Cholinergic Dysfunction Alters Synaptic Integration between Thalamostriatal and Corticostriatal Inputs in DYT1 Dystonia
نویسندگان
چکیده
منابع مشابه
Cholinergic dysfunction alters synaptic integration between thalamostriatal and corticostriatal inputs in DYT1 dystonia.
Projections from thalamic intralaminar nuclei convey sensory signals to striatal cholinergic interneurons. These neurons respond with a pause in their pacemaking activity, enabling synaptic integration with cortical inputs to medium spiny neurons (MSNs), thus playing a crucial role in motor function. In mice with the DYT1 dystonia mutation, stimulation of thalamostriatal axons, mimicking a resp...
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DYT1 early-onset generalized torsion dystonia (DYT1 dystonia) is an inherited movement disorder caused by mutations in one allele of DYT1 (TOR1A), coding for torsinA. The most common mutation is a trinucleotide deletion (ΔGAG), which causes a deletion of a glutamic acid residue (ΔE) in the C-terminal region of torsinA. Although recent studies using cultured cells suggest that torsinA contribute...
متن کاملCorticostriatal and thalamostriatal synapses have distinctive properties.
The two principal excitatory glutamatergic inputs to striatal medium spiny neurons (MSNs) arise from neurons in the cerebral cortex and thalamus. Although there have been many electrophysiological studies of MSN glutamatergic synapses, little is known about how corticostriatal and thalamostriatal synapses differ. Using mouse brain slices that allowed each type of synapse to be selectively activ...
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Parvalbumin-containing fast-spiking interneurons (FSIs) exert a powerful feed-forward GABAergic inhibition on striatal medium spiny neurons (MSNs), playing a critical role in timing striatal output. However, how glutamatergic inputs modulate their firing activity is still unexplored. Here, by means of a combined optogenetic and electrophysiological approach, we provide evidence for a differenti...
متن کاملTorsinA and DYT1 dystonia: a synaptopathy?
DYT1 dystonia is an autosomal dominant movement disorder, characterized by early onset of involuntary sustained muscle contractions. It is caused by a 3-bp deletion in the DYT1 gene, which results in the deletion of a single glutamate residue in the C-terminus of the protein TA (torsinA). TA is a member of the AAA+ (ATPase associated with various cellular activities) family of chaperones with m...
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ژورنال
عنوان ژورنال: Journal of Neuroscience
سال: 2012
ISSN: 0270-6474,1529-2401
DOI: 10.1523/jneurosci.0041-12.2012