No abstract

Objectives Long-term cannabis use has been associated with the appearance of psychotic symptoms and schizophrenia-like cognitive impairments; however these studies may be confounded by concomitant use of tobacco by cannabis users. We aimed to determine if previously observed cannabis-associated deficits in sensory gating would be seen in cannabis users with no history of tobacco use, as evidenced by changes in the P50, N100, and P200 event-related potentials. A secondary objective of this study was to examine the effects of acute nicotine administration on cannabis users with no tobacco use history. Methods Three components (P50, N100, P200) of the mid-latency auditory-evoked response (MLAER) were elicited by a paired-stimulus paradigm in 43 healthy, non-tobacco smoking male volunteers between the ages of 18-30. Cannabis users (CU, n = 20) were administered nicotine (6 mg) and placebo gum within a randomized, double-blind design. Non-cannabis users (NU, n = 23) did not receive nicotine. Results Between-group sensory gating effects were only observed for the N100, with CUs exhibiting a smaller N100 to S 1 of the paired stimulus paradigm, in addition to reduced dN100 (indicating poorer gating). Results revealed no significant sensory gating differences with acute administration of nicotine compared to placebo cannabis conditions. Conclusions These findings suggest a relationship between gating impairment and cannabis use; however, acute nicotine administration nicotine does not appear to impact sensory gating function.Keywords P50 . MLAEP . Mid-latency auditory-evoked potential . Event-related potential . Marijuana . Nicotine Cannabis, schizophrenia, and sensory gatingCannabis is the collective term of any consumable product or extract from the Cannabis sativa plant with its major psychoactive constituent being Δ-9-tetrahydrocannabinol (THC; Sundram 2006). Consumption of THC, an exogenous cannabinoid, influences the CNS through the endocannabinoid receptors, including CB1, and the changes it induces in the nervous system may ultimately lead to dependence (Fernandez-Espejo et al. 2009).Overall, both acute and chronic THC have been shown to induce memory impairments similar to those seen in schizophrenia (SZ) including working memory, episodic memory encoding, impaired retrieval, and attentional deficits (Skosnik et al. 2001;Fletcher and Honey 2006); it has been hypothesized that deficits in these higher-order cognitive functions in SZ are in part related to an inability to inhibit irrelevant sensory input, leading to an overload of information reaching consciousness (Patterson et al. 2008). There is also This article belongs to a Special Issue on Cannabis and Cannabinoids * Derek J. Fisher