Compare and contrast the mechanisms employed by Cocaine, Ecstasy, Heroin, and Cannabis to stimulate dopamine release in the brain and how this relates to their abuse potential

Introduction

This essay will compare and contrast the different ways that drugs such as cocaine, ecstasy (indirect agonists) heroin and cannabis (direct agonists) stimulate the brains reward pathways differently in order to create excited states and how this relates to their abuse potential. Key to the excited state that illicit drugs such as cocaine stimulate is Dopamine (DA), the principal catecholamine neurotransmitter in the brain, which is created by the mesencephalic neurons in the substantia nigra (SN) and ventral tegmental area (VTA). Dopamine neurons originate in these nuclei and move to other parts of the brain including the striatum, cortex, limbic system and hypothalamus. It is through these pathways, that it regulates many of the body’s physiological functions, like movements, emotional behaviour and motivation (Tritsch and Sabatini 2012).

Main body

Stimulation of the DA system in reward-related behaviours is of vital importance because of the severe consequences of dysfunction in this circuit, especially drug addiction although other addictions like the food reward are also causing havoc such as high obesity prevalence in the west (Nestler and Carlezon 2006). Research has now accepted the fact that repeated exposure to addictive stimulants leads to adaptive transformation of the DA meso-cortico-limbic pathway at the molecular and cellular level, key pathway that regulates motivational behavior and organizes emotional and contextual behaviors (Nestler and Carlezon, 2006; Tritsch and Sabatini 2012; Julien et al 2010; Thomas et al 2008; Spanagel and Heilig 2005; Volkow et al 2006). 

These changes to the meso-cortico-limbic pathway are thought to lead to chronic drug dependence, and continued relapse where drug users risk life and limb in order to get their fix of dopamine (Thomas et al., 2008).

Cocaine and ecstasy DA stimulation mechanism