Cortical Axonal Secretion of BDNF in the Striatum Is Disrupted in the Mutant-huntingtin Knock-in Mouse Model of Huntington's Disease
- Authors
- Park, Hyungju
- Issue Date
- Jun-2018
- Publisher
- KOREAN SOC BRAIN & NEURAL SCIENCE, KOREAN SOC NEURODEGENERATIVE DISEASE
- Keywords
- BDNF; Huntington' s disease; antisense oligonucleotide; corticostriatal synapse
- Citation
- EXPERIMENTAL NEUROBIOLOGY, v.27, no.3, pp.217 - 225
- Journal Title
- EXPERIMENTAL NEUROBIOLOGY
- Volume
- 27
- Number
- 3
- Start Page
- 217
- End Page
- 225
- URI
- http://scholarworks.bwise.kr/kbri/handle/2023.sw.kbri/739
- DOI
- 10.5607/en.2018.27.3.217
- ISSN
- 1226-2560
- Abstract
- Deficient BDNF signaling is known to be involved in neurodegenerative diseases such as Huntington's disease (HD). Mutant huntingtin (mhtt)-mediated disruption of either BDNF transcription or transport is thought to be a factor contributing to striatal atrophy in the HD brain. Whether and how activity-dependent BDNF secretion is affected by the mhtt remains unclear. In the present study, I provide evidence for differential effects of the mhtt on cortical BDNF secretion in the striatum during HD progression. By two-photon imaging of fluorescent BDNF sensor (BDNF-pHluorin and -EGFP) in acute striatal slices of HD knock-in model mice, I found deficient cortical BDNF secretion regardless of the HD onset, but antisense oligonucleotide (ASO)-mediated reduction of htts only rescues BDNF secretion in the early HD brain before the disease onset. Although secretion modes of individual BDNF-containing vesicle were not altered in the pre-symptomatic brain, the full-fusion and partial-fusion modes of BDNF-containing vesicles were significantly altered after the onset of HD symptoms. Thus, besides abnormal BDNF transcription and transport, our results suggest that mhtt-mediated alteration in activity-dependent BDNF secretion at corticostriatal synapses also contributes to the development of HD.
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