Abstract

Cocaine is a stimulant and an extremely addictive drug. Its effects at the synaptic level are extremely prominent in the NAc (Adinoff, 2004). Cocaine works by competitively blocking the dopamine transporter (DAT) located on the presynaptic neuron, thereby blocking the reuptake of DA and potentiating its reinforcing effects. This can cause users to feel euphoric and later continue chasing that high feeling (Beuming et al., 2008). The route of administration can also influence the addictive properties of cocaine as it determines the speed and duration of the high. For example, when smoking, the maximal concentration and effects of cocaine are attained almost instantly (Quenzer and Meyer, 2013). In contrast, intranasal administration produces a slower achievement of peak drug concentration as well as lower reports on the intensity of the high (Kiluk et al., 2013). Thus, these differences in the rate and The Role of Synaptic Plasticity in the Pathophysiology of Cocaine Addiction