RT Journal Article
SR Electronic
T1 Neuroprotection by Δ<sup>9</sup>-Tetrahydrocannabinol, the Main Active Compound in Marijuana, against Ouabain-Induced <em>In Vivo</em> Excitotoxicity
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 6475
OP 6479
DO 10.1523/JNEUROSCI.21-17-06475.2001
VO 21
IS 17
A1 van der Stelt, M.
A1 Veldhuis, W. B.
A1 Bär, P. R.
A1 Veldink, G. A.
A1 Vliegenthart, J. F. G.
A1 Nicolay, K.
YR 2001
UL http://www.jneurosci.org/content/21/17/6475.abstract
AB Excitotoxicity is a paradigm used to explain the biochemical events in both acute neuronal damage and in slowly progressive, neurodegenerative diseases. Here, we show in a longitudinal magnetic resonance imaging study that Δ9-tetrahydrocannabinol (Δ9-THC), the main active compound in marijuana, reduces neuronal injury in neonatal rats injected intracerebrally with the Na+/K+-ATPase inhibitor ouabain to elicit excitotoxicity. In the acute phase Δ9-THC reduced the volume of cytotoxic edema by 22%. After 7 d, 36% less neuronal damage was observed in treated rats compared with control animals. Coadministration of the CB1 cannabinoid receptor antagonist SR141716 prevented the neuroprotective actions of Δ9-THC, indicating that Δ9-THC afforded protection to neurons via the CB1 receptor. In Δ9-THC-treated rats the volume of astrogliotic tissue was 36% smaller. The CB1 receptor antagonist did not block this effect. These results provide evidence that the cannabinoid system can serve to protect the brain against neurodegeneration.