The transition function impaired between goal-directed and habitual behavioral strategy are the main reasons of the formation of habitual drug-seeking behavior. Previous studies thought that the weakening ability of the prefrontal cortex to control the dorsomedial striatum, which is in charge of goal-directed system, mediated the habitual behavior. However, recent studies have found that the direct and indirect pathways of the dorsolateral striatum (DLS) can selectively regulate goal-directed and habitual systems. In addition, the projects from motor cortex to DLS can modulate the neurons’ synaptic plasticity of dopamine D1 receptor (D1DR) and D2 receptor (D2DR) bidirectional, regulating the synergistic or antagonistic effects between direct and indirect pathways. Recent studies have also revealed that the amygdala, as a key brain area for regulating emotions, can mediate the functional connection between the nucleus accumbens and DLS in the habitual drug-seeking behavior through the functional transformation between the central amygdala and the basolateral amygdala. Moreover, there is a competitive relationship for the regulation of habitual drug-seeking behavior between D1DR and D2DR neurons in the striatum. In view of these, this paper will focus on the mechanism of abnormal brain functions, which are associated with the defects of the conversion in behavioral strategies accompanying with habitual drug use, in the cell-specific and the circuit-specific ways.