Skip to main content
. 2017 Dec 6;37(49):11894–11911. doi: 10.1523/JNEUROSCI.2397-17.2017

Figure 4.

Figure 4.

S831A GluA1 mutant mice have a deficit in extinction of cocaine CPP and lower levels of GluA1 in synaptosomal fractions but not at the hippocampal PSD. A, Total and phosphorylated GluA1 at S831 were significantly higher in the PSD-enriched fraction of the hippocampus after extinction of cocaine CPP compared with saline control mice. *p < 0.05, **p < 0.01. B, Phosphorylated GluA1 at S831 was not altered in the PSD-enriched fraction of the hippocampus in mice that underwent cocaine CPP acquisition followed by home cage exposure without extinction training compared with saline control mice. C, Total GluA1 was not altered in the cytoplasmic fraction of the hippocampus after extinction of cocaine CPP compared with saline control mice. D, S831A mutant mice displayed no difference in acquisition of cocaine CPP, but demonstrated an extinction deficit compared with WT mice. *p < 0.05, **p < 0.01, ***p < 0.001 compared with baseline test; #p < 0.05 compared with acquisition test. E, After extinction, there was no difference in levels of GluA1 in PSD fractions generated from the hippocampus of S831A mutant mice compared with WT mice, whereas synaptosomal fractions had significantly lower levels of GluA1 in mutants compared with WT mice. ***p < 0.001. Data are presented as mean ± SEM.