Current Drug Abuse Reviews - Volume 6, Issue 3, 2013

Objective: High rates of smoking and nicotine dependence have a profoundly negative impact on the health and well being of individuals with schizophrenia. Treating smoking is a critical step in improving the health and quality of life of people affected by this illness. This paper reviews the literature on smoking cessation interventions in schizophrenia and discusses potential barriers to effective treatment with this population. Methods: The criteria used to select studies for inclusion were: (1) Sample included 50% or more individuals with schizophrenia spectrum diagnosis (SSD); (2) Some individual or group intervention for smoking cessation was provided; and (3) Some smoking-related outcome variable was measured (self-reported smoking, breath carbon monoxide, etc). Results: Both pharmacologic and psychosocial smoking cessation treatments have been found to be useful in helping individuals with schizophrenia reduce and quit smoking in the short term. Few interventions have been found to be effective in promoting smoking abstinence in the long term. Conclusions: Intervention development must include strategies to overcome barriers to smoking cessation that are most relevant to individuals with schizophrenia and focus on translating short term gains into long term abstinence.

An active lifestyle throughout the life cycle seems to delay cognitive aging and dementia and has also been evaluated as an intervention against addiction to cocaine and other drugs of abuse. In epidemiological studies with humans, it has proved difficult to separate the cognitive, social and physical components from other variables that influence lifestyle. Studies in animal models are useful for evaluating the impact of each of these factors and for uncovering the underlying mechanisms of the benefits of complex environments. Preclinical studies have employed the Environmental Enrichment paradigm (EE) which has been proposed as a preclinical model of positive life experiences in humans. EE has been associated with protective effects against addiction to some drugs, but few studies have been carried out in order to evaluate how its actions interact with nicotine addiction. In this context, the main aim of this review is to provide an analysis of the preclinical studies evaluating the interaction between exposure to enriched environments with the neurobiological and behavioral effects of nicotine administration. These studies will contribute to the development of future preventive and therapeutic applications of enriched environments and positive experiences for drug addiction in human beings, taking into account individual vulnerability. They also may shed light on new approaches to the treatment of nicotine addiction, as interventions based in physical exercise in interaction with other environmental variables.

While poorly controlled alcohol drinking is a prominent symptom of alcohol abuse, its environmental determinants remain poorly understood. The Sign-Tracking Model (STM), developed by Tomie and his associates, postulates that poorly controlled alcohol drinking is due to the development of signal-directed behaviors induced by Pavlovian sign-tracking procedures. In laboratory studies of animal learning, presentation of the lever (conditioned stimulus, CS) followed by the presentation of the food (unconditioned stimulus, US) induces sign-tracking conditioned response (CR) performance, wherein rats approach and contact, then express consummatory-like responses (i.e., licking, gnawing, and chewing) directed at the lever CS. The Pavlovian sign-tracking CR is an involuntary acquired reflexive response. It is poorly controlled and elicited by the presentation of the CS. STM proposes that poorly controlled alcohol drinking in humans may be due to repeated pairings of the alcohol sipper (e.g., cocktail glass) CS with alcohol’s rewarding effects US, resulting in sign-tracking CR performance. The cocktail glass CS will elicit Pavlovian sign-tracking CR performance of reflexive and involuntary alcohol intake. This paper reviews evidence in the Pavlovian conditioning literature that in animals the positive contingency between the alcohol sipper CS and alcohol US induces sign-tracking of alcohol drinking. Also reviewed is evidence that in human beings alcohol drinking is a direct function of the positive contingency between a particular alcohol glassware CS and alcohol US. Implications of these findings for the Sign- Tracking Model (STM) are discussed.

Methadone has been used as a pharmacotherapy for the treatment of opiate dependence since the mid-1960s. Many studies examining the benefits of methadone maintenance treatment (MMT) for opiate dependence have documented a significant reduction in both criminal behavior and the use of other opiates. Nevertheless, emerging evidence suggests that MMT may impair cognitive function. However, it is unclear as to the part methadone dose, duration of MMT or plasma level may play in any observed deficits. Given the large number of people enrolled in MMT world-wide and the potential for deficits in cognitive function, a systematic review of the research investigating the association between MMT and cognitive function seemed warranted. The following databases were searched with a combination of free-text and thesaurus terms (methadone AND cognition): MEDLINE In-Process, EMBASE, PsycINFO and EBM Reviews-Cochrane Central Register of Controlled Trials. Seventy-eight articles were retrieved of which 35 met the inclusion criteria. The majority of research suggests that MMT is associated with impaired cognitive function and that deficits extended across a range of domains. However, caution is required when interpreting these results due to the methodological limitations associated with many studies. Further research that includes a combination of psychological and physiological measures within well-controlled group comparison studies is required to more accurately assess which cognitive domains are affected.

Ghrelin is a gut-brain hormone that regulates energy balance through food consumption. While ghrelin is well known for its role in hypothalamic activation and homeostatic feeding, more recent evidence suggests that ghrelin also is involved in hedonic feeding through the dopaminergic reward pathway. This paper investigated how ghrelin administration (intraperitoneal, intracerebroventricular, or directly into dopaminergic reward-relevant brain regions) activates the dopaminergic reward pathway and associated reward-relevant behavioral responses in rodents. A total of 19 empirical publications that examined one or more of these variables were included in this review. Overall, ghrelin administration increases dopamine levels in the nucleus accumbens, as well as reward-relevant behaviors such as food (both standard chow and palatable foods) and alcohol consumption. Ghrelin administration also increases operant responding for sucrose, and conditioned place preference. Following a review of the small body of literature examining the effects of ghrelin administration on the dopamine reward pathway, we present a model of the relationship between ghrelin and dopaminergic reward activation. Specifically, ghrelin acts on ghrelin receptors (GHS-R1A) in the ventral tegmental area (VTA) and lateral dorsal tegmental nucleus (LDTg) to stimulate the mesolimbic dopamine reward pathway, which results in increased rewarding behaviors in rodents. Results from this review suggest that selective antagonism of the ghrelin system may serve as potential treatment for addictive drug use. This review highlights gaps in the literature, including a lack of examination of sex- or age-related differences in the effects of ghrelin on dopamine reward processes. In light of vulnerability to drug abuse among female and adolescent populations, future studies should target these individual difference factors.