Abstract
Release of both D-[3H]aspartate and endogenous amino acids was measured in primary cultures of cerebellar granule cells. Two hour-pretreatment with the glycosphingolipids, GM1 or GT1b, attenuated the stimulation of excitatory amino acid release induced by depolarizing concentrations of K+ (50 mM). Gangliosides inhibited the phencyclidine (PCP)-sensitive component of depolarization-induced release, i.e. the amplification of release that follows activation of NMDA receptors by the endogenous glutamate.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Amino Acids / metabolism*
-
Animals
-
Aspartic Acid / metabolism
-
Cerebellum / cytology
-
Cerebellum / drug effects
-
Cerebellum / metabolism*
-
Chromatography, High Pressure Liquid
-
Gangliosides / pharmacology*
-
Glutamates / metabolism
-
Neurons / drug effects
-
Neurons / metabolism*
-
Phencyclidine / pharmacology
-
Potassium Chloride / pharmacology
-
Rats
-
Receptors, N-Methyl-D-Aspartate
-
Receptors, Neurotransmitter / physiology*
-
Tetradecanoylphorbol Acetate / pharmacology
Substances
-
Amino Acids
-
Gangliosides
-
Glutamates
-
Receptors, N-Methyl-D-Aspartate
-
Receptors, Neurotransmitter
-
Aspartic Acid
-
Potassium Chloride
-
Phencyclidine
-
Tetradecanoylphorbol Acetate