Abstract
![Figure][1] CREDIT: SHEN ET AL. While the existence of a period of reduced learning coinciding with the onset of puberty in mice is well characterized, the underlying cellular and molecular mechanisms remain unclear. Shen et al. (p. [1515][2]) assessed the role of specific γ-aminobutyric acid type A (GABAA) receptors for restricting hippocampal plasticity during puberty. At puberty, but not in adults or the very young, GABA receptors containing the α4 and δ subunits were targeted perisynaptically to excitatory synapses, shunting the depolarizing current necessary for N -methyl-d-aspartate (NMDA) receptor activation. As a consequence, signal transmission was affected and spatial learning reduced. [1]: pending:yes [2]: /lookup/doi/10.1126/science.1184245
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