Effects of cannabinoid receptor stimulation and blockade on catalepsy produced by dopamine receptor antagonists

The endocannabinoid system: a physiological perspective on its role in psychomotor control

“…Administration of exogenous cannabinoids was found to increase dopamine release in rat nucleus accumbens (Chen et al, 1990;Gessa et al, 1998;Gardner and Vorel, 1998) and to excite dopaminergic neurons in the ventral tegmental area and substantia nigra (French et al, 1997). However, other studies indicate that cannabinoids potentiate the behavioral effects of dopamine antagonists (neuroleptics) (Anderson et al, 1996) and reduce electrically evoked dopamine release from rat striatal slices (Cadogan et al, 1997). The possibility suggested by these results, that cannabinoids may regulate dopamine functions is supported by several biochemical and behavioral studies.…”

2,5-Dimethoxy-4-iodoamphetamine (DOI) Inhibits Δ9-Tetrahydrocannabinol-Induced Catalepsy-Like Immobilization in Mice

“…This effect is attenuated by the cannabinoid CB 1 -receptor antagonist rimonabant (2,3), indicating that it is mediated by CB 1 receptors. In contrast, rimonabant is unable to affect catalepsy induced by the D 2 -receptor antagonists haloperidol and raclopride (4,5), indicating that catalepsy induced by D 2 blockade does not involve stimulation of CB 1 receptors. The mechanism mediating THC-induced catalepsy is different from that mediating D 2 -receptor antagonistinduced catalepsy.…”

AVE1625, a cannabinoid CB1 receptor antagonist, as a co-treatment with antipsychotics for schizophrenia: improvement in cognitive function and reduction of antipsychotic-side effects in rodents

“…It is unlikely that CB1 receptors interfere directly with the activity of dopaminergic neurons, but they can modify dopamine transmission through mechanisms involving inhibitory GABAergic striatal efferent terminals on which CB1 receptors are located (see van der Stelt and Di Marzo 2003, for a thorough review on the endocannabinoid/ dopamine interaction), and this effect may explain at least in part the APD-induced catalepsy attenuation of AVE1625. It is interesting to note that stimulation of CB1 receptors has been shown to increase catalepsy produced by administration of dopamine receptor antagonists (Anderson et al 1996). Together, these findings suggest that AVE1625 may potentially ameliorate some of the APD-induced side effects seen in patients.…”