The brain in schizophrenia

AUDITORY SYSTEM Enables humans to hear and understand speech. In schizophrenia, overactivity of the speech area (called Wernicke’s area) can create auditory hallucinations—the illusion that internally generated thoughts are real voices coming from the outside.

BASAL GANGLIA Involved in movement and emotions and in integrating sensory information. Abnormal functioning in schizophrenia is thought to contribute to paranoia and hallucinations. (Excessive blockade of dopamine receptors in the basal ganglia by traditional antipsychotic medicines leads to motor side effects.)

FRONTAL LOBE Critical to problem solving, insight and other high-level reasoning. Perturbations in schizophrenia lead to difficulty in planning actions and organizing thoughts.

LIMBIC SYSTEM Involved in emotion. Disturbances are thought to contribute to the agitation frequently seen in schizophrenia.

SOME SCIENTISTS have proposed that too much dopamine leads to symptoms emanating from the basal ganglia and that too little dopamine leads to symptoms associated with the frontal cortex. Insufficient glutamate signaling could produce those same symptoms, however.

IN THE FRONTAL CORTEX, where dopamine promotes cell firing (by acting on D1 receptors), glutamate’s stimulatory signals amplify those of dopamine; hence, a shortage of glutamate would decrease neural activity, just as if too little dopamine were present.

OCCIPITAL LOBE Processes information about the visual world. People with schizophrenia rarely have full-blown visual hallucinations, but disturbances in this area contribute to such difficulties as interpreting complex images, recognizing motion, and reading emotions on others’ faces.

HIPPOCAMPUS Mediates learning and memory formation, intertwined functions that are impaired in schizophrenia.

IN THE REST OF THE CORTEX, glutamate is prevalent, but dopamine is largely absent.

IN THE BASAL GANGLIA, where dopamine normally inhibits cell firing (by acting on D2 receptors on nerve cells), glutamate’s stimulatory signals oppose those of dopamine; hence, a shortage of glutamate would increase inhibition, just as if too much dopamine were present.

IN THE FRONTAL CORTEX, where dopamine promotes cell firing (by acting on D1 receptors), glutamate’s stimulatory signals amplify those of dopamine; hence, a shortage of glutamate would decrease neural activity, just as if too little dopamine were present.

SOME SCIENTISTS have proposed that too much dopamine leads to symptoms emanating from the basal ganglia and that too little dopamine leads to symptoms associated with the frontal cortex. Insufficient glutamate signaling could produce those same symptoms, however.

MANY BRAIN REGIONS and systems operate abnormally in schizophrenia, including those highlighted below. Imbalances in the neurotransmitter dopamine were once thought to be the prime cause of schizophrenia. But new findings suggest that impoverished signaling by the more pervasive neurotransmitter glutamate—or, more specifically, by one of glutamate’s key targets on neurons (the NMDA receptor)—better explains the wide range of symptoms in this disorder.

COPYRIGHT 2003 SCIENTIFIC AMERICAN, INC.
52 SCIENTIFIC AMERICAN JANUARY 2004

ALFRED T. KAMAJIAN
From Katrine elizabeth sackett32463(5’3)(5’21/2)(whitelady)
Information found under google in internet
july 30 2019

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