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. 2012 Jan 30;109(7):E442–E451. doi: 10.1073/pnas.1118803109

Fig. 7.

Fig. 7.

β-Arrestin-2 KO mice exhibit normal LTP, but significantly impaired LTD, in acute hippocampal slices. (A) LTP of Schaffer collateral-CA1 synapses evoked by two trains of 100-Hz pulses at 1 s duration in WT (solid symbols) and β-arrestin-2 KO (shaded symbols) mice. Graph shows mean ± SEM (WT, n = 7; β-arrestin-2 KO, n = 7). (B) Quantitative analysis of extracellular field excitatory postsynaptic potentials (fEPSPs) for minutes 60–75 in WT (solid bar) and β-arrestin-2 KO (shaded bar) mice. Histogram shows mean ± SEM; Student's t test, not significant (NS). (C) LTD of Schaffer collateral-CA1 synapses evoked by paired-pulse LFS at 1 Hz for 15 min in WT (solid symbols) and β-arrestin-2 KO (shaded symbols) mice. Graph shows mean ± SEM (WT, n = 9; β-arrestin-2 KO, n = 10). (D) Quantitative analysis of fEPSPs for minutes 75–90 in WT (solid bar) and β-arrestin-2 KO (shaded bar) mice. Histogram shows mean ± SEM; Student's t test, *P = 0.027. (E) Input/output (I/O) curves as an indication of basal synaptic transmission for WT (solid symbols) and β-arrestin-2 KO (shaded symbols) mice. Graph shows mean ± SEM (WT, n = 17; β-arrestin-2 KO, n = 15); Student's t test, not significant (NS).