Question

How are third-generation antipsychotic drugs different than first-generation antipsychotic drugs?

Explain the difference between the glutamate hypothesis, dopamine hypothesis, and the serotonin-dopamine hypothesis of psychosis.

Answer 1

• The glutamate hypothesis of schizophrenia models the subset of pathologic mechanisms linked to glutamatergic signaling. The hypothesis was initially based on a set of clinical, neuropathological, and, later, genetic findings pointing at a hypofunction of glutamatergic signaling via NMDA receptors.
• The theory that decreased activity of the excitatory neurotransmitter glutamate is responsible for the clinical expression of schizophrenia. Developed by observing symptoms induced by phencyclidine that act as antagonists at NMDA receptors.
• The dopamine hypothesis of schizophrenia suggests that a dysregulated dopamine system contributes to positive, negative, and cognitive symptoms of the disease.The dopamine hypothesis of schizophrenia postulates that hyperactivity of dopamine D2 receptor neurotransmission in subcortical and limbic brain regions contributes to positive symptoms of schizophrenia, whereas negative and cognitive symptoms of the disorder can be attributed to hypofunctionality of dopamine D1 receptor neurotransmission in the prefrontal cortex.
• The serotonin (5-hydroxytryptamine; 5-HT) hypothesis of schizophrenia is based on the early studies of interactions between the hallucinogenic drug lysergic acid diethylamide (LSD) and 5-HT. Observations of the psychotogenic effects of LSD and the antipsychotic effects of serotonin-dopamine antagonists, such as clozapine and risperidone, have led to increased interest in the interaction between these two neurotransmitter systems as a possible pathophysiological target in schizophrenia
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