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Merck
CN

FMRP regulates an ethanol-dependent shift in GABA

Nature communications (2016-09-27)
Sarah A Wolfe, Emily R Workman, Chelcie F Heaney, Farr Niere, Sanjeev Namjoshi, Luisa P Cacheaux, Sean P Farris, Michael R Drew, Boris V Zemelman, R Adron Harris, Kimberly F Raab-Graham
摘要

Alcohol promotes lasting neuroadaptive changes that may provide relief from depressive symptoms, often referred to as the self-medication hypothesis. However, the molecular/synaptic pathways that are shared by alcohol and antidepressants are unknown. In the current study, acute exposure to ethanol produced lasting antidepressant and anxiolytic behaviours. To understand the functional basis of these behaviours, we examined a molecular pathway that is activated by rapid antidepressants. Ethanol, like rapid antidepressants, alters γ-aminobutyric acid type B receptor (GABA

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抗-α微管蛋白抗体,小鼠单克隆抗体, clone B-5-1-2, purified from hybridoma cell culture
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Anti-Rabbit IgG (Fc specific), highly cross adsorbed-Biotin antibody produced in goat, affinity isolated antibody, lyophilized powder