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Chunk #13 — Results — LTP fails to stabilize in slices from BAF53b mutant mice

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The neuron-specific chromatin regulatory subunit BAF53b is necessary for synaptic plasticity and memory.
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We next tested if the higher expression of mutant BAF53bΔHD in BAF53ΔHDhigh mice would reproduce the total loss of LTP found in the Baf53b+/− het mice. Slices prepared from BAF53ΔHDhigh mice had unexpected responses to ten theta bursts. Initial potentiation was greatly amplified (% facilitation at two minute post-TBS was 239±31% compared to 156±10% for widltypes; p=0.003) but then showed a failure to stabilize similar to the BAF53bΔHDlow and Baf53b+/− het mice (Fig 5D). Collectively, the above findings suggest that BAF53b is required for consolidation of lasting changes in synaptic strength and that somewhat lower levels are needed to maintain STP within normal boundaries.