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Spatial component of: CELSR3 deficiency leads to tic-related behaviors and dopaminergic alterations in the striatum

ABSTRACT: Spatial component of: CELSR3 deficiency leads to tic-related behaviors and dopaminergic alterations in the striatum

PROVIDER: PRJNA1180076 | ENA |

REPOSITORIES: ENA

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			Action	DRS
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	SRR31173800_1.fastq.gz	Fastqsanger.gz
	SRR31173800_2.fastq.gz	Fastqsanger.gz
	SRR31173794_1.fastq.gz	Fastqsanger.gz
	SRR31173794_2.fastq.gz	Fastqsanger.gz

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CELSR3 deficiency leads to tic-related behaviors and dopaminergic alterations in the striatum

Project description:CELSR3 deficiency leads to tic-related behaviors and dopaminergic alterations in the striatum

| PRJNA1051112 | ENA

Spatial component of: CELSR3 deficiency leads to tic-related behaviors and dopaminergic alterations in the striatum

Project description:The gene CELSR3 (cadherin EGF LAG seven‐pass-G‐type receptor 3) has been recently recognized as a high-confidence risk factor for tic disorders (TD). Celsr3 mutant mice displayed tic-like grooming stereotypies and jerks, as well as sensorimotor gating deficits, which were opposed by TD therapies. Spatial transcriptomic analyses revealed that Celsr3 mutants featured abnormalities of the extracellular matrix in the striatum. Notably, there are alterations in collagen and extracellular organization.

2025-06-12 | GSE280709 | GEO

CELSR3 deficiency leads to tic-related behaviors and dopaminergic alterations in the striatum

Project description:The gene CELSR3 (cadherin EGF LAG seven‐pass-G‐type receptor 3) has been recently recognized as a high-confidence risk factor for tic disorders (TD). Celsr3 mutant mice displayed tic-like grooming stereotypies and jerks, as well as sensorimotor gating deficits, which were opposed by TD therapies. Single-nucleus transcriptomic analyses revealed that Celsr3 mutants featured a unique group of eccentric striatal projection neurons. Notably, the Drd3 gene, encoding the dopamine D3 receptor, was significantly upregulated in these cells as well as striosomal D1-positive neurons, while it was reduced in calretinin-positive GABAergic interneurons.

2025-06-12 | GSE249902 | GEO

In vitro Modeling of the Human Dopaminergic System using spatially arranged ventral Midbrain-Striatum-Cortex Assembloids [Smartseq]

Project description:Dopaminergic neurons located in the ventral Midbrain (vMid) innervate the striatum and cortex and are involved in movement control and reward-related cognition. Degeneration of dopaminergic neurons causes Parkinson’s disease (PD), while their over-activation is implicated in addiction. Thus, modeling the dopaminergic system is of broad relevance for disease research and drug discovery, although limited availability of patient material and inherent differences in animal model systems are restricting the study of distinctive human specific features such as development and neurodegeneration. Here, we show that spatially arranged assembloids can recapitulate dopaminergic innervation of striatum and cortex and offer methods for their use in cell replacement therapy and addiction research. We describe improved protocols for growing vMid, striatal and cortical organoids and use custom embedding molds to fuse them in a linear manner. Linear assembloids form functional long-range dopaminergic connections with striatal and cortical tissues that can release dopamine. We demonstrate that vMid grafts derived from hPSCs for cell replacement therapy of PD can integrate into the tissue and structurally mature. Additionally, we demonstrate that our model can be used to study dopaminergic circuit perturbations in the example of chronic cocaine treatment which causes morphological, functional and transcriptional changes that remained altered even after drug withdrawal. Our method opens new avenues for dopaminergic cell replacement therapy and the analysis of drugs affecting the dopaminergic system, directly in a human system.

