Striatal circuit development and its alterations in Huntington's disease

Lebouc, Margaux; Richard, Quentin; Garret, Maurice; Baufreton, Jérôme

doi:10.1016/j.nbd.2020.105076

Cited by 27 publications

(20 citation statements)

References 147 publications

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“… 1 , 2 The coordination of these roles relies on striatal neurons integrating information received from surrounding brain areas including the cortex, midbrain and thalamus. 2 , 3 Dysfunction in striatal regulation has been associated with a variety of diseases such as Parkinson's disease, 4 , 5 Huntington's disease 6 , 7 and addiction. 8 , 9 Additionally, recent studies have shown that striatal dysregulation may also correlate with obsessive‐compulsive disorder, 10 , 11 eating disorders, 12 , 13 schizophrenia, 14 , 15 and bipolar disorder.…”

Section: Introductionmentioning

confidence: 99%

Functional dissociation of behavioral effects from acetylcholine and glutamate released from cholinergic striatal interneurons

et al. 2022

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In the striatum, cholinergic interneurons (CINs) have the ability to release both acetylcholine and glutamate, due to the expression of the vesicular acetylcholine transporter (VAChT) and the vesicular glutamate transporter 3 (VGLUT3). However, the relationship these neurotransmitters have in the regulation of behavior is not fully understood. Here we used reward-based touchscreen tests in mice to assess the individual and combined contributions of acetylcholine/glutamate co-transmission in behavior. We found that reduced levels of the VAChT from CINs negatively impacted dopamine signalling in response to reward, and disrupted complex responses in a sequential chain of events. In contrast, diminished VGLUT3 levels had somewhat opposite effects. When mutant mice were treated with haloperidol in a cue-based task, the drug did not affect the performance of VAChT mutant mice, whereas VGLUT3 mutant mice were highly sensitive to haloperidol. In mice where both vesicular transporters were deleted from CINs, we observed altered rewardevoked dopaminergic signalling and behavioral deficits that resemble, but wereThis is an open access article under the terms of the Creat ive Commo ns Attri butio n-NonCo mmerc ial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

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Section: Introductionmentioning

confidence: 99%

Functional dissociation of behavioral effects from acetylcholine and glutamate released from cholinergic striatal interneurons

et al. 2022

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“…Collectively, the previous studies have potential to reveal spatiotemporal and cell-type specific mechanism of HD pathology. The future challenges in HD research are brought by the complexity of the pathology from biochemical level [293][294][295][296][297][298][299][300][301][302][303] to system level [304][305][306][307][308]. Accordingly, the ultimate mechanisms of HD pathology can be further scrutinized by state-of-the art research methods such as multi-omics approach combining transcriptome, proteome, and interactome [309], big data analysis with machine learning [310], and meta-analysis combining the publicly available data [311].…”

Section: Discussionmentioning

confidence: 99%

Non-Cell Autonomous and Epigenetic Mechanisms of Huntington’s Disease

Kim

Yousefian-Jazi

Choi

et al. 2021

IJMS

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Huntington’s disease (HD) is a rare neurodegenerative disorder caused by an expansion of CAG trinucleotide repeat located in the exon 1 of Huntingtin (HTT) gene in human chromosome 4. The HTT protein is ubiquitously expressed in the brain. Specifically, mutant HTT (mHTT) protein-mediated toxicity leads to a dramatic degeneration of the striatum among many regions of the brain. HD symptoms exhibit a major involuntary movement followed by cognitive and psychiatric dysfunctions. In this review, we address the conventional role of wild type HTT (wtHTT) and how mHTT protein disrupts the function of medium spiny neurons (MSNs). We also discuss how mHTT modulates epigenetic modifications and transcriptional pathways in MSNs. In addition, we define how non-cell autonomous pathways lead to damage and death of MSNs under HD pathological conditions. Lastly, we overview therapeutic approaches for HD. Together, understanding of precise neuropathological mechanisms of HD may improve therapeutic approaches to treat the onset and progression of HD.

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“…The neuropathological changes in HD include atrophy and cell loss in the caudate putamen of the striatum, where medium spiny neurons are the most vulnerable [ 154 , 155 , 156 ]. This has led to the striatum being the center of attention for molecular, structural, and functional studies of HD [ 157 , 158 , 159 ]. However, other brain regions such as the hippocampus are also affected in HD [ 160 ].…”

Section: Hippocampal Dysfunction In Neurodegenerative Diseasesmentioning

confidence: 99%

Structural Plasticity of the Hippocampus in Neurodegenerative Diseases

Weerasinghe-Mudiyanselage

Ang

Kang

et al. 2022

IJMS

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Neuroplasticity is the capacity of neural networks in the brain to alter through development and rearrangement. It can be classified as structural and functional plasticity. The hippocampus is more susceptible to neuroplasticity as compared to other brain regions. Structural modifications in the hippocampus underpin several neurodegenerative diseases that exhibit cognitive and emotional dysregulation. This article reviews the findings of several preclinical and clinical studies about the role of structural plasticity in the hippocampus in neurodegenerative diseases, including Alzheimer’s disease, Parkinson’s disease, Huntington’s disease, and multiple sclerosis. In this study, literature was surveyed using Google Scholar, PubMed, Web of Science, and Scopus, to review the mechanisms that underlie the alterations in the structural plasticity of the hippocampus in neurodegenerative diseases. This review summarizes the role of structural plasticity in the hippocampus for the etiopathogenesis of neurodegenerative diseases and identifies the current focus and gaps in knowledge about hippocampal dysfunctions. Ultimately, this information will be useful to propel future mechanistic and therapeutic research in neurodegenerative diseases.

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Striatal circuit development and its alterations in Huntington's disease

Cited by 27 publications

References 147 publications

Functional dissociation of behavioral effects from acetylcholine and glutamate released from cholinergic striatal interneurons

Functional dissociation of behavioral effects from acetylcholine and glutamate released from cholinergic striatal interneurons

Non-Cell Autonomous and Epigenetic Mechanisms of Huntington’s Disease

Structural Plasticity of the Hippocampus in Neurodegenerative Diseases

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