Effects of morphine-3-glucuronide and morphine on the K+-evoked release of [3H]-glutamic acid and [14C]-gamma-aminobutyric acid from rat brain synaptosomes.

The effects of morphine-3-glucuronide (M3G) and morphine on the K+-evoked release of [14C]-gamma-aminobutyric acid (GABA) and [3 H]-glutamic acid were investigated in rat brain synaptosomes using superfusion techniques. K+-evoked release of both [14C]-GABA and [3H]-glutamic acid from rat brain synaptosomes was eliminated in the absence of calcium, indicating that K+-evoked neurotransmitter release was from vesicular stores in a manner analagous to that which occurs in vivo following an action potential (1). Addition of M3G or morphine in a range of concentrations (0.1-10 microM) to the superfusion medium did not alter the K+-evoked release of [14C]-GABA or [3H]-glutamic acid from rat brain synaptosomes, suggesting that the CNS excitation observed following central administration of M3G (2-5) and supra-analgesic doses of morphine (2,3,6,7) does not occur by a generalized inhibition of GABA release or facilitation of glutamic acid release from pre-synaptic nerve terminals.