Abstract
Whole-cell recording in the superficial layers of the developing superior colliculus (sSC) reveals a large drop in NMDA receptor (NMDAR) current decay time synchronized across all neurons and occurring consistently between P10 and P11. We show that blocking the Ca2+/calmodulin-dependent phosphatase calcineurin (CaN) in the postsynaptic neuron can abolish this drop. The regulation is induced prematurely by 1-2 hr of electrical stimulation in P10 collicular slices only if CaN and NMDAR currents can be activated in the neuron. These data suggest that a long-lasting, CaN-mediated control of NMDAR kinetics is rapidly initiated by heightened activity of the NMDAR itself and demonstrate a novel developmental and tonic function of CaN that can play an important role in modulating the plasticity of the developing CNS.
Publication types
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Research Support, U.S. Gov't, P.H.S.
MeSH terms
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Action Potentials / drug effects
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Calcineurin / metabolism*
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Calcineurin / pharmacology
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Calcineurin Inhibitors
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Dose-Response Relationship, Drug
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Down-Regulation / genetics*
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Electric Stimulation
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Enzyme Inhibitors / pharmacology
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Excitatory Amino Acid Antagonists / pharmacology
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Excitatory Postsynaptic Potentials / physiology
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Gene Expression Regulation, Developmental / drug effects
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In Vitro Techniques
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Ion Transport / drug effects
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Neuronal Plasticity / physiology
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Neurons / cytology
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Neurons / metabolism
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Patch-Clamp Techniques
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Piperidines / pharmacology
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Receptors, N-Methyl-D-Aspartate / genetics
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Receptors, N-Methyl-D-Aspartate / metabolism*
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Superior Colliculi / cytology
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Superior Colliculi / metabolism*
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Synapses / metabolism
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Tacrolimus / pharmacology
Substances
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Calcineurin Inhibitors
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Enzyme Inhibitors
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Excitatory Amino Acid Antagonists
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NR1 NMDA receptor
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NR2A NMDA receptor
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NR2B NMDA receptor
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Piperidines
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Receptors, N-Methyl-D-Aspartate
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Calcineurin
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ifenprodil
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Tacrolimus