期刊
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
卷 99, 期 12, 页码 8366-8371出版社
NATL ACAD SCIENCES
DOI: 10.1073/pnas.122210599
关键词
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资金
- NIMH NIH HHS [MH 48432, R37 MH044754, R01 MH048432, MH 44754] Funding Source: Medline
- NINDS NIH HHS [NS 37444, P01 NS037444] Funding Source: Medline
We investigated the role of A-type K+ channels for the induction of long-term potentiation (LTP) of Schaffer collateral inputs to hippocampal CA1 pyramidal neurons. When low-amplitude excitatory postsynaptic potentials (EPSPs) were paired with two postsynaptic action potentials in a theta-burst pattern, N-methyl-D-aspartate (NMDA)-receptor-dependent LTP was induced. The amplitudes of the back-propagating action potentials were boosted in the dendrites only when they were coincident with the EPSPs. Mitogen-activated protein kinase (MAPK) inhibitors PD 098059 or U0126 shifted the activation of dendritic K+ channels to more hyperpolarized potentials, reduced the boosting of dendritic action potentials by EPSPs, and suppressed the induction of LTP. These results support the hypothesis that dendritic K+ channels and the boosting of back-propagating action potentials contribute to the induction of LTP in CA1 neurons.
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