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Figure 1 Dopaminergic Dysfunction The dopamine (DA) hypothesis for SZ features the imbalances in dopaminergic neurotransmission throughout the brain, such as presynaptic abnormalities of DA neurons that are described in both SZ and high-risk populations ( in vivo findings of decreased dopaminergic activity in the dorsolateral prefrontal cortex has been associated with cognitive impairment severity, such as worsened working memory, as well as negative symptom severity ( Glutamatergic and GABAergic Dysfunction A more recent hypothesis for SZ pathology involves glutamatergic dysfunction, involving the hypofunction of N -methyl-D-aspartate (NMDA) receptors of which glutamate, the major excitatory transmitter in the brain, binds ( Additionally, NMDARs, which influence both glutamate and GABA, highly influence dopamine synthesis and transmission ( DA, GLU, GABA, and Nicotine Nicotine modulates dopaminergic transmission in both subcortical and cortical regions

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