The active principle of marijuana and hashish, D 9 cannabinol (THC), seems to be accountable for the drugs' central affects. Both forms are prepared from the leaves of a plant, Cannabis sativa.
THC is lipophilic, quickly dissolving through plasmatic membranes and having a heterogenous distribution in the brain.
THC seems to stimulate phospholipase A2, increasing the production of arachdonic acid, diacylglycerol (DAG), and inositol triphosphate. Perhaphs this system is responsible for THC-induced inhibition of a Ca++ voltage-dependent channel that regulates neurotransmitter release.
In 1992 an endogenous ligand, with high binding affinity to THC, was described. This substance, named amandamide (N-arachnil-ethanolamide) is an ethanolamide of arachdonic acid. There are plenty of these binding places and they can be found in the pallidum, hippocampus, and brain stem. Clones of the protein G-bound receptor have already been obtained.
THC is described as a neuromodulator substance, acting via a receptor located in the cellular membrane that modifies the production of a second messenger regulated by another neurotransmitter.
THC causes a biphasic alteration, euphoria (stimulating phase) and sedation (depressive phase). During the stimulating phase, there are reports of an action similar to a dream, with the possibility of distortions in vision and time-experience. Concentration may be impaired. Memory decreases and appetite is suppressed, respectively reflecting THC effects upon acetylcholine and serotonine receptors. After the stimulating phase, lethargy and sleep are common.
Psychic effects are use-dependent. There are reports about anxiety phenomena that are almost panic-like. Amotivational syndrome is characteristic of the subject’s personality.