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Journal of Neuroscience, Vol 7, 2910-2916, Copyright © 1987 by Society for Neuroscience
Excitatory amino acid-induced release of 3H-GABA from cultured mouse cerebral cortex interneurons
J Drejer, T Honore and A Schousboe
A newly developed continuous superfusion model was used for studies of
3H-GABA release from cultured mouse cerebral cortex neurons. It was found
that a series of excitatory amino acids (EAAs) representing all receptor
subtypes evoked Ca2+- dependent release of 3H-GABA from the neurons.
Quisqualate was the most potent agonist tested, with an EC50 value of 75
nM. L-Glutamate, N-methyl-D-aspartate (NMDA), and kainate showed EC50
values of 12, 16 and 29 microM, respectively. The EAA- evoked 3H-GABA
release could be blocked by a series of EAA antagonists. The highly
selective NMDA antagonist D-2-amino-5-phosphonovaleric acid (D-APV) was
found to block NMDA responses, whereas the nonselective antagonists
cis-2,3-piperidine dicarboxylic acid (PDA) and gamma-D-
glutamyl-aminomethyl sulphonic acid (GAMS) blocked responses to all
agonists. NMDA responses were found to be sensitive to Mg+ blockade. EAA-
as well as potassium-induced 3H-GABA release from the neurons could be
detected as early as day 5 in culture. However, during the culture period
up to 12 d, the responses to K+, quisqualate, and NMDA were increased. The
ontogenetic development of binding sites for quisqualate, kainate, and NMDA
in mouse cortex was studied using the radioligands
3H-alpha-amino-3-hydroxy-5-methyl-4-isoxasole propionate (3H-AMPA),
3H-kainate, and 3H-L-glutamate, respectively. The development of binding
sites for the different EAA-receptor subtypes showed a good correlation
with the development of neuronal 3H-GABA release evoked by the excitatory
amino acids.(ABSTRACT TRUNCATED AT 250 WORDS)
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