Open AccessNeurotrophin‐3 restores synaptic plasticity in the striatum of a mouse model of Huntington's disease
Author(s) -
GómezPineda Victor G.,
TorresCruz Francisco M.,
VivarCortés César I.,
HernándezEcheagaray Elizabeth
Publication year - 2018
Publication title -
cns neuroscience and therapeutics
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.403
H-Index - 69
eISSN - 1755-5949
pISSN - 1755-5930
DOI - 10.1111/cns.12824
Subject(s) - striatum , long term potentiation , synaptic plasticity , neuroscience , biology , huntington's disease , neurotransmission , neurotrophin , tropomyosin receptor kinase c , trk receptor , neuroplasticity , receptor , medicine , dopamine , biochemistry , platelet derived growth factor receptor , disease , growth factor
Summary 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 mRNA s 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.