Journal
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
Volume 109, Issue 7, Pages 2642-2647Publisher
NATL ACAD SCIENCES
DOI: 10.1073/pnas.1109099109
Keywords
electrophysiological recordings; neuronal culture; fear conditioning; sucrose preference; open-field
Categories
Funding
- Josef Cohn Center for Biomembrane Research
- Israeli Science Foundation [207/09]
- David and Fela Shapell Family Center for Genetic Disorders Research
- Nella and Leon Benoziyo Center for Neurological Diseases
- Foundation Jerome le Jeune
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G protein-activated inwardly rectifying K+ channels (GIRK) generate slow inhibitory postsynaptic potentials in the brain via G(i/o) protein-coupled receptors. GIRK2, a GIRK subunit, is widely abundant in the brain and has been implicated in various functions and pathologies, such as learning and memory, reward, motor coordination, and Down syndrome. Down syndrome, the most prevalent cause of mental retardation, results from the presence of an extra maternal chromosome 21 (trisomy 21), which comprises the Kcnj6 gene (GIRK2). The present study examined the behaviors and cellular physiology properties in mice harboring a single trisomy of the Kcnj6 gene. Kcnj6 triploid mice exhibit deficits in hippocampal-dependent learning and memory, altered responses to rewards, hampered depotentiation, a form of excitatory synaptic plasticity, and have accentuated long-term synaptic depression. Collectively the findings suggest that triplication of Kcnj6 gene may play an active role in some of the abnormal neurological phenotypes found in Down syndrome.
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