作者: Y. Perez , C.A. Chapman , G. Woodhall , R. Robitaille , J.-C. Lacaille
DOI: 10.1016/S0306-4522(98)00531-4
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摘要: Abstract Tetanization of Schaffer collaterals, which induces long-term potentiation excitatory transmission in the hippocampus rat, also affects local inhibitory circuits. Mechanisms controlling plasticity early and late components postsynaptic potentials CA1 pyramidal cells were studied using intracellular recordings Ca 2+ imaging rat hippocampal slices. High-frequency stimulation (100 Hz/s) collaterals resulted no change mean amplitude or 30 min post-tetanus. However, injection chelator 1,2-bis(2-aminophenoxy)ethane- N , ′, ′-tetra-acetate unmasked a significant increase both post-tetanus induction this was blocked by -methyl- d -aspartate receptor antagonist (±)-2-amino-5-phosphopentanoic acid. In contrast to high-frequency tetanization, “theta-burst” normal medium This antagonist. The more physiological tetanization pattern, mimics endogenous theta rhythm, therefore an -aspartate-dependent inhibition Calcium during whole-cell from revealed differences signal associated with theta-burst stimulations. During time peak signals significantly longer, area under response larger than stimulation. These results indicate that long-lasting synaptic involves interaction between -mediated depression -aspartate-mediated GABA A B inhibition, these processes are differentially sensitive parameters.