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. Author manuscript; available in PMC: 2016 Jul 1.
Published in final edited form as: Neuron. 2010 Mar 11;65(5):585–596. doi: 10.1016/j.neuron.2010.02.014

Figure 2. The Dopamine Hypothesis of Schizophrenia.

Figure 2

(A) Organization of the nigrostriatal and mesocortical midbrain dopaminergic projections. The dopaminergic midbrain neurons topographically project to the striatum but with an inverse dorsal-to-ventral organization. The mesocortical projections arise from the dorsal and medial dopamine cells.

(B) The original dopamine hypothesis of schizophrenia. The original dopamine hypothesis proposed that a global hyperactivity of the dopaminergic projections in the brain may lead to the symptoms of schizophrenia.

(C) The revised dopamine hypothesis of schizophrenia. The revised dopamine hypothesis proposed that a hyperactive nigrostriatal dopaminergic projection leads to positive symptoms but a hypoactive mesocortical projection is responsible for cognitive and negative symptoms.

(D) Results of brain imaging studies in schizophrenia. Brain imaging studies show that an increase in amphetamine-induced dopamine release in the striatum is highest in the associative striatum. Moreover, the density and occupancy of striatal D2 receptors is increased in drug-free or drug-naive patients.

PFC, prefrontal cortex; dSTR, dorsal striatum; vSTR, ventral striatum; VTA, ventral tegmental area; SNc, substantia nigra pars compacta; SNr, substantia nigra pars reticulata; D2R, dopamine D2 receptor.