V. Nadler et al., BLOCKADE OF CA-45(2-METHYL-D-ASPARTATE RECEPTOR-ION CHANNEL BY THE NON-PSYCHOACTIVE CANNABINOID HU-211() INFLUX THROUGH THE N), Brain research, 622(1-2), 1993, pp. 79-85
The effects of the synthetic non-psychoactive cannabinoid (+)-(3S,4S)-
7-hydroxy-DELTA6-tetrahydrocannabinoL 1,1-dimethylheptyl (HU-211) on t
he activity of the N-methyl-D-aspartate (NMDA) receptor/ion channel we
re examined. HU-211 non-competitively blocks the increase in binding o
f [H-3]N-[1-(2-thienyl)-cyclohexyl]piperidine ([H-3]TCP) induced by th
e polyamines spermine and spermidine or by glutamate and glycine. HU-2
11 does not, however, affect the direct binding of [H-3]glycine and [H
-3]glutamate to their binding sites on the NMDA receptor, which sugges
ts that the effects of HU-211 are not mediated via the binding sites o
f glutamate-, glycine- and phencyclidine-like drugs or of polyamines.
HU-211 can also block Ca-45(2+) uptake through the NMDA-receptor/ion c
hannel in primary cell cultures of rat forebrain. All of the above inh
ibitory effects of HU-211 on the NMDA-receptor/ion channel activity ar
e stereospecific, since the (-)(3R,4R) enantiomer (HU-210) is ineffect
ive.