This group of findings demonstrates a number of ways in which smoking might enhance neurotransmission through cortico–basal ganglia–thalamic circuits (Alexander et al. 1990), in addition to demonstrating direct effects of chronic nicotine exposure on nAChR availability (Fig. 1). Given that the thalamus (Groenewegen et al. 1999; Herrero et al. 2002; Sommer 2003) and ventral striatum/NAc (Groenewegen et al. 1999; Herrero et al. 2002) function as relay centers for information and for paralimbic and motor processing in the brain, the net effect of smoking may be to enhance neurotransmission along cortico–basal ganglia–thalamic loops originating in the paralimbic cortex. Neurotransmission through these circuits may be stimulated directly by the interconnected (Sherman 2001; Sillito and Jones 2002) nAChR-rich thalamus and visual systems, and/or indirectly through effects on MAO inhibition and DA release in the ventral striatum/NAc, as well as through nicotine stimulation of excitatory glutamatergic input to the dopaminergic system (Mansvelder et al. 2002). In the thalamus, for example, nicotine has direct agonist action on excitatory thalamocortical projection neurons and local circuit neurons, although nicotine also stimulates GABAergic interneurons, so that the relationship
