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05), reflecting a greater contribution of GluA2-containing AMPARs in the presence of TBOA than in its absence. As a percentage of the total integral in TBOA, the PhTx-resistant EPSC was predominant (Figure ?(Figure4C,4C, n = 8, PhTx-resistant, 85 �� 8%; PhTx-sensitive, 15 �� 7%). When the kinetics of the PhTx-resistant EPSC in TBOA were directly compared to those of the PhTx-sensitive EPSC in TBOA, the decay of the PhTx-sensitive EPSC was not clearly slower than that of the PhTx-resistant MMP23B EPSC (Figure ?(Figure4D);4D); a tri-exponential fit failed to reveal any significant differences between the decay time constants of the fast (n = 8, 9.8 �� 1.5 ms; n = 6, 12.8 �� 2.4 ms; p = 0.622), slow (n = 8, 570 �� 106 ms; n = 6, 485 �� 195 ms, p = 0.691), or uptake-suppressed (n = 8, 2489 �� 395 ms; n = 4, 1497 �� 474 ms; p > 0.05) components of the PhTx-resistant and��sensitive currents of the TBOA-enhanced tail. There was also no click here difference between the relative proportions of the fast (n = 8, 0.5 �� 0.08; n = 6, 0.46 �� 0.08; p > 0.05), slow (n = 8, 0.29 �� 0.08; n = 6, 0.36 �� 0.09; p > 0.05), or uptake-suppressed (n = 8, 0.21 �� 0.05; n = 6, 0.19 �� 0.07; p > 0.05) EPSCs. We conclude that the slow EPSC recruited by TBOA is not composed predominantly of GluA2-lacking AMPARs, and in this respect it is clearly distinct from the slow EPSC when uptake is intact. Figure 4 Blockade of EAAT1 recruits extrasynaptic AMPARs that predominantly contain GluA2. (A) Representative traces of before (black) and after addition of TBOA (green). TBOA results in a small reduction of the fast component and a major enhancement of the tail ... The Slow AMPAR EPSC is Developmentally Downregulated As we performed these experiments, we noted that the slow EPSC in our present set of experiments was smaller than expected based on our previous studies. One difference between the current results and previous ones is that the current BTK inhibitor set of experiments was done in mice while earlier studies were done in rats, both at about the same developmental stage (2�C3 weeks). Reasoning that rats have a slower developmental entry into adulthood than mice, we considered that a developmental downregulation of the slow AMPAR EPSC might account for the smaller expression of the slow EPSC in mice. To test this idea directly, we divided the subjects by age (