The metabotropic glutamate receptor antagonist ( + )-α-methyl-4-carboxyphenylglycine protects hippocampal CA1 neurons of the rat from in vitro hypoxia/hypoglycemia

1994 ◽  
Vol 33 (5) ◽  
pp. 715-717 ◽  
Author(s):  
T. Opitz ◽  
P. Richter ◽  
K.G. Reymann
Keyword(s):  
Receptor Antagonist ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
Glutamate Receptor Antagonist ◽  
Ca1 Neurons ◽  
Metabotropic Glutamate ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1 ◽  
Metabotropic Glutamate Receptor Antagonist

Weak excitation and simultaneous inhibition induce long-term depression in hippocampal CA1 neurons

1994 ◽  
Vol 71 (4) ◽  
pp. 1586-1590 ◽  
Author(s):  
X. D. Yang ◽  
J. A. Connor ◽  
D. S. Faber
Keyword(s):  
Receptor Antagonist ◽  
Glutamate Receptor ◽  
Metabotropic Glutamate Receptor ◽  
High Frequency Stimulation ◽  
Long Term Depression ◽  
Ca1 Neurons ◽  
Metabotropic Glutamate ◽  
Hippocampal Ca1 Neurons ◽  
Hippocampal Ca1

1. Weak excitation to rat hippocampal CA1 neurons via Schaffer collaterals at a frequency of 0.1 or 0.2 Hz accompanied by repeated brief exposures to the inhibitory transmitter gamma-amino-butyric acid (GABA) causes a long-term depression (LTD, up to 90% of the control) of the stimulated pathway. This depression can be reversed by high-frequency stimulation. 2. Although inhibition is necessary for the induction of this LTD, the depression can be produced with either the GABAA or the GABAB receptor agonists. 3. This conjunctive LTD could not be blocked by the N-methyl-D-aspartate receptor antagonist, 2-amino-5-phosphonovaleric acid. 4. It was, however, blocked by the metabotropic glutamate receptor antagonist L-2-amino-3-phosphonopropionic acid and (RS)-alpha-methyl-4-carboxyphenylglycine, indicating that activation of a metabotropic glutamate receptor is necessary for the LTD. Induction also appeared to require an intracellular Ca2+ increase. 5. Because GABAergic inhibition often modulates glutamatergic transmission in the brain, we propose that this form of synaptic modification is of potential importance for neural plasticity.

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