ArticleCellular and molecular neurobiology
Elevated expression of the G-protein-activated inwardly rectifying potassium channel 2 (GIRK2) in cerebellar unipolar brush cells of a Down syndrome mouse model.
Article in Cellular and molecular neurobiology. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 45 citations in OpenAlex.
- Differential Modulation of Cerebellar Flocculus Unipolar Brush Cells during Vestibular Compensation.Biomedicines · 2023Article
- Glutamatergic synaptic deficits in the prefrontal cortex of the Ts65Dn mouse model for Down syndrome.Frontiers in neuroscience · 2023Article
- Enhanced GIRK2 channel signaling in Down syndrome: A feasible role in the development of abnormal nascent neural circuits.Frontiers in genetics · 2022Review
- GIRK2 Channels in Down Syndrome and Alzheimer's Disease.Current Alzheimer research · 2022Article
- GABACurrent topics in behavioral neurosciences · 2022Review
- Rethinking Intellectual Disability from Neuro- to Astro-Pathology.International journal of molecular sciences · 2020Review
- Proteomic analysis of six- and twelve-month hippocampus and cerebellum in a murine Down syndrome model.Neurobiology of aging · 2018Article
- A KCNJ6 gene polymorphism modulates theta oscillations during reward processing.International journal of psychophysiology : official journal of the International Organization of Psychophysiology · 2017Article
- Altered intrinsic and network properties of neocortical neurons in the Ts65Dn mouse model of Down syndrome.Physiological reports · 2015Article
- Human chromosome 21 orthologous region on mouse chromosome 17 is a major determinant of Down syndrome-related developmental cognitive deficits.Human molecular genetics · 2014Article
- 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
- Down syndrome: the brain in trisomic mode.Nature reviews. Neuroscience · 2012Review
- Electrophysiological, morphological, and topological properties of two histochemically distinct subpopulations of cerebellar unipolar brush cells.Cerebellum (London, England) · 2012Article
- Increased excitability and altered action potential waveform in cerebellar granule neurons of the Ts65Dn mouse model of Down syndrome.Brain research · 2012Article
- Trisomy of the G protein-coupled K+ channel gene, Kcnj6, affects reward mechanisms, cognitive functions, and synaptic plasticity in mice.Proceedings of the National Academy of Sciences of the United States of America · 2012Article
- Dysfunctional hippocampal inhibition in the Ts65Dn mouse model of Down syndrome.Experimental neurology · 2012Article
- Molecular and cellular alterations in Down syndrome: toward the identification of targets for therapeutics.Neural plasticity · 2012Review
- The unipolar brush cell: a remarkable neuron finally receiving deserved attention.Brain research reviews · 2011Review
- Down's syndrome suppression of tumour growth and the role of the calcineurin inhibitor DSCR1.Nature · 2009Article
- Functional genomic analysis of amniotic fluid cell-free mRNA suggests that oxidative stress is significant in Down syndrome fetuses.Proceedings of the National Academy of Sciences of the United States of America · 2009Article
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
Abstract
1. Down syndrome (DS) arises from the presence of three copies of chromosome (Chr.) 21. Fine motor learning deficits found in DS from childhood to adulthood result from expression of extra genes on Chr. 21, however, it remains unclear which if any of these genes are the specific causes of the cognitive and motor dysfunction. DS cerebellum displays morphological abnormalities that likely contribute to the DS motor phenotype. 2. The G-protein-activated inwardly rectifying potassium channel subunit 2 (GIRK2) is expressed in cerebellum and can shunt dendritic conductance and attenuate postsynaptic potentials. We have used an interbreeding approach to cross a genetic mouse model of DS (Ts65Dn) with Girk2 knockout mice and examined its relative expression level by quantitative real-time RT-PCR, Western blotting and immunohistochemistry. 3. We report here for the first time that GIRK2 is expressed in unipolar brush cells, which are excitatory interneurons of the vestibulocerebellum and dorsal cochlear nucleus. Analysis of disomic-Ts65Dn/Girk2((+/+/-)) and heterozygous-Diploid/Girk2((+/-)) mice shows that GIRK2 expression in Ts65Dn lobule X follows gene dosage. The lobule X of Ts65Dn mice contain greater numbers of unipolar brush cells co-expressing GIRK2 and calretinin than the control mouse groups. 4. These results demonstrate that gene triplication can impact specific cell types in the cerebellum. We hypothesize that GIRK2 overexpression will adversely affect cerebellar circuitry in Ts65Dn vestibulocerebellum and dorsal cochlear nucleus due to GIRK2 shunting properties and its effects on resting membrane potential.
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