Adenylyl cyclase I regulates AMPA receptor trafficking during mouse cortical 'barrel' map development

Supplementary Fig. 1. (gif 20K)
The kinetics of evoked miniature-EPSCs and the decay kinetics of NMDAR mediated evoked EPSCs for control and barrelless neurons. (a) Summary data of the rise time from barrelless and control neurons (wt neurons, 0.757 0.131 msec, n=7; barrelless neurons, 0.686 0.077 msec, n= 7). Data taken from same neurons as reported in figure 2. Examples of the raw data traces are presented in figure 2. Rise time measurements show no difference between genotypes (P=0.61 for the comparison). (b) Summary data of fall time from n=7 barrelless and control neurons. The falling phase of the average evoked mEPSCs was fit with a double exponential. The fall times on average were longer in the control animals (4.957 0.131 msec, n=7) than in barrelless neurons (3.0714 0.337 msec, n=7; P < 0.05 for the difference). (c) Example average evoked mEPSCs from barrelless and control neurons. (d) Normalized average evoked mEPSCs from barrelless and control neurons show that the rise times are similar, but the fall times are somewhat longer in control animals. This is consistent with the direct effect of PKA phosphorylation on AMPA receptor open time in the control animals. (e) Summary measurements of the decay kinetics for NMDAR mediated evoked EPSCs at thalamocortical synapses. The developmental decrease in NMDAR decay time constant occurred in both control and barrelless thalamocortical synapses, consistent with a shift from NR2B to NR2A mediated currents as reported in Fig. 1C. There is no difference in the NMDAR kinetics between control and barrelless neurons for both age groups (For P3-5: the mean weighted time constant, 274 32.6 msec, n=8 for wild type neurons; 233 15.0 msec, n=6 for barrelless neurons; P=0.67 for the comparison; for P9-11: the mean weighted time constant, 160 15.4 msec, n=7 for wild type neurons; 171 28.2 msec, n=7 for barrelless neurons; P=0.99 for the comparison).

Top