2023-09-20 | GSE219246 | GEO

In vitro Modeling of the Human Dopaminergic System using spatially arranged ventral Midbrain-Striatum-Cortex Assembloids [scRNAseq]

2023-09-20 | GSE219245 | GEO

Zonisamide facilitates survival of human iPS cell-derived dopaminergic neurons in the rat striatum

Project description:It is reported that the transplantation of dopaminergic (DA) progenitors derived from pluripotent stem cells improves the behavior of Parkinson's disease (PD) model animals. However, the number of survived DA neurons was reported to be about 10% of the transplanted cells. This low survivability limits the clinical application of this stem cell-based therapy for PD. Recently, it was reported that zonisamide (ZNS) increased the number of survived DA neurons upon the transplantation of mouse induced pluripotent stem (iPS) cell-derived DA progenitors in the mouse striatum. It is not known, however, whether ZNS exerts the same effect on human DA neurons. We induced DA progenitors from human iPS cells and transplanted them into the rat striatum with daily administration of ZNS. The number of survived DA neurons was evaluated one and four months after transplantation by immunohistochemistry. To assess the mechanism of action of ZNS, we performed a microarray analysis to compare the gene expression profile in striatum treated with or without ZNS. The immunofluorescense study at one and four months revealed that the number of survived DA neurons was significantly increased with the administration of ZNS. The microarray analysis revealed that the expression of Slitrk6 was up-regulated in rat striatum treated with ZNS. SLIT and NTRK like protein 6 (SLITRK6) was expressed by cholinergic neurons in the striatum. In addition, survival and neurite extension were enhanced when human iPS cell-derived DA progenitors were cultured on SLITRK6-expressing HEK293T cells. ZNS promotes the survival of DA neurons after the transplantation of human iPS cell-derived DA progenitors in the rat striatum. SLITRK6 is suggested to be involved in this supportive effect of ZNS by modulating the environment of the host brain.

2019-04-26 | GSE112624 | GEO

The Obesity-associated Fto gene regulates activity of the dopaminergic midbrain circuitry [WT]

Project description:Here we use MeRIP-Seq to analyze global adenosine methylation (m6A) in mRNAs in the midbrain and striatum of Fto-deficient mice. We find that Fto deficiency leads to increased methylation within a subset of mRNAs important for neuronal signaling, including many within the dopaminergic signaling pathway. Collectively, our results show that Fto regulates demethylation of specific mRNAs in vivo, and this activity relates to control of dopaminergic transmission. Profiling of m6A in midbrain and striatum from wild type mice

2013-06-15 | E-GEOD-47215 | biostudies-arrayexpress

The Obesity-associated Fto gene regulates activity of the dopaminergic midbrain circuitry [FTO KO]

2013-06-15 | E-GEOD-47216 | biostudies-arrayexpress

Disrupted iron homeostasis causes dopaminergic neurodegeneration in mice

Project description:Disruption of local iron homeostasis is a common feature of neurodegenerative diseases. We focused on dopaminergic neurons, asking how iron transport proteins modulate iron homeostasis in vivo. Inactivation of the transmembrane iron exporter ferroportin had no apparent consequences. However, loss of the transferrin receptor 1, involved in iron uptake, caused profound, age-progressive neurodegeneration with features similar to Parkinson’s disease. There was gradual loss of dopaminergic projections in the striatum with subsequent death of dopaminergic neurons in the substantia nigra. After depletion of 30% of the neurons the mice developed neurobehavioral parkinsonism, with evidence of mitochondrial dysfunction and impaired mitochondrial autophagy. Molecular analysis revealed strong signatures indicative of attempted axonal regeneration, a metabolic switch to glycolysis and the unfolded protein response. We speculate that cellular iron deficiency may contribute to neurodegeneration in human patients Using Ribotag technology, from mouse ventral midbrain lysates, we isolated actively translated mRNA species from control and Transferrin receptor 1-null dopaminergic neurons. Two mouse ages were used 3 wks (early neurodegeration) 10 wks (late neurodegeneration)

2015-03-11 | E-GEOD-66730 | biostudies-arrayexpress

Zonisamide facilitates survival of human iPS cell-derived dopaminergic neurons in the rat striatum

Project description:Zonisamide facilitates survival of human iPS cell-derived dopaminergic neurons in the rat striatum

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