| First Author | Shen H | Year | 2010 |
| Journal | Science | Volume | 327 |
| Issue | 5972 | Pages | 1515-8 |
| PubMed ID | 20299596 | Mgi Jnum | J:158728 |
| Mgi Id | MGI:4440362 | Doi | 10.1126/science.1184245 |
| Citation | Shen H, et al. (2010) A critical role for alpha4betadelta GABAA receptors in shaping learning deficits at puberty in mice. Science 327(5972):1515-8 |
| abstractText | The onset of puberty defines a developmental stage when some learning processes are diminished, but the mechanism for this deficit remains unknown. We found that, at puberty, expression of inhibitory alpha4betadelta gamma-aminobutyric acid type A (GABAA) receptors (GABAR) increases perisynaptic to excitatory synapses in CA1 hippocampus. Shunting inhibition via these receptors reduced N-methyl-D-aspartate receptor activation, impairing induction of long-term potentiation (LTP). Pubertal mice also failed to learn a hippocampal, LTP-dependent spatial task that was easily acquired by delta-/- mice. However, the stress steroid THP (3alphaOH-5alpha[beta]-pregnan-20-one), which reduces tonic inhibition at puberty, facilitated learning. Thus, the emergence of alpha4betadelta GABARs at puberty impairs learning, an effect that can be reversed by a stress steroid. |
