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Plasticity of mature hippocampal CA1 synapses is dependent on L-alpha-amino-3-- hydroxy-5-methylisoxazole-4-propionate (AMPA) receptors containing the glutamate receptor A (GluR-A) subunit. In GluR-A-deficient mice, plasticity could be restored by controlled expression of green fluorescent protein (GFP)-tagged GluRA, which contributes to channel formation and displayed the developmental redistribution of AMPA receptors in CA1 pyramidal neurons. Long-term potentiation (LTP) induced by pairing or tetanic stimulation was rescued in adult GluR-A^sup -/-^ mice when ^sup GFP^GluR-A expression was constitutive or induced in already fully developed pyramidal cells. This shows that GluR-A-independent forms of synaptic plasticity can mediate the establishment of mature hippocampal circuits that are prebuilt to express GluR-A-dependent LTP.
Of the four AMPA receptor subunits (GluR-- A to GluR-D) constituting one family of glutamate-gated ion channels (1-3), GluR-A is essential for adult hippocampal LTP but not for spatial learning in a water maze task (4). Studies on mice lacking GluR-A provided evidence that after tetanic stimulation, increased transmission at Schaffer collateral (SC/CA1) synapses is established by an augmented response of AMPA receptors. The selective, strong reduction of somatic AMPA receptor currents in GluR-A-deficient mice
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