TY - JOUR
T1 - A glycine receptor antagonist, strychnine, blocked NMDA receptor activation in the neonatal mouse neocortex
AU - Miyakawa, Naohisa
AU - Uchino, Shigeo
AU - Yamashita, Takayuki
AU - Okada, Hidetsugu
AU - Nakamura, Takeshi
AU - Kaminogawa, Shuichi
AU - Miyamoto, Yusei
AU - Hisatsune, Tatsuhiro
PY - 2002/9/16
Y1 - 2002/9/16
N2 - The NMDA receptor (NMDAR) is a Ca2+-permeable cation channel that plays a critical role in neural network formation during brain development. Since it is blocked in a voltage-dependent manner by extracellular Mg2+, in order for the NMDA to be activated, the membrane must be strongly depolarized. Immature neurons in the developing neocortex can be depolarized by ligand-gated Cl- channels, such as the glycine receptor (GlyR) or GABAA receptor (GABAAR). We here assess the contribution of GlyRs to Ca2+ influx via NMDARs in neonatal mouse cortical neurons. The GlyR antagonist, strychnine, was more effective in suppressing post-synaptic Ca2+ influx than the GABAAR antagonist, picrotoxin, suggesting greater potentiation of NMDARs by GlyRs than by GABAARs. The GlyR, known to be endogenously activated at this stage, may play a critical role in neocortical development.
AB - The NMDA receptor (NMDAR) is a Ca2+-permeable cation channel that plays a critical role in neural network formation during brain development. Since it is blocked in a voltage-dependent manner by extracellular Mg2+, in order for the NMDA to be activated, the membrane must be strongly depolarized. Immature neurons in the developing neocortex can be depolarized by ligand-gated Cl- channels, such as the glycine receptor (GlyR) or GABAA receptor (GABAAR). We here assess the contribution of GlyRs to Ca2+ influx via NMDARs in neonatal mouse cortical neurons. The GlyR antagonist, strychnine, was more effective in suppressing post-synaptic Ca2+ influx than the GABAAR antagonist, picrotoxin, suggesting greater potentiation of NMDARs by GlyRs than by GABAARs. The GlyR, known to be endogenously activated at this stage, may play a critical role in neocortical development.
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U2 - 10.1097/00001756-200209160-00020
DO - 10.1097/00001756-200209160-00020
M3 - Article
C2 - 12352624
AN - SCOPUS:0037120330
SN - 0959-4965
VL - 13
SP - 1667
EP - 1673
JO - Neuroreport
JF - Neuroreport
IS - 13
ER -