Journal: Philosophical Transactions of the Royal Society B: Biological Sciences

Article Title: Src dependency of the regulation of LTP by alternative splicing of GRIN1 exon 5

doi: 10.1098/rstb.2023.0236

Figure Lengend Snippet: Src family kinase activating peptide, pYEEI, enhances EPSPs in GluN1a but not in GluN1b neurons ( a ). Scatter plot of normalized peak EPSPs from GluN1a neurons. The intracellular solution had no pYEEI peptide added ( n = 6 neurons from three animals), or pYEEI included without ( n = 7 neurons from three animals) or with bath-applied (2R)-amino-5-phosphonovaleric acid (APV) ( n = 6 neurons from three animals). ( b ). Scatter plot of normalized peak EPSPs from GluN1b neurons. The intracellular solution had no pYEEI peptide added ( n = 6 neurons from four animals), pYEEI included ( n = 7 neurons from four animals). ( c ) Histograms of average normalized EPSPs peak amplitude for WT ( n = 6 neurons from three animals (with peptide) and 6 neurons from four animals (no peptide)), the GluN1a or the GluN1b neurons with treatment indicated below each bar. The average amplitude was calculated for 25–30 min after breakthrough. The run-up of the peak amplitude with no added pYEEI was not statistically significantly different across the three genotypes. * p < 0.05; ** p < 0.01; ns, p > 0.05. All experiments shown in this figure were done with whole-cell patch recording in current-clamp mode. EPSPs were evoked by stimulating Schaffer collateral inputs to CA1. In all panels, response amplitudes were normalized to those evoked in the first 2 min after patch breakthrough. Inset traces in a and b show a representative average of 10 EPSPs recorded at the beginning (1) and the end (2) of the 30 min period shown. Scale bars in a , b , 10 mV; 50 ms.

Article Snippet: Intracellularly administrated Src activating peptide (2 mM), inactive control peptide (2 mM) [ ] and Src inhibitory peptide Src40–58 (0.03 mg/ml) [ ] were from GenScript.

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