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Opioid Effects on 45 Ca 2+ Uptake and Glutamate Release in Rat Cerebral Cortex in Primary Culture
Author(s) -
Vlaskovska Mila,
Schramm Michael,
Nylander Ingrid,
Kasakov Lubomir,
You ZhiBing,
HerreraMarschitz Mario,
Terenius Lars
Publication year - 1997
Publication title -
journal of neurochemistry
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.75
H-Index - 229
eISSN - 1471-4159
pISSN - 0022-3042
DOI - 10.1046/j.1471-4159.1997.68020517.x
Subject(s) - glutamate receptor , nmda receptor , depolarization , dynorphin , (+) naloxone , chemistry , opioid , pharmacology , opioid peptide , antagonist , biophysics , biochemistry , receptor , biology
Primary cultures of rat cortex, conveniently prepared from newborn animals, were used to study opioid effects on 45 Ca 2+ uptake and glutamate release. 45 Ca 2+ uptake, induced by treatment with glutamate or NMDA, was largely blocked by the NMDA antagonist MK‐801. K + depolarization‐induced 45 Ca 2+ uptake was also reduced by MK‐801, indicating that the effect was mediated by glutamate release. Direct analysis verified that glutamate, and aspartate, were indeed released. Opioid peptides of the prodynorphin system were also released and these, or other peptides, were functionally active, because naloxone treatment increased glutamate release, as well as the 45 Ca 2+ uptake induced by depolarization. Opioid agonists, selective for μ‐, κ‐, and δ‐receptors, inhibited the 45 Ca 2+ uptake induced by K + depolarization. The combination of low concentrations of MK‐801 and opioid agonists resulted in additive inhibition of K + ‐ induced 45 Ca 2+ uptake. The results indicate that this system may be useful as an in vitro CNS model for studying modulation by opioids of glutamate release and Ca 2+ uptake under acute, and perhaps also chronic, opiate treatment.