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BDNF increases rat brain mitochondrial respiratory coupling at complex I, but not complex II.

Authors: Markham, A  Cameron, I  Franklin, P  Spedding, M 
Citation: Markham A, etal., Eur J Neurosci 2004 Sep;20(5):1189-96.
Pubmed: (View Article at PubMed) PMID:15341590
DOI: Full-text: DOI:10.1111/j.1460-9568.2004.03578.x

Brain-derived neurotrophic factor (BDNF) governs both the selective survival of neurons during development and the experience-based regulation of synaptic strength throughout life. BDNF produced a concentration-dependent increase in the respiratory control index (RCI, a measure of the efficiency of respiratory coupling, ATP synthesis and organelle integrity) of rat brain mitochondria. This effect was mediated via a MAP kinase pathway and highly specific for oxidation of glutamate plus malate (complex I) by brain mitochondria. The oxidation by brain mitochondria of the complex II substrate succinate was unaffected by BDNF. The failure of BDNF to modify respiratory activity associated with mitochondrial preparations isolated from rat liver indicates that the actions of the neurotrophin are tissue specific. BDNF also increased the RCI values associated with Ca2+ -induced respiration to a similar extent. This is the first demonstration that BDNF, in addition to modifying neuronal plasticity, can modify brain metabolism and the efficiency of oxygen utilization. The finding that neurotrophins can alter mitochondrial oxidative efficiency has important implications for neurodegenerative and psychiatric diseases.

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CRRD Object Information
CRRD ID: 1358393
Created: 2005-06-10
Species: All species
Last Modified: 2005-06-10
Status: ACTIVE



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