Tags

Type your tag names separated by a space and hit enter

Brain-derived neurotrophic factor functions as a metabotrophin to mediate the effects of exercise on cognition.
Eur J Neurosci. 2008 Dec; 28(11):2278-87.EJ

Abstract

Brain-derived neurotrophic factor (BDNF) has been shown to mediate the effects of exercise on synaptic plasticity and cognitive function, in a process in which energy metabolism probably plays an important role. The purpose of the present study was to examine the influence of exercise on rat hippocampal expression of molecules involved in the regulation of energy management and cognitive function, and to determine the role of BDNF in these events. One week of voluntary exercise that enhanced learning and memory performance elevated the expression of molecular systems involved in the metabolism of energy [AMP-activated protein kinase (AMPK), ubiquitous mitochondrial creatine kinase (uMtCK) and uncoupling protein 2] and molecules that work at the interface of energy and synaptic plasticity [BDNF, insulin-like growth factor I (IGF-I) and ghrelin]. The levels of BDNF mRNA were associated with the mRNA levels of AMPK, uMtCK, IGF-I and ghrelin. Inhibiting the action of BDNF during exercise abolished an exercise-mediated enhancement in spatial learning and increased the expression of all of the molecular systems studied. BDNF blocking also disrupted the association between learning speed and levels of AMPK, uMtCK, ghrelin and IGF-I mRNAs. These findings suggest that the effects of exercise on synaptic plasticity and cognitive function involve elements of energy metabolism, and that BDNF seems to work at the interface between the two processes as a metabotrophin.

Authors+Show Affiliations

Department of Physiological Science, UCLA Brain Injury Research Center, Los Angeles, CA, USA. fgomezpi@ucla.eduNo affiliation info availableNo affiliation info available

Pub Type(s)

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

Language

eng

PubMed ID

19046371

Citation

Gomez-Pinilla, Fernando, et al. "Brain-derived Neurotrophic Factor Functions as a Metabotrophin to Mediate the Effects of Exercise On Cognition." The European Journal of Neuroscience, vol. 28, no. 11, 2008, pp. 2278-87.
Gomez-Pinilla F, Vaynman S, Ying Z. Brain-derived neurotrophic factor functions as a metabotrophin to mediate the effects of exercise on cognition. Eur J Neurosci. 2008;28(11):2278-87.
Gomez-Pinilla, F., Vaynman, S., & Ying, Z. (2008). Brain-derived neurotrophic factor functions as a metabotrophin to mediate the effects of exercise on cognition. The European Journal of Neuroscience, 28(11), 2278-87. https://doi.org/10.1111/j.1460-9568.2008.06524.x
Gomez-Pinilla F, Vaynman S, Ying Z. Brain-derived Neurotrophic Factor Functions as a Metabotrophin to Mediate the Effects of Exercise On Cognition. Eur J Neurosci. 2008;28(11):2278-87. PubMed PMID: 19046371.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Brain-derived neurotrophic factor functions as a metabotrophin to mediate the effects of exercise on cognition. AU - Gomez-Pinilla,Fernando, AU - Vaynman,Shoshanna, AU - Ying,Zhe, PY - 2008/12/3/pubmed PY - 2009/2/21/medline PY - 2008/12/3/entrez SP - 2278 EP - 87 JF - The European journal of neuroscience JO - Eur. J. Neurosci. VL - 28 IS - 11 N2 - Brain-derived neurotrophic factor (BDNF) has been shown to mediate the effects of exercise on synaptic plasticity and cognitive function, in a process in which energy metabolism probably plays an important role. The purpose of the present study was to examine the influence of exercise on rat hippocampal expression of molecules involved in the regulation of energy management and cognitive function, and to determine the role of BDNF in these events. One week of voluntary exercise that enhanced learning and memory performance elevated the expression of molecular systems involved in the metabolism of energy [AMP-activated protein kinase (AMPK), ubiquitous mitochondrial creatine kinase (uMtCK) and uncoupling protein 2] and molecules that work at the interface of energy and synaptic plasticity [BDNF, insulin-like growth factor I (IGF-I) and ghrelin]. The levels of BDNF mRNA were associated with the mRNA levels of AMPK, uMtCK, IGF-I and ghrelin. Inhibiting the action of BDNF during exercise abolished an exercise-mediated enhancement in spatial learning and increased the expression of all of the molecular systems studied. BDNF blocking also disrupted the association between learning speed and levels of AMPK, uMtCK, ghrelin and IGF-I mRNAs. These findings suggest that the effects of exercise on synaptic plasticity and cognitive function involve elements of energy metabolism, and that BDNF seems to work at the interface between the two processes as a metabotrophin. SN - 1460-9568 UR - https://www.unboundmedicine.com/medline/citation/19046371/Brain_derived_neurotrophic_factor_functions_as_a_metabotrophin_to_mediate_the_effects_of_exercise_on_cognition_ L2 - https://doi.org/10.1111/j.1460-9568.2008.06524.x DB - PRIME DP - Unbound Medicine ER -