No abstract

Disinhibition is present in various maladaptive behaviors, including substance use disorders. Most previous research has assumed that disinhibition is a psychological construct that is relatively stable within individuals. However, recent evidence suggests that the ability to inhibit behavior fluctuates in response to environmental and psychological triggers. In this review we discuss some of the factors that cause (dis)inhibition to fluctuate, we examine whether these fluctuations contribute to subjective craving and substance consumption, and we ask if they might increase the risk of relapse in those who are attempting to abstain. The research that we discuss has furthered our understanding of the causal relationships between disinhibition and substance use disorders, and it also highlights opportunities to develop novel treatment interventions. We conclude that substance misusers and their therapists should be made aware of the triggers that can cause disinhibition to fluctuate, and we highlight the need for more research to investigate the effectiveness of inhibitory control training in clinical settings.

This report of an association with a polymorphic site within the IL-1 locus and AS suggests that genes other than B27 may well be involved in the pathogenesis of AS.

Current information is reviewed on the mechanism of secretion in small intestine, including how it is altered by cyclic 3',5'-adenosine monophosphate and on the structures and properties of cholera and both heat-labile and heat-stable Escherichia coli enterotoxins. Two separate active ion transport processes are altered by cyclic 3',5'-adenosine monophosphate: 1) coupled absorption of NaCl is inhibited in villus cells and 2) active anion secretion is stimulated, probably in crypt cells. Cholera and heat-labile E. coli toxins exert their secretory effect by stimulating intestinal mucosal adenylate cyclase. This stimulation results from the A1 subunit catalyzed transfer of adenosine diphosphate ribose from NAD to a membrane-bound guanosine triphosphatase, thereby inhibiting the enzyme, which normally represses adenylate cyclase. Heat-stable E. coli enterotoxin stimulates intestinal mucosal guanylate cyclase, which appears to be the basis for its enterotoxicity.

Background: Approach and avoidance motivation for alcohol are relatively independent, and they operate in both automatic (or implicit) and controlled processes. In this study, we adapted methods previously used in the appetite literature and implicitly primed an alcohol-related motivational orientation (approach or avoidance) in order to investigate its influence on the opposing motivational orientation, in a group of non-dependent heavy drinkers. Methods: Participants (N = 110) completed computerised measures of attentional bias and avoidance for alcohol cues (visual probe task) and behavioural approach and avoidance for alcohol cues (Stimulus-response Compatibility (SRC) task). Word primes were subliminally presented during each trial of these tasks. Participants were randomly allocated to groups that were exposed to alcohol-appetitive primes, alcohol-aversive primes, or neutral primes. Results: Contrary to hypotheses, word primes had no effect on responding during the visual probe or SRC tasks. Supplementary analyses revealed that participants showed attentional avoidance of alcohol cues combined with slower behavioural avoidance responses to alcohol cues. Attentional bias was positively correlated with scores on the Alcohol Use Disorders Identification Test. Conclusions: In contrast to previous findings from the appetite domain, our findings suggest that automatic alcohol cognitions are unaffected by implicit priming of motivational orientations, although features of our novel methodology may account for these results.