zhuohao; Jia, Caixia; Feng, Shengjie; Zhou, Kesong; Tai, Yilin; Bai, Xue; Wang, Yizheng

doi:10.1523/jneurosci.6363-11.2012

Cited by 40 publications

(28 citation statements)

References 80 publications

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“…It has been speculated that by allowing different patterns of Ca 2ϩ influx, diverse TRPC channels may perform distinct regulatory functions in neurons. Indeed, a recent study demonstrated that TRPC5-mediated Ca 2ϩ elevation activates CaMKII␣, whereas TRPC6-mediated Ca 2ϩ elevation activates CaMKIV, resulting in inhibition and promotion of neuronal dendritic growth, respectively (42). In our experiments, it is likely that at presynaptic sites TRPC3 forms heteromers with TRPC6 and is activated by BDNF, allowing Ca 2ϩ influx and resulting in higher intracellular Ca 2ϩ at the synaptic sites, which leads to more mitochondrial docking at synaptic sites regardless of anterograde or retrograde movement of mitochondria.…”

Section: Discussionmentioning

confidence: 99%

Brain-derived Neurotrophic Factor (BDNF)-induced Mitochondrial Motility Arrest and Presynaptic Docking Contribute to BDNF-enhanced Synaptic Transmission

Su¹,

Ji²,

Sun

et al. 2014

Journal of Biological Chemistry

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Background: Appropriate mitochondrial transport and localization are highly associated with neuronal activities. Results: BDNF induces mitochondrial motility arrest via Miro1 binding with Ca 2ϩ , which facilitates BDNF-enhanced neurotransmitter release. Conclusion: BDNF-regulated mitochondrial motility is essential for BDNF-enhanced synaptic transmission. Significance: These results provide novel insights into the mechanistic link between BDNF-dependent mitochondrial motility and BDNF-mediated synaptic transmission.

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Section: Discussionmentioning

confidence: 99%

Brain-derived Neurotrophic Factor (BDNF)-induced Mitochondrial Motility Arrest and Presynaptic Docking Contribute to BDNF-enhanced Synaptic Transmission

Su¹,

Ji²,

Sun

et al. 2014

Journal of Biological Chemistry

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“…Cells were treated with the following reagents: ethylene glycol tetraacetic acid (EGTA), SKF96365, mibefradil, nimodipine, D(−)-2-amino-5-phosphonopentanoic acid (D-APV), 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), cobalt chloride (CoCl 2 ), 1-oleoyl-2-acetyl-sn-glycerol (OAG), thapsigargin, 2-aminoethyl diphenylborinate (2-APB), MG132 and dimethyloxalylglycine N-(methoxyoxoacetyl)-glycine methyl ester (DMOG), all purchased from Sigma; U73122 from Calbiochem; suramin from Santa Cruz Biotechnology; pazopanib, canertinib dihydrochloride and BMS-754807 from MedChem Express; and K252a from Merck. The 3-nitrocoumarin and 7-OH-3-nitrocoumarin were gifts from Renata Tisi and Enzo Martegani (Milano-Bicocca University, Milan, Italy) (He et al, 2012). Recombinant human IGF-1 was from PeproTech.…”

Section: Cell Cultures Reagents and Antibodiesmentioning

confidence: 99%

Critical role of TRPC6 in maintaining the stability of HIF-1α in glioma cells under hypoxia

Wang

et al. 2015

Journal of Cell Science

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Hypoxia-inducible factor-1 (HIF-1) is a key transcription factor responsible for the expression of a broad range of genes that facilitate acclimatization to hypoxia. Its stability is predominantly controlled by rapid hydroxylation of two proline residues in its α-subunit. However, how the rapid hydroxylation of HIF-1α is regulated is not fully understood. Here, we report that transient receptor potential canonical (TRPC) 6 channels control hydroxylation and stability of HIF-1α in human glioma cells under hypoxia. TRPC6 was rapidly activated by IGF-1R-PLCγ-IP 3 R pathway upon hypoxia. Inhibition of TRPC6 enhanced the levels of α-ketoglutarate and promoted hydroxylation of HIF-1α to suppress HIF-1α accumulation without affecting its transcription or translation. Dimethyloxalylglycine N-(methoxyoxoacetyl)-glycine methyl ester (DMOG), an analog of α-ketoglutarate, reversed the inhibition of HIF-1α accumulation. Moreover, TRPC6 regulated GLUT1 (also known as SLC2A1) expression in a manner that was dependent on HIF-1α accumulation to affect glucose uptake during hypoxia. Our results suggest that TRPC6 regulates metabolism to affect HIF-1α stability and consequent glucose metabolism in human glioma cells under hypoxia.

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“…In neuronal cell development, establishment of morphological and functional polarity of dendrites and an axon are crucial in the formation of neural circuits and for efficient transmission of information across neurons (Gomez 2005). Recent findings define a novel function for TRPC5 that TRPC5 regulate dendrite morphogenesis in neurons and connectivity in the brain (He et al 2012;Puram et al 2011). Additionally, TRPC5 contributes to promote axon formation through activating the CaMKK/CaMKIγ cascade in cultured hippocampal neurons (Davare et al 2009).…”

Section: Introductionmentioning

confidence: 99%

Increased Expression of TRPC5 in Cortical Lesions of the Focal Cortical Dysplasia

Shu

Yue

et al. 2014

J Mol Neurosci

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Focal cortical dysplasias (FCDs) are frequently associated with the medical refractory epilepsy in both children and adults. Transient receptor potential canonical channel 5 (TRPC5), a receptor-operated cation channel, has been well recognized as a regulator in the central nervous system. Here, we examined the expression and cellular distribution of TRPC5 in the specimens from patients with FCDIa (n = 14), FCDIIa (n = 12), and FCDIIb (n = 12) compared with the age-matched control cortex (CTX). TRPC5 mRNA and protein levels were significantly higher in FCDs compared with CTX. Immunohistochemical data showed that TRPC5 was strongly expressed in the misshapen cells, particularly in neuronal microcolumns, dysmorphic neurons, and balloon cells. Moreover, the double-label immunofluorescence analyses demonstrated that TRPC5 localized on NeuN-positive neurons. In addition, its co-localization with glutamate and gamma-aminobutyric acid (GABA) indicated that TRPC5 was distributed on both glutamatergic and GABAergic neurons. Taken together, these results suggested that increased expression of TRPC5 in FCDs and the cell-specific distribution patterns of TRPC5 in the misshapen neurons in FCDs could potentially contribute to the epileptogenesis of FCDs.

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TRPC5 Channel Is the Mediator of Neurotrophin-3 in Regulating Dendritic Growth via CaMKII in Rat Hippocampal Neurons

Abstract: Neurotrophin-3 (NT-3) plays numerous important roles in the CNS

Cited by 40 publications

References 80 publications

Brain-derived Neurotrophic Factor (BDNF)-induced Mitochondrial Motility Arrest and Presynaptic Docking Contribute to BDNF-enhanced Synaptic Transmission

Brain-derived Neurotrophic Factor (BDNF)-induced Mitochondrial Motility Arrest and Presynaptic Docking Contribute to BDNF-enhanced Synaptic Transmission

Critical role of TRPC6 in maintaining the stability of HIF-1α in glioma cells under hypoxia

Increased Expression of TRPC5 in Cortical Lesions of the Focal Cortical Dysplasia

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