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Interest in the relationship between cannabis use and psychosis has increased dramatically in recent years, in part because of concerns related to the growing availability of cannabis and potential risks to health and human functioning. There now exists a plethora of scientific articles addressing this issue, but few provide a clear verdict about the causal nature of the cannabis-psychosis association. Here, we review recent research reports on cannabis and psychosis, giving particular attention to how each report provides evidence relating to two hypotheses: (1) cannabis as a contributing cause and (2) shared vulnerability. Two primary kinds of data are brought to bear on this issue: studies done with schizophrenic patients and studies of first-episode psychosis. Evidence reviewed here suggests that cannabis does not in itself cause a psychosis disorder. Rather, the evidence leads us to conclude that both early use and heavy use of cannabis are more likely in individuals with a vulnerability to psychosis. The role of early and heavy cannabis use as a prodromal sign merits further examination, along with a variety of other problem behaviors (e.g., early or heavy use of cigarettes or alcohol and poor school performance). Future research studies that focus exclusively on the cannabis-psychosis association will therefore be of little value in our quest to better understand psychosis and how and why it occurs.

The effects of several doses of d-amphetamine, chlordiazepoxide (CDP), chlorpromazine (CPZ), LSD, pentobarbital, and scopolamine were examined in rats trained to respond to the brighter of two keys. On each of the 100 trials during a daily session, the rat pressed the key that was brighter (correct key) and received a food pellet, or pressed the incorrect key and terminated the trial without food, or pressed neither key for 10 s, allowing the trial to terminate. Within a session, trials were mixed randomly such that on 50 trials the incorrect key was not lit (easy trials,) and on 50 trials the incorrect key was dimly lit (difficult trials). Amphetamine (0.5–2.0 mg/kg) reduced percent correct responses, with a greater effect of difficult than on easy trials. CDP (4.0–16.0 mg/kh) and pentobarbital (2.0–16.0 mg/kg) reduced percent correct responses on the difficult trials at the highest doses tested. Scopolamine (0.12–1.0 mg/kg) reduced both percent correct (more so on the difficult trials) and percent of trials on which a response was made, in a dose-related fashion. CPZ (1.0–4.0 mg/kg) reduced trial responding at 2.0 and 4.0 mg/kg and reduced percent correct on the difficult trials at 4.0 mg/kg. LSD (0.08–0.32 mg/kh) did not significantly alter behavior in this study.

Repeated exposure to nicotine increases both the number of central nicotinic receptors and the behavioral stimulant effect of nicotine. In the present experiments, the behavioral response to nicotine was examined in photocell activity cages. Groups of rats were tested using doses from 0.1 to 1.6 mg/kg both before and after all rats were exposed for 5 days to a common dose of 0.2 mg/kg/day. Prior to the 5-day exposure, there was a dose-related stimulant response to nicotine, with a maximum response seen at 0.4 mg/kg. After the 5-day exposure, the dose-effect curve was shifted upward, so that greater stimulation was produced at each test dose of nicotine. Other groups of rats were exposed for 5 days to doses of nicotine ranging from 0.01 to 0.30 mg/kg/day. On the 6th day all rats received a common test dose of 0.2 mg/kg and their response was measured in the activity cages. In animals exposed to 0.01 mg/kg/day, the test day response was not different from saline controls, but the groups exposed to higher doses showed increased stimulation in response to the common test dose. Measurements of nicotinic receptor binding using [3H]-acetylcholine found increased binding in groups receiving 0.03 mg/kg/day or more, but not in the group that received 0.01 mg/kg/day. The correspondence between the doses that increase behavioral stimulant reactions to nicotine and the doses that increase nicotinic binding suggest that increased receptor numbers may be responsible for the increased behavioral stimulation. However, rats given high doses (1.6 mg/kg, twice per day) did not show increased behavioral stimulation to a test dose of 0.2 mg/kg.(ABSTRACT TRUNCATED AT 250 WORDS)

Chickens that were given up to 1.0 mg/kg scopolamine hydrobromide 15 min before testing did not show a reduced duration of tonic immobility when a 15-sec restraint procedure was used to induce immobility. Chickens given 2.0 mg/kg scopolamine did not show decreased duration or probability of induction of tonic immobility compared to chickens injected with physiological saline. These results contradict those of a previous study.

Pigeons responded under compound fixed-interval (FI) fixed-ratio (FR) schedules of food presentation. Distinctive discrimininative stimuli were either continuously present during each component schedule (multiple FI FR) or were present only for a brief period at the beginning of each component (primed FI FR). Similar rates and patterns of responding were maintained under the multiple and primed schedules. Pentobarbital, scopolamine, and d-amphetamine decreased FR responding, but promazine had little effect at the doses studied. d-Amphetamine and promazine increased FI responding at certain doses, pentobarbital had little effect, and scopolamine decreased responding. There were no systematic differences in the effects of drugs under the multiple and primed schedules, in spite of the differences in discriminative stimuli under the conditions.

Three groups of rats received either kainic acid or vehicle in the ventral pallidum or no operation, and were then tested in photocell activity cages following recovery from surgery. Locomotor activity was measured following injections of saline, nicotine (0.1, 0.2, 0.4 mg/kg) or d-amphetamine (0.5, 1.0 mg/kg). The lesioned rats showed an enhanced locomotor response after injections of nicotine compared with sham operated or unoperated controls. In contrast, both lesioned and control rats showed increased activity after amphetamine; this effect was not influenced by the lesion. Since these lesions are known to produce neurochemical and cellular changes resembling those seen in human Alzheimer's disease, this increased response to nicotine might also be found in Alzheimer's patients and serve as the basis for a diagnostic test.