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Increasing knowledge of the genome sequences of several organisms and the development of genome-wide, high-throughput screening techniques for gene expression are likely to generate a vast amount of data aimed at elucidating the molecular mechanisms of addiction. These findings are likely to have potential for future addiction pharmacotherapies. However, it is important to employ animal models that dissociate the molecular and cellular consequences of the direct pharmacological effects of addictive drugs from those that result from the cognitive processes associated with self-administration of these drugs. In this article, we suggest that the short-term and long-term neuroadaptive effects of addictive drugs in the brain depend crucially on the drug-exposure paradigm used [i.e. passive (non-contingent) drug exposure and active (contingent) self-administration]. This has important ramifications for future molecular and cellular studies of drug addiction.

Adaptation of circadian rhythms to the environmental light-dark cycle is necessary for the survival of organisms. This synchronization or entrainment is only caused by light (photic input) during the dark period, according to the internal biological clock of an organism. During the light period, internal factors (non-photic input), rather than light, are able to entrain circadian rhythms. In this article, the data that implicate the neurotransmitter system for histamine in circadian entrainment are reviewed. Furthermore, we speculate that histamine receptors are the final gate at which both photic and non-photic entrainment mechanisms converge before sending a resetting signal to the intracellular biological clock.