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. 2023 Mar 1;43(9):1475–1491. doi: 10.1523/JNEUROSCI.1857-22.2023

Figure 2.

Figure 2.

SYT1, but not SYT9, supports evoked neurotransmitter release in cortical and hippocampal neurons. A, Averaged eIPSC traces recorded from Syt1 cKO cortical neurons with quantification of peak eIPSC amplitude – CRE (n = 20; 1.09 ± 0.141 nA) and + CRE (n = 23; 0.158 ± 0.0237 nA). B, Same as in A, but with hippocampal neurons (– CRE n = 22; 1.16 ± 0.221 nA; + CRE n = 26; 0.131 ± 0.0170 nA). C, D, Same as in A, B, but using Syt9 KO neurons; cortical neurons (WT n = 26; 1.81 ± 0.193 nA; KO n = 17; 1.50 ± 0.225 nA); hippocampal neurons (WT n = 23; 1.54 ± 0.192 nA; KO n = 22; 1.74 ± 0.226 nA). eIPSCs were disrupted in Syt1 cKO + CRE cortical (p < 0.0001; unpaired t test t = 6.96, df = 41) and hippocampal neurons (p < 0.0001; unpaired t test t = 5.07, df = 46). In contrast, eIPSCs were unaffected in Syt9 KO cortical (p = 0.3231; unpaired t test t = 1.000, df = 41) and hippocampal neurons (p = 0.4966; unpaired t test t = 0.686, df = 43).