D. Besusso
BDNF-TrkB signaling in striatopallidal neurons controls inhibition of locomotor behaviour
Besusso, D.; Geibel, M.; Kramer, D.; Schneider, T.; Pendolino, V.; Picconi, B.; Calabresi, P.; Minichiello, L.; Bannerman, D.M.
Authors
M. Geibel
D. Kramer
T. Schneider
V. Pendolino
B. Picconi
P. Calabresi
L. Minichiello
D.M. Bannerman
Abstract
The physiology of brain-derived neurotrophic factor signaling in enkephalinergic striatopallidal neurons is poorly understood. Changes in cortical Bdnf expression levels, and/or impairment in brain-derived neurotrophic factor anterograde transport induced by mutant huntingtin (mHdh) are believed to cause striatopallidal neuron vulnerability in early-stage Huntington’s disease. Although several studies have confirmed a link between altered cortical brain-derived neurotrophic factor signaling and striatal vulnerability, it is not known whether the effects are mediated via the brain-derived neurotrophic factor receptor TrkB, and whether they are direct or indirect. Using a novel genetic mouse model, here, we show that selective removal of brain-derived neurotrophic factor–TrkB signaling from enkephalinergic striatal targets unexpectedly leads to spontaneous and drug-induced hyperlocomotion. This is associated with dopamine D2 receptor-dependent increased striatal protein kinase C and MAP kinase activation, resulting in altered intrinsic activation of striatal enkephalinergic neurons. Therefore, brain-derived neurotrophic factor/TrkB signaling in striatopallidal neurons controls inhibition of locomotor behavior by modulating neuronal activity in response to excitatory input through the protein kinase C/MAP kinase pathway.
Citation
Besusso, D., Geibel, M., Kramer, D., Schneider, T., Pendolino, V., Picconi, B., …Bannerman, D. (2013). BDNF-TrkB signaling in striatopallidal neurons controls inhibition of locomotor behaviour. Nature Communications, 4, https://doi.org/10.1038/ncomms3031
Journal Article Type | Article |
---|---|
Publication Date | Jun 18, 2013 |
Deposit Date | Jan 17, 2014 |
Publicly Available Date | Aug 13, 2014 |
Journal | Nature Communications |
Publisher | Nature Research |
Peer Reviewed | Peer Reviewed |
Volume | 4 |
DOI | https://doi.org/10.1038/ncomms3031 |
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This article is licensed under a Creative Commons Attribution 3.0 Unported Licence. To view a copy of this licence visit http://creativecommons.org/licenses/by/3.0/.
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