The Dopaminergic Pathways

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Dopaminergic Pathways And Antipsychotics

Figure 4.6 Representation of the primary dopamine-containing tracts in the human brain. The nigrostriatal tract is primarily involved in motor control, but also in reward- and goal-directed behavior. Blockade of D2 receptors here produces some of the antipsychotic effects of antipsychotics, but high levels of blockade (> 80%) produce parkinsonian side-effects. Blockade of D2 receptors in the tuberoinfundibular pathway increases plasma prolactin. It is thought that it is the blockade of D2 and D2-like receptors in the mesolimbic and mesocortical tracts that underlies the primary antipsychotic effects of all currently available antipsychotics

Figure 4.6 Representation of the primary dopamine-containing tracts in the human brain. The nigrostriatal tract is primarily involved in motor control, but also in reward- and goal-directed behavior. Blockade of D2 receptors here produces some of the antipsychotic effects of antipsychotics, but high levels of blockade (> 80%) produce parkinsonian side-effects. Blockade of D2 receptors in the tuberoinfundibular pathway increases plasma prolactin. It is thought that it is the blockade of D2 and D2-like receptors in the mesolimbic and mesocortical tracts that underlies the primary antipsychotic effects of all currently available antipsychotics dopaminergic innervation supplies fibers to the medial surface of the frontal lobes and to the parahippocampus and cingulate cortex, the latter two being part of the limbic system. Because of this anatomic representation it is thought that this tract is where antipsychotic medication exerts its beneficial effect. The third major pathway is termed the tuberoinfundibular tract. The cell bodies for this tract reside in the arcuate nucleus and periventricular area of the hypothalamus. They project to the infundibulum and the anterior pituitary. Dopamine acts within this tract to inhibit the release of prolactin. The blockade of these receptors by antipsychotics removes the inhibitory drive from prolactin release and leads to prolactinemia.

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