Abstract
Glutamate application at synapses between hippocampal neurons in culture produces long-term potentiation of the frequency of spontaneous miniature synaptic currents, together with long-term potentiation of evoked synaptic currents. The mini frequency potentiation is initiated postsynaptically and requires activity of NMDA receptors. Although the frequency of unitary quantal responses increases strongly, their amplitude remains little changed with potentiation. Tests of postsynaptic responsiveness rule out recruitment of latent glutamate receptor clusters. Thus, postsynaptic induction can lead to enhancement of presynaptic transmitter release. The sustained potentiation of mini frequency is expressed even in the absence of Ca2+ entry into presynaptic terminals.
Publication types
-
Research Support, Non-U.S. Gov't
-
Research Support, U.S. Gov't, P.H.S.
MeSH terms
-
6-Cyano-7-nitroquinoxaline-2,3-dione
-
Animals
-
Animals, Newborn
-
Calcium / pharmacology
-
Cells, Cultured
-
Evoked Potentials / drug effects
-
Glutamates / pharmacology*
-
Glutamic Acid
-
Hippocampus / physiology*
-
Kinetics
-
Magnesium / pharmacology
-
Membrane Potentials
-
Neurons / drug effects
-
Neurons / physiology*
-
Pyramidal Tracts / physiology
-
Quinoxalines / pharmacology
-
Rats
-
Receptors, N-Methyl-D-Aspartate / drug effects
-
Receptors, N-Methyl-D-Aspartate / physiology
-
Synapses / drug effects
-
Synapses / physiology*
-
Tetrodotoxin / pharmacology
-
Time Factors
Substances
-
Glutamates
-
Quinoxalines
-
Receptors, N-Methyl-D-Aspartate
-
Glutamic Acid
-
Tetrodotoxin
-
6-Cyano-7-nitroquinoxaline-2,3-dione
-
Magnesium
-
Calcium