We then investigated which aspects of the complex series of events leading to induction, expression, and consolidation of LTP are negatively affected by manipulations of BAF53b by examining conventional measures of transmission and the responses to theta bursts. Input / output curves (number of axons stimulated / magnitude of post-synaptic response) were comparable for wildtypes vs. Baf53b+/− het mice or BAF53bΔHDlow but there was a marked depression of the curve in the BAF53bΔHDhigh mice (Fig 5E). The most straightforward interpretation of these results is that high expression of the BAF53ΔHD mutation affects axon excitability. In accord with this idea, the slope of the relationship between stimulation current and the amplitude of the fiber volley, a measure of the number of responsive axons, was reduced for the BAF53ΔHDhigh slices, but not for the other two genotypes, relative to controls (Fig 5F). We then tested the genotypes for differences in transmitter release kinetics using paired pulse facilitation, a measure of the extent to which release triggered by a single stimulation pulse increases release by a slightly delayed second pulse. The Baf53b+/− het
