Neurotrophin-3 restores synaptic plasticity in the striatum of a mouse model of Huntington's disease.
CNS Neurosci Ther
; 24(4): 353-363, 2018 04.
Article
em En
| MEDLINE
| ID: mdl-29453932
ABSTRACT
AIMS:
Neurotrophin-3 (NT-3) is expressed in the mouse striatum; however, it is not clear the NT-3 role in striatal physiology. The expression levels of mRNAs and immune localization of the NT-3 protein and its receptor TrkC are altered in the striatum following damage induced by an in vivo treatment with 3-nitropropionic acid (3-NP), a mitochondrial toxin used to mimic the histopathological hallmarks of Huntington's disease (HD). The aim of this study was to evaluate the role of NT-3 on corticostriatal synaptic transmission and its plasticity in both the control and damaged striatum.METHODS:
Corticostriatal population spikes were electrophysiologically recorded and striatal synaptic plasticity was induced by high-frequency stimulation. Further, the phosphorylation status of Trk receptors was tested under conditions that imitated electrophysiological experiments.RESULTS:
NT-3 modulates both synaptic transmission and plasticity in the striatum; nonetheless, synaptic plasticity was modified by the 3-NP treatment, where instead of producing striatal long-term depression (LTD), long-term potentiation (LTP) was obtained. Moreover, the administration of NT-3 in the recording bath restored the plasticity observed under control conditions (LTD) in this model of striatal degeneration.CONCLUSION:
NT-3 modulates corticostriatal transmission through TrkB stimulation and restores striatal LTD by signaling through its TrkC receptor.Palavras-chave
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Base de dados:
MEDLINE
Assunto principal:
Doença de Huntington
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Transmissão Sináptica
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Corpo Estriado
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Neurotrofina 3
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Plasticidade Neuronal
Idioma:
En
Ano de publicação:
2018
Tipo de documento:
Article