ArticleBrain research2012
Increased excitability and altered action potential waveform in cerebellar granule neurons of the Ts65Dn mouse model of Down syndrome.
Article in Brain research, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 13 citations in OpenAlex.
- A Dive Into Cerebellar Dysfunction, Motor Deficits and GABAergic Signaling in Down Syndrome.Cureus · 2025Review
- Optimization of Efficient Neuron Models With Realistic Firing Dynamics. The Case of the Cerebellar Granule Cell.Frontiers in cellular neuroscience · 2020Article
- VU0810464, a non-urea G protein-gated inwardly rectifying KBritish journal of pharmacology · 2019Article
- Emerging connections between cerebellar development, behaviour and complex brain disorders.Nature reviews. Neuroscience · 2019Review
- The GABAergic Hypothesis for Cognitive Disabilities in Down Syndrome.Frontiers in cellular neuroscience · 2017Review
- Altered intrinsic and network properties of neocortical neurons in the Ts65Dn mouse model of Down syndrome.Physiological reports · 2015Article
- Reversing excitatory GABAAR signaling restores synaptic plasticity and memory in a mouse model of Down syndrome.Nature medicine · 2015Article
- Size does not always matter: Ts65Dn Down syndrome mice show cerebellum-dependent motor learning deficits that cannot be rescued by postnatal SAG treatment.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2013Article
- Hedgehog agonist therapy corrects structural and cognitive deficits in a Down syndrome mouse model.Science translational medicine · 2013Article
- Weaker control of the electrical properties of cerebellar granule cells by tonically active GABAA receptors in the Ts65Dn mouse model of Down's syndrome.Molecular brain · 2013Article
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Down syndrome (DS) is characterized by intellectual disability and impaired motor control. Lack of coordinated movement, poor balance, and unclear speech imply dysfunction of the cerebellum, which is known to be reduced in volume in DS. The principal cause of the smaller cerebellum is a diminished number of granule cells (GCs). These neurons form the 'input layer' of the cerebellar cortex, where sensorimotor information carried by incoming mossy fibers is transformed before it is conveyed to Purkinje cells and inhibitory interneurons. However, it is not known how processing of this information is affected in the hypogranular cerebellum that characterizes DS. Here we explore the possibility that the electrical properties of the surviving GCs are changed. We find that in the Ts65Dn mouse model of DS, GCs have a higher input resistance at voltages approaching the threshold for firing, which causes them to be more excitable. In addition, they fire narrower and larger amplitude action potentials. These subtly modified electrical properties may result in atypical transfer of information at the input layer of the cerebellum.
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