Opioid effects on 45Ca2+ uptake and glutamate release in rat cerebral cortex in primary culture

• Primary cultures of rat cortex, conveniently prepared from newborn animals, were used to study opioid effects on 45Ca2+ uptake and glutamate release. 45Ca2+ uptake, induced by treatment with glutamate or NMDA, was largely blocked by the NMDA antagonist MK-801. K+ depolarization-induced 45Ca2+ 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 45Ca2+ uptake induced by depolarization. Opioid agonists, selective for mu-, kappa-, and delta-receptors, inhibited the 45Ca2+ uptake induced by K+ depolarization. The combination of low concentrations of MK-801 and opioid agonists resulted in additive inhibition of K(+)-induced 45Ca2+ 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 Ca2+ uptake under acute, and perhaps also chronic, opiate treatment.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Medicinska och farmaceutiska grundvetenskaper -- Farmaceutiska vetenskaper (hsv//swe)

MEDICAL AND HEALTH SCIENCES  -- Basic Medicine -- Pharmaceutical Sciences (hsv//eng)

Keyword

primary culture

rat cerebral cortex

dynorphin peptides

glutamate release

Ca-45(2+) uptake

opiate agonists

naloxone

MEDICINE

MEDICIN

PHARMACY

FARMACI

Publication and Content Type

ref (subject category)

art (subject category)