Abstract
A variety of processes limit NMDA (N-methyl-D-aspartate) receptor (NMDAR) activity in response to agonist exposure, including rundown--the decline of peak current with repeated, sustained agonist application. Here we report that calcium and tyrosine phosphorylation differentially regulate rundown of synaptic versus extrasynaptic NMDAR-mediated current in rat hippocampal pyramidal neurons.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Animals
-
Calcium / metabolism
-
Calcium Signaling / drug effects
-
Calcium Signaling / physiology
-
Cell Membrane / drug effects
-
Cell Membrane / metabolism
-
Cells, Cultured
-
Endocytosis / drug effects
-
Endocytosis / physiology
-
Excitatory Amino Acid Antagonists / pharmacology
-
Excitatory Postsynaptic Potentials / drug effects
-
Excitatory Postsynaptic Potentials / physiology*
-
Hippocampus / cytology
-
Hippocampus / drug effects
-
Hippocampus / metabolism*
-
N-Methylaspartate / pharmacology
-
Phosphoric Monoester Hydrolases / metabolism
-
Piperidines / pharmacology
-
Protein Transport / drug effects
-
Protein Transport / physiology
-
Protein-Tyrosine Kinases / antagonists & inhibitors
-
Protein-Tyrosine Kinases / metabolism
-
Pyramidal Cells / cytology
-
Pyramidal Cells / drug effects
-
Pyramidal Cells / metabolism*
-
Rats
-
Receptors, N-Methyl-D-Aspartate / drug effects
-
Receptors, N-Methyl-D-Aspartate / metabolism*
-
Synapses / drug effects
-
Synapses / metabolism*
-
Synaptic Transmission / drug effects
-
Synaptic Transmission / physiology*
Substances
-
Excitatory Amino Acid Antagonists
-
NR2A NMDA receptor
-
NR2B NMDA receptor
-
Piperidines
-
Receptors, N-Methyl-D-Aspartate
-
N-Methylaspartate
-
Protein-Tyrosine Kinases
-
Phosphoric Monoester Hydrolases
-
ifenprodil
-
Calcium