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Abstract: Excess inhibition in the brain of individuals carrying an extra copy of chromosome 21 could be responsible for cognitive deficits observed throughout their lives. A change in the excitatory/inhibitory balance in adulthood would alter synaptic plasticity, potentially triggering learning and memory deficits. - Aminobutyric acid (GABA) is the major inhibitory neurotransmitter in the mature central nervous system and binds to GABAA receptors, opens a chloride channel, and reduces neuronal excitability. In this review we discuss methods to alleviate neuronal inhibition in a mouse model of Down syndrome, the Ts65Dn mouse, using either an antagonist (pentylenetetrazol) or two different inverse agonists selective for the 5-subunit containing receptor. Both inverse agonists, which reduce inhibitory GABAergic transmission, could rescue learning and memory deficits in Ts65Dn mice. We also discuss safety issues since modulation of the excitatory-inhibitory balance to improve cognition without inducing seizures remains particularly difficult when using GABA antagonists.
Fuente: Neuroscience and Biobehavioral Reviews, 2014, 46 Pt 2, 218-227
Editorial: Elsevier
Fecha de publicación: 09/01/2014
Nº de páginas: 10
Tipo de publicación: Artículo de Revista
DOI: 10.1016/j.neubiorev.2013.12.008
ISSN: 0149-7634,1873-7528
Url de la publicación: https://doi.org/10.1016/j.neubiorev.2013.12.008
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CARMEN MARTINEZ-CUE PESINI
DELATOUR, BENOÎT
POTIER, MARIE-CLAUDE
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