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Wolfe, SA, Workman, ER, Heaney, CF, Niere, F, Namjoshi, S, Cacheaux, LP, Farris, SP, Drew, MR, Zemelman, BV, Harris, RA and Raab-Graham, KF (2016) FMRP regulates an ethanol-dependent shift in GABABR function and expression with rapid antidepressant properties. Nat Commun 7:12867
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 (GABABR) expression and signalling, to increase dendritic calcium. Furthermore, new GABABRs are synthesized in response to ethanol treatment, requiring fragile-X mental retardation protein (FMRP). Ethanol-dependent changes in GABABR expression, dendritic signalling, and antidepressant efficacy are absent in Fmr1-knockout (KO) mice. These findings indicate that FMRP is an important regulator of protein synthesis following alcohol exposure, providing a molecular basis for the antidepressant efficacy of acute ethanol exposure.
|Gene product||Qualifier||GO Term||Evidence Code||with/from||Aspect||Extension||Notes||Status|
|GO:0017148: negative regulation of translation||
Figure 3 (c-g) shows that in mutant mice cells with no FMRP protein production, there was an increased expression of GABAbR1 and GABAbR2 proteins. This means that in the presence of FMRP, translation of GABAbR1 and GABAbR2 is repressed. This shows FMRP negatively regulates the expression of these proteins.
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