To assess whether pathogenic PrP mutations influenced this interaction, we immunoprecipitated PrP from hippocampal homogenates of WT, FFI and CJD mice and immunoblotted the precipitated proteins with antibodies against GluA1 and GluA2, the two main AMPAR subunits expressed at hippocampal synapses. The gene discussed is GRIA2; the disease is Creutzfeldt Jacob disease.