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Coupling energy metabolism with a mechanism to support brain-derived neurotrophic factor-mediated synaptic plasticity.
Neuroscience. 2006; 139(4):1221-34.N

Abstract

Synaptic plasticity and behaviors are likely dependent on the capacity of neurons to meet the energy demands imposed by neuronal activity. We used physical activity, a paradigm intrinsically associated with energy consumption/expenditure and cognitive enhancement, to study how energy metabolism interacts with the substrates for neuroplasticity. We found that in an area critical for learning and memory, the hippocampus, exercise modified aspects of energy metabolism by decreasing oxidative stress and increasing the levels of cytochrome c oxidase-II, a specific component of mitochondrial machinery. We infused 1,25-dihydroxyvitamin D3, a modulator of energy metabolism, directly into the hippocampus during 3 days of voluntary wheel running and measured its effects on brain-derived neurotrophic factor-mediated synaptic plasticity. Brain-derived neurotrophic factor is a central player for the effects of exercise on synaptic and cognitive plasticity. We found that 25-dihydroxyvitamin D3 decreased exercise-induced brain-derived neurotrophic factor but had no significant effect on neurotrophin-3 levels, thereby suggesting a level of specificity for brain-derived neurotrophic factor in the hippocampus. 25-Dihydroxyvitamin D3 injection also abolished the effects of exercise on the consummate end-products of brain-derived neurotrophic factor action, i.e. cyclic AMP response element-binding protein and synapsin I, and modulated phosphorylated calmodulin protein kinase II, a signal transduction cascade downstream to brain-derived neurotrophic factor action that is important for learning and memory. We also found that exercise significantly increased the expression of the mitochondrial uncoupling protein 2, an energy-balancing factor concerned with ATP production and free radical management. Our results reveal a fundamental mechanism by which key elements of energy metabolism may modulate the substrates of hippocampal synaptic plasticity.

Authors+Show Affiliations

Department of Physiological Science, UCLA, Los Angeles, CA 90095, USA.No affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural

Language

eng

PubMed ID

16580138

Citation

Vaynman, S, et al. "Coupling Energy Metabolism With a Mechanism to Support Brain-derived Neurotrophic Factor-mediated Synaptic Plasticity." Neuroscience, vol. 139, no. 4, 2006, pp. 1221-34.
Vaynman S, Ying Z, Wu A, et al. Coupling energy metabolism with a mechanism to support brain-derived neurotrophic factor-mediated synaptic plasticity. Neuroscience. 2006;139(4):1221-34.
Vaynman, S., Ying, Z., Wu, A., & Gomez-Pinilla, F. (2006). Coupling energy metabolism with a mechanism to support brain-derived neurotrophic factor-mediated synaptic plasticity. Neuroscience, 139(4), 1221-34.
Vaynman S, et al. Coupling Energy Metabolism With a Mechanism to Support Brain-derived Neurotrophic Factor-mediated Synaptic Plasticity. Neuroscience. 2006;139(4):1221-34. PubMed PMID: 16580138.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Coupling energy metabolism with a mechanism to support brain-derived neurotrophic factor-mediated synaptic plasticity. AU - Vaynman,S, AU - Ying,Z, AU - Wu,A, AU - Gomez-Pinilla,F, Y1 - 2006/03/31/ PY - 2005/07/28/received PY - 2006/01/19/revised PY - 2006/01/26/accepted PY - 2006/4/4/pubmed PY - 2006/7/27/medline PY - 2006/4/4/entrez SP - 1221 EP - 34 JF - Neuroscience JO - Neuroscience VL - 139 IS - 4 N2 - Synaptic plasticity and behaviors are likely dependent on the capacity of neurons to meet the energy demands imposed by neuronal activity. We used physical activity, a paradigm intrinsically associated with energy consumption/expenditure and cognitive enhancement, to study how energy metabolism interacts with the substrates for neuroplasticity. We found that in an area critical for learning and memory, the hippocampus, exercise modified aspects of energy metabolism by decreasing oxidative stress and increasing the levels of cytochrome c oxidase-II, a specific component of mitochondrial machinery. We infused 1,25-dihydroxyvitamin D3, a modulator of energy metabolism, directly into the hippocampus during 3 days of voluntary wheel running and measured its effects on brain-derived neurotrophic factor-mediated synaptic plasticity. Brain-derived neurotrophic factor is a central player for the effects of exercise on synaptic and cognitive plasticity. We found that 25-dihydroxyvitamin D3 decreased exercise-induced brain-derived neurotrophic factor but had no significant effect on neurotrophin-3 levels, thereby suggesting a level of specificity for brain-derived neurotrophic factor in the hippocampus. 25-Dihydroxyvitamin D3 injection also abolished the effects of exercise on the consummate end-products of brain-derived neurotrophic factor action, i.e. cyclic AMP response element-binding protein and synapsin I, and modulated phosphorylated calmodulin protein kinase II, a signal transduction cascade downstream to brain-derived neurotrophic factor action that is important for learning and memory. We also found that exercise significantly increased the expression of the mitochondrial uncoupling protein 2, an energy-balancing factor concerned with ATP production and free radical management. Our results reveal a fundamental mechanism by which key elements of energy metabolism may modulate the substrates of hippocampal synaptic plasticity. SN - 0306-4522 UR - https://www.unboundmedicine.com/medline/citation/16580138/Coupling_energy_metabolism_with_a_mechanism_to_support_brain_derived_neurotrophic_factor_mediated_synaptic_plasticity_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0306-4522(06)00138-2 DB - PRIME DP - Unbound Medicine ER -