抄録
The molecular and cellular mechanisms underlying experience-dependent plasticity of brain function are poorly understood. Recent in vitro studies have identified the regulated trafficking of AMPA receptors (-Rs) into synapses as a major molecular component of neural plasticity. Here we ask if experience-driven plasticity in the developing rat barrel cortex is accompanied by and/or requires AMPA-R delivery to synapses. By combining in vivo gene delivery with in vitro recordings, we show that experience drives recombinant GluR1, an AMPA-R subunit, into synapses formed between layer 4 and layer 2/3 neurons. Furthermore, expression of the GluR1 cytoplasmic tail in layer 2/3 neurons, a construct that inhibits synaptic delivery of endogenous AMPA receptors during long-term potentiation, blocks experience-driven synaptic potentiation. These studies show that synaptic delivery of AMPA-Rs contributes to plasticity driven by natural stimuli in the mammalian brain. [J Physiol Sci. 2007;57 Suppl:S58]
