Phasic dopamine signalling induced by drug administration can also trigger neuroadaptations in basal ganglia circuits. Here, drug-induced phasic dopamine release triggers the ability of drug-paired cues to increase dopamine levels. Activation of the ventral striatum leads to the recruitment of striatal-globus pallidalthalamocortical loops that engage the dorsal striatum, resulting in habit formation45 and triggering what is hypothesised to underlie compulsive responding for drugs (table 2, circuits 3 and 4).59 Key synaptic changes involve glutamate-modulated N-methyl-D-aspartate (NMDA) receptors and α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid (AMPA) receptors in glutamatergic projections from the prefrontal cortex and amygdala to the ventral tegmental area and nucleus accumbens (table 2, circuit 4).32,43,46
