Up-regulation of transient receptor potential vanilloid (TRPV) and down-regulation of brain-derived neurotrophic factor (BDNF) expression in patients with functional dyspepsia (FD)

2017 ◽  
Vol 30 (2) ◽  
pp. e13176 ◽  
Author(s):  
C. K. Y. Cheung ◽  
L. L. Lan ◽  
M. Kyaw ◽  
A. D. P. Mak ◽  
A. Chan ◽  
...  
Keyword(s):  
Functional Dyspepsia ◽  
Neurotrophic Factor ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Brain Derived Neurotrophic Factor ◽  
Transient Receptor Potential Vanilloid ◽  
Bdnf Expression ◽  
Down Regulation ◽  
Transient Receptor

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

2013 ◽  
Vol 289 (3) ◽  
pp. 1213-1226 ◽  
Author(s):  
Bo Su ◽  
Yun-Song Ji ◽  
Xu-lu Sun ◽  
Xiang-Hua Liu ◽  
Zhe-Yu Chen
Keyword(s):  
Synaptic Transmission ◽  
Neurotrophic Factor ◽  
Hippocampal Neurons ◽  
Transient Receptor Potential ◽  
Receptor Potential ◽  
Brain Derived Neurotrophic Factor ◽  
High Energy ◽  
Mitochondrial Transport ◽  
Mitochondrial Motility ◽  
Transient Receptor

Appropriate mitochondrial transport and distribution are essential for neurons because of the high energy and Ca2+ buffering requirements at synapses. Brain-derived neurotrophic factor (BDNF) plays an essential role in regulating synaptic transmission and plasticity. However, whether and how BDNF can regulate mitochondrial transport and distribution are still unclear. Here, we find that in cultured hippocampal neurons, application of BDNF for 15 min decreased the percentage of moving mitochondria in axons, a process dependent on the activation of the TrkB receptor and its downstream PI3K and phospholipase-Cγ signaling pathways. Moreover, the BDNF-induced mitochondrial stopping requires the activation of transient receptor potential canonical 3 and 6 (TRPC3 and TRPC6) channels and elevated intracellular Ca2+ levels. The Ca2+ sensor Miro1 plays an important role in this process. Finally, the BDNF-induced mitochondrial stopping leads to the accumulation of more mitochondria at presynaptic sites. Mutant Miro1 lacking the ability to bind Ca2+ prevents BDNF-induced mitochondrial presynaptic accumulation and synaptic transmission, suggesting that Miro1-mediated mitochondrial motility is involved in BDNF-induced mitochondrial presynaptic docking and neurotransmission. Together, these data suggest that mitochondrial transport and distribution play essential roles in BDNF-mediated synaptic transmission.

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