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Hi all! There are five key dopamine pathways, including the thalamic, tuberoinfundibular, nigrostriatal, mesolimbic, and mesocortical dopamine pathways (Stahl, 2021, p. 84). To begin, the thalamic dopamine pathway extends to the thalamus and emerges from various locations, including the ventral mesencephalon, periaqueductal gray, lateral parabrachial nucleus, and hypothalamic nuclei (Stahl, 2021, p. 85). The overall function of the thalamic dopamine pathway is not fully understood. That said, it is thought it be involved in arousal and sleep processes by controlling information that passes through the thalamus to other brain areas, such as the cortex (Stahl, 2021, p. 85). There is not much of an implication for antipsychotic use in this pathway given that no evidence currently exists showing atypical processing of this pathway in schizophrenia (Stahl, 2021, p. 85). Second, the tuberoinfundibular pathway includes dopamine neurons that extend from the hypothalamus to the anterior pituitary gland (Stahl, 2021, p. 85). The main purpose of this pathway is to regulate prolactin secretion into circulation, with dopamine acting as a prolactin secretion inhibitor (Stahl, 2021, p. 85). Dopamine antagonists result in increased prolactin levels and could cause symptoms such as amenorrhea and galactorrhea (Stahl, 2021, p. 165). Thirdly, the nigrostriatal dopamine pathway extends from dopamine cell bodies located in the brainstem substantia nigra by ways of axons which end in the striatum (Stahl, 2021, p. 85). This pathway is part of the extrapyramidal nervous system and plays a role in the regulation of motor movements (Stahl, 2021, p. 85). A decrease in dopamine can cause parkinsonism, with symptoms including rigidity, tremor, bradykinesia, and akinesia (Stahl, 2021, p. 87). An excess of dopamine can result in hyperkinetic motor movements, including dyskinesias and tics (Stahl, 2021, p. 87). This said, medication administration can be tricky when it comes to the nigrostriatal dopamine pathway. Acutely, dopamine antagonists can result is motor symptoms associated with drug-induced parkinsonism (Stahl, 2021, p. 165). On the other hand, blocking dopamine receptors chronically can result in tardive dyskinesia (Stahl, 2021, p. 166). Next, the mesolimbic dopamine pathway extends from the ventral tegmental area located within the brainstem to the nucleus accumbens (Stahl, 2021, p. 90). This system is involved in a variety of behaviors including euphoria associated with drug abuse, sensations of pleasure, and hallucinations and delusions of psychosis (Stahl, 2021, pp. 84-85). A hyperactive state of this pathway is connected with positive symptoms of psychosis and drug-induced highs (Stahl, 2021, p. 90). On the other hand, a hypoactive state of this pathway is connected with manifestations including apathy, anhedonia, negative symptoms of schizophrenia, and lack of energy (Stahl, 2021, p. 90). Decreasing dopamine within the mesolimbic system through the use of antipsychotic medications results in a reduction of positive symptoms of schizophrenia (Stahl, 2021, p. 90-92). It is interesting to note that typical and atypical antipsychotics have the ability to decrease dopamine, however, atypical antipsychotics may have a higher ability to do so (Grinchii & Dremencov, 2020). Lastly, the mesocortical dopamine pathway extends from the midbrain ventral tegmental area to the prefrontal cortex (Stahl, 2021, p. 85). This pathway plays a role in mediating affective and cognitive symptoms of schizophrenia (Stahl, 2021, p. 85). In addition, many professionals believe that negative symptoms of schizophrenia are related to deficiency of dopamine in the mesocortical pathway (Stahl, 2021, p. 93). That said, antipsychotics that can increase dopamine levels, such as various atypical antipsychotics, would result in a reduction of negative symptoms of schizophrenia (Grinchii & Dremencov, 2020).
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