Electrodermal responses to sources of dual-task interference.

There is a response selection bottleneck that is responsible for dual-task interference. How the response selection bottleneck operates was addressed in three dual-task experiments. The overlap between two tasks (as indexed by the stimulus onset asynchrony [SOA]) was systematically manipulated, and both reaction time and electrodermal activity were measured. In addition, each experiment also manipulated some aspect of the difficulty of either task. Both increasing task overlap by reducing SOA and increasing the difficulty of either task lengthened reaction times. Electrodermal response was strongly affected by task difficulty but was only weakly affected by SOA, and in a different manner from reaction time. A fourth experiment found that the subjectively perceived difficulty of a dual-task trial was affected both by task difficulty and by SOA, but in different ways than electrodermal activity. Overall, the results were not consistent with a response selection bottleneck that involves processes of voluntary, executive attention. Instead, the results converge with findings from neural network modeling to suggest that the delay of one task while another is being processed reflects the operation of a routing mechanism that can process only one stream of information for action at a time and of a passive, structural store that temporarily holds information for the delayed task. The results suggest that conventional blocked or event-related neuroimaging designs may be inadequate to identify the mechanism of operation of the response selection bottleneck.

Pharmacological activation of CB1 and D2 receptors in rats: predominant role of CB1 in the increase of alcohol relapse.

The classical dopamine D2 receptor has been widely studied in alcoholism. Recently, different studies have explored the role of the CB1 receptor in alcohol-related behavior. In alcohol addiction, relapse is one of the central features. In light of this, we investigated the functional roles of and interactions between CB1 and D2 receptors in alcohol relapse. We used the learned task of alcohol operant self-administration in Wistar rats. In order to evaluate alcohol relapse, we set up a protocol essentially based on the alcohol deprivation effect. We found that subchronic activation of CB1 (WIN 55,212-2, 2 mg/kg), but not D2 receptors (quinpirole, 1 mg/kg), during a period of alcohol deprivation increased long-lasting alcohol relapse. The cannabinoid-induced potentiation of alcohol relapse was mediated by a motivational and appetitive component, and not merely by alcohol consumption. This potentiation was prevented by the pharmacological inactivation of D2 receptors (raclopride, 0.1-0.3 mg/kg). Together, these results essentially demonstrate that activation of CB1 receptors plays a key role in the increase of alcohol relapse, whereas inactivation of D2 receptors modulates this aberrant behavior. We suggest that there exists a functional and interactive relationship between both receptor systems, which controls alcohol relapse and alcohol-learned tasks.