There are four major dopamine pathways. The mesolimbic pathway is responsible for the functions usually associated with dopamine, which are reward and pleasure. The pathway originates in the ventral tegmental area, a dopamine-rich nucleus in the midbrain from where action potentials are emitted to the nucleus accumbens (Guy-Evans, 2022). The mesocortical pathway also originates from the ventral tegmental area but moves to the prefrontal cortex. A disturbance in this process may cause various dysfunctions including issues with working memory, cognition, and decision-making. The dopamine is relocated from the substantia nigra to the caudate and putamen through the nigrostriatal pathway (Guy-Evans, 2022). Reduction in dopamine levels within this pathway may result in poorer motor planning. The tuberoinfundibular pathway releases dopamine in order to reduce prolactin release. It begins in the arcuate and periventricular nuclei and moves to the infundibular region within the hypothalamus.
Within the mesolimbic pathway, every antipsychotic drug can reduce dopaminergic levels. A decrease in dopamine levels in the nucleus accumbens can cause fewer cravings for dopamine-producing activities (Guy-Evans, 2022). On the other hand, overstimulation with an increase in dopamine dramatically expands this craving. Though the use of antipsychotics or other medication on the mesocortical pathway may increase or decrease motor capabilities, it has the potential for negative side effects on the mesolimbic pathway. Antipsychotics that limit dopamine in the nigrostriatal pathway may cause motor control impairment. A disbalance caused by D2 antagonists, which may be first-generation antipsychotics, can lead to symptoms such as contractions, spasms, parkinsonism, tremors, and more (Guy-Evans, 2022). In the tuberoinfundibular pathway, antipsychotics may contribute to higher prolactin levels and can lead to hyperprolactinemia.
Reference
Guy-Evans, O. (2022). The Role of Dopamine as a Neurotransmitter in the Human Brain. Simply Psychology. Web.