A different form of long-lasting potentiation revealed in tissue plasminogen activator mutant mice

作者：Uwe Frey, Martin Müller, Dietmar Kuhl · 发表于：Journal of Neuroscience · 年份：1996 · DOI：10.1523/jneurosci.16-06-02057.1996 · 被引用次数：201 · 研究领域：Protease and Inhibitor Mechanisms、Calpain Protease Function and Regulation、S100 Proteins and Annexins

The establishment of hippocampal long-term (LTP) requires protein and mRNA synthesis, suggesting that neuronal activity resulting in LTP initiates a cascade of gene expression. The expression of the gene for the extracellular serine protease tissue plasminogen activator (t-PA) is induced during LTP. Here we analyze long-lasting LTP (L-LTP,>4 hr)in CA1 hippocampal slices of mice homozygous for disrupted t-PA genes. Although mutant mice appear to exhibit long-term potentiation, we provide evidence that these mice are devoid of conventional homosynaptic L-LTP at the Schaffer collateral-CA1 pyramidal cell synapse. Most remarkably, t-PA-deficient mice exhibit a different form of long-lasting potentiation that is characterized by an NMDA receptor-dependent modification of GABA transmission in the CA1 region.