Cholinergic interneurons amplify corticostriatal synaptic responses in the Q175 model of huntington’s disease
Frontiers in Systems Neuroscience, ISSN: 1662-5137, Vol: 10, Issue: DEC, Page: 102
2016
- 24Citations
- 34Captures
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Example: if you select the 1-year option for an article published in 2019 and a metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019. If you select the 3-year option for the same article published in 2019 and the metric category shows 90%, that means that the article or review is performing better than 90% of the other articles/reviews published in that journal in 2019, 2018 and 2017.
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Metrics Details
- Citations24
- Citation Indexes24
- 24
- CrossRef11
- Captures34
- Readers34
- 34
Article Description
Huntington’s disease (HD) is a neurodegenerative disorder characterized by deficits in movement control that are widely viewed as stemming from pathophysiological changes in the striatum. Giant, aspiny cholinergic interneurons (ChIs) are key elements in the striatal circuitry controlling movement, but whether their physiological properties are intact in the HD brain is unclear. To address this issue, the synaptic properties of ChIs were examined using optogenetic approaches in the Q175 mouse model of HD. In ex vivo brain slices, synaptic facilitation at thalamostriatal synapses onto ChIs was reduced in Q175 mice. The alteration in thalamostriatal transmission was paralleled by an increased response to optogenetic stimulation of cortical axons, enabling these inputs to more readily induce burst-pause patterns of activity in ChIs. This adaptation was dependent upon amplification of cortically evoked responses by a post-synaptic upregulation of voltage-dependent Na channels. This upregulation also led to an increased ability of somatic spikes to invade ChI dendrites. However, there was not an alteration in the basal pacemaking rate of ChIs, possibly due to increased availability of Kv4 channels. Thus, there is a functional “re-wiring” of the striatal networks in Q175 mice, which results in greater cortical control of phasic ChI activity, which is widely thought to shape the impact of salient stimuli on striatal action selection.
Bibliographic Details
http://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85007432902&origin=inward; http://dx.doi.org/10.3389/fnsys.2016.00102; http://www.ncbi.nlm.nih.gov/pubmed/28018188; http://journal.frontiersin.org/article/10.3389/fnsys.2016.00102/full; https://dx.doi.org/10.3389/fnsys.2016.00102; https://www.frontiersin.org/articles/10.3389/fnsys.2016.00102/full
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