原创力文档a post-burst afterdepolarization is mediated by group i metabotropic glutamate receptor-dependent upregulation of cav2.3 r-type calcium channels in ca1 pyramidal neurons英文论文.pdfVIP
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a post-burst afterdepolarization is mediated by group i metabotropic glutamate receptor-dependent upregulation of cav2.3 r-type calcium channels in ca1 pyramidal neurons英文论文
A Post-Burst Afterdepolarization Is Mediated by Group I
Metabotropic Glutamate Receptor-Dependent
Upregulation of Cav2.3 R-Type Calcium Channels in CA1
Pyramidal Neurons
1 1¤a 1¤b 1¤b 1¤c
Jin-Yong Park , Stefan Remy , Juan Varela , Donald C. Cooper , Sungkwon Chung , Ho-Won
2 2 1
Kang , Jung-Ha Lee , Nelson Spruston *
1 Department of Neurobiology and Physiology, Northwestern University, Evanston, Illinois, United States of America, 2 Department of Life Science and Basic Science
Institute for Cell Damage Control, Sogang University, Seoul, Korea
Abstract
Activation of group I metabotropic glutamate receptors (subtypes mGluR1 and mGluR5) regulates neural activity in a variety
of ways. In CA1 pyramidal neurons, activation of group I mGluRs eliminates the post-burst afterhyperpolarization (AHP) and
produces an afterdepolarization (ADP) in its place. Here we show that upregulation of Cav2.3 R-type calcium channels is
responsible for a component of the ADP lasting several hundred milliseconds. This medium-duration ADP is rapidly and
reversibly induced by activation of mGluR5 and requires activation of phospholipase C (PLC) and release of calcium from
internal stores. Effects of mGluR activation on subthreshold membrane potential changes are negligible but are large
following action potential firing. Furthermore, the medium ADP exhibits a biphasic activity dependence consisting of short-
term facilitation and longer-term inhibition. These findings suggest that mGluRs may dramatically alter the firing of CA1
pyramidal neurons via a complex, activity-dependent modulation of Cav2.3 R-type channels that are activated durin
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