M. Klarica et al., PHARMACOLOGY OF N-METHYL-D-ASPARTATE-EVOKED [H-3] NORADRENALINE RELEASE IN ADULT-RAT SPINAL-CORD, European journal of pharmacology, 308(2), 1996, pp. 135-144
N-Methyl-D-aspartate (NMDA) produced a concentration-related increase
in [H-3]noradrenaline release from adult rat cervical spinal cord slic
es. Its potency was relatively low and the response concentrated in do
rsal spinal regions although also observed in ventral slices. NMDA did
not increase the release of radiolabelled glutamate, aspartate, gamma
-aminobutyric acid (GABA), acetylcholine or serotonin. In comparison w
ith previously characterised NMDA responses in the striatum, (release
of dopamine, GABA, acetylcholine or spermidine) the spinal response wa
s particularly sensitive to MK-801 and magnesium and to L-689,560 but
not to other glycine receptor antagonists (7-chlorokynurenate, CNQX (6
-cyano-7-nitroquinoxaline-2,3-dione), DNQX (6,7-dichloroquinoxaline-2,
3-dione), (+)-HA966). Dextrorphan and dextromethorphan produced partia
l or biphasic inhibition curves suggesting a subdivision of NMDA recep
tors. NMDA-evoked [3H]noradrenaline release was moderately sensitive t
o CPP and CGP37849 but insensitive to arcaine. These characteristics d
istinguish the native spinal NMDA receptor subtype(s) from those so fa
r characterised in the striatum suggesting a unique spinal NMDA recept
or subtype.