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Re‐expression of NR2B‐containing NMDA receptors in vitro by suppression of neuronal activity
Author(s) -
Kiyosue Kazuyuki,
Hiyama Takeshi Y.,
Nakayama Kimiko,
Kasai Michiki,
Taguchi Takahisa
Publication year - 2004
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2003.12.007
Subject(s) - ifenprodil , nmda receptor , synapse formation , neuroscience , glutamate receptor , synapse , receptor , microbiology and biotechnology , chemistry , patch clamp , biology , electrophysiology , biochemistry
N ‐methyl‐ d ‐aspartate receptors (NMDARs) are known to play critical roles in the development of the nervous system, and their expression is regulated in an activity‐dependent fashion during development. However, the regulation of NMDAR expression after circuit formation is less well understood. To examine this, we performed patch‐clamp recordings from chick cerebral neurons in an activity‐controlled culture. Analysis of NMDAR channels from neurons before synapse formation showed that there are two components in channel open kinetics. The major slow component is clearly blocked by ifenprodil, a specific inhibitor of NR2B‐containing NMDARs. In contrast, slow component of NMDAR channel opening from neurons after synapse formation became minor and ifenprodil had little effect on the NMDAR channel openings. Furthermore, this change is reversibly regulated by neuronal activity, in that suppression induces the re‐expression of NR2B‐containing NMDARs, even after circuit formation.