Cocaine is a widely abused illicit substance and has been gaining global popularity in recent years. It is understood that cocaine alters the normal functioning of the brain’s dopaminergic system to increase the amount of dopamine (DA) available to bind to receptors, subsequently potentiating DA’s euphoric effects. Knowledge regarding cocaine’s long-term addictive qualities is limited. Findings presented in this review demonstrate that DA D1 receptors (D1R) modulate the activity of the transcription factor ΔFosB, a marker of synaptic plasticity. Following cocaine use, dopaminergic activity is increased, subsequently causing the upregulation of ΔFosB. This upregulation of ΔFosB is correlated with an increase in expression of the N-methyl-d-aspartate receptor (NMDAR), which acts as a core component of long-term potentiation (LTP), a process underlying learning and memory. Thus, alterations to the normal synaptic functioning involved in learning and memory could explain the long-term impact of cocaine addiction, such as relapse. Based on the findings discussed in this review, further investigation of the role of these pathways in cocaine addiction is warranted.