CBD possesses sedative properties (Carlini and Cunha, 1981), and a clinical
trial showed that it reduces the anxiety and other unpleasant psychological
side effects provoked by pure THC (Zuardi et al. 1982). CBD modulates the
pharmacokinetics of THC by three mechanisms: (1) it has a slight affinity for
cannabinoid receptors (Ki at CB1 = 4350 nM, compared to THC = 41 nM,
Showalter et al. 1996), and it signals receptors as an antagonist or reverse agonist
(Petitet et al. 1998), (2) CBD may modulate signal transduction by perturbing
the fluidity of neuronal membranes, or by remodeling G-proteins that
carry intracellular signals downstream from cannabinoid receptors, and (3)CBD
is a potent inhibitor of cytochrome P450 3A11 metabolism, thus it blocks the
hydroxylation of THC to its 11-hydroxy metabolite (Bornheim et al. 1995).
The 11-hydroxy metabolite is four times more psychoactive than unmetabolized
THC (Browne and Weissman 1981), and four times more immunosuppressive
(Klein et al. 1987).
CBD provides antipsychotic benefits (Zuardi et al. 1995). It increases dopamine
activity, serves as a serotonin uptake inhibitor, and enhances norepinephrine
activity (Banerjee et al. 1975; Poddar and Dewey 1980). CBD protects
neurons from glutamate toxicity and serves as an antioxidant, more potently
than ascorbate and α-tocopherol (Hampson et al. 1998). Auspiciously, CBD
does not decrease acetylcholine (ACh) activity in the brain (Domino 1976;
Cheney et al. 1981). THC, in contrast, reduces hippocampal ACh release in
rats (Carta et al. 1998), and this correlates with loss of short-term memory consolidation.
In the hippocampus THC also inhibits N-methyl-D-aspartate (NMDA)
receptor activity (Misner and Sullivan 1999; Shen and Thayer 1999), and
NMDA synaptic transmission is crucial for memory consolidation (Shimizu et
al. 2000). CBD, unlike THC, does not dampen the firing of hippocampal cells
(Heyser et al. 1993) and does not disrupt learning (Brodkin and Moerschbaecher
1997).
Consroe (1998) presented an excellent review of CBD in neurological disorders.
In some studies, it ameliorates symptoms of Huntington’s disease, such
as dystonia and dyskinesia. CBD mitigates other dystonic conditions, such as
torticollis, in rat studies and uncontrolled human studies. CBD functions as an
anticonvulsant in rats, on a par with phenytoin (Dilantin, a standard antiepileptic
drug).
CBD demonstrated a synergistic benefit in the reduction of intestinal motility
in mice produced by THC (Anderson, Jackson, and Chesher 1974). This
may be an important component of observed benefits of cannabis in inflammatory
bowel diseases.

--"Cannabis and Cannabis Extracts:
Greater Than the Sum of Their Parts?
John M. McPartland
Ethan B. Russo"