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. Author manuscript; available in PMC: 2012 Sep 1.
Published in final edited form as: Nat Neurosci. 2012 Jan 22;15(3):431–S1. doi: 10.1038/nn.3033

Figure 5. Disruption of mGluR5-Homer interactions mediates prolonged neocortical UP states in Fmr1 KO mice.

Figure 5

A,B. Genetic deletion of H1a rescues prolonged UP states in the Fmr1 KO. A. Representative extracellular multiunit recordings of spontaneous, persistent activity or UP states from layer 4 of somatosensory, barrel neocortical slices from each genotype. B. Group averages reveal that the UP state duration is prolonged in the Fmr1 KO slices (n = 13) in comparison to WT (n = 22) UP state duration in the H1a/Fmr1 KO (n = 44 slices) is reduced from the Fmr1 KO and is not different from WT. There is no difference between WT and H1a single KO (n = 18), suggesting that the rescue is dependent on Fmr1, and not a general decrease in excitability due to loss of H1a. C. Representative UP state recordings from WT and Fmr1 KO slices treated with the appropriate peptide. D. Pretreatment of WT neocortical slices with mGluR5CT peptide (CT; 4 hours; 5 μM; n = 15 slices) to acutely disrupt mGluR5-Homer interactions increases UP state duration in comparison to slices pretreated with control (mGluR5MU; MU; 5 μM; n = 13) peptide. In contrast, treatment of Fmr1KO slices (n = 12) with CT peptide had no effect on UP state duration in comparison to MU treated slices (n = 15). **p< 0.01; ***p<0.001.