If postsynaptic membrane depolarizes and glutamate releases from presynaptic neurons, postsynaptic neuron proteins {NMDA receptor, neuron} {N-methyl-D-aspartate receptor} can bind glutamate [Miller et al., 1989] [Tang et al., 1999] [Watkins and Collingridge, 1989] [Wittenberg and Tsien, 2002]. Binding is fast.
effects
Binding opens sodium ion channels, opens potassium ion channels, opens calcium ion channels, and excites or inhibits. Binding increases cell response non-linearly. Binding rapidly controls connectivity between cells, allowing transient cell assemblies.
In neocortex pyramidal cells, binding causes slow, long lasting ESP that rises to peak in 10 milliseconds to 75 milliseconds and can stay altered for days or years.
process
NMDA receptors have magnesium ion inside. Glutamate binding removes magnesium ion and allows calcium-ion flow. Calcium ion aids protein-kinase phosphorylation. Protein kinases then phosphorylate AMPA receptors for early LTP. Protein kinase A (PKA), MAP kinase (MAPK), and calcium/calmodulin protein kinase (CaMK) phosphorylate CREB. In cell nucleus, CREB activation turns on genes that make late LTP proteins. Active synapses have chemical sites {molecular tag} that bind late LTP proteins.
factors
Brain-derived neurotrophic factor (BDNF) increases NMDA-receptor phosphate binding.
antagonists
Ap5, CGS 19755, CPP, and D-CPP-ene affect NMDA receptor. NMDA antagonists can block visually induced activity in visual-cortex superficial layers, but not deep layers.
Biological Sciences>Zoology>Organ>Nerve>Neural Chemical>Receptor
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Date Modified: 2022.0224