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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