Work

Dendritic K + channels contribute to spike-timing dependent long-term potentiation in hippocampal pyramidal neurons

Year: 2002

Type: article

Abstract: 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.

Source: Proceedings of the National Academy of Sciences

DOI: 10.1073/pnas.122210599

Authors: Shigeo Watanabe, Dax A. Hoffman, Michele Migliore, Daniel Johnston

Institutions: Baylor College of Medicine, Yale University

Language: English

Topic: Neuroscience and Neuropharmacology Research

Subfield: Cellular and Molecular Neuroscience

Field: Neuroscience

Domain: Life Sciences

Open Access status: green

Funders: National Institute of Mental Health, National Institute of Neurological Disorders and Stroke

Awards: PHARMACOLOGY OF MOSSY FIBER SYNAPTIC PLASTICITY, CELLULAR INFORMATION PROCESSING IN THE HIPPOCAMPUS, Regulation of Neuronal Excitability