Basal ganglia pathology in schizophrenia: dopamine connections and anomalies
Article first published online: 20 JAN 2010
© 2010 The Authors. Journal Compilation © 2010 International Society for Neurochemistry
Journal of Neurochemistry
Volume 113, Issue 2, pages 287–302, April 2010
How to Cite
Perez-Costas, E., Melendez-Ferro, M. and Roberts, R. C. (2010), Basal ganglia pathology in schizophrenia: dopamine connections and anomalies. Journal of Neurochemistry, 113: 287–302. doi: 10.1111/j.1471-4159.2010.06604.x
- Issue published online: 16 MAR 2010
- Article first published online: 20 JAN 2010
- Received October 9, 2009; revised manuscript received January 11, 2010; accepted January 13, 2010.
- psychiatric disorders;
- substantia nigra;
- tyrosine hydroxylase
J. Neurochem. (2010) 113, 287–302.
Schizophrenia is a severe mental illness that affects 1% of the world population. The disease usually manifests itself in early adulthood with hallucinations, delusions, cognitive and emotional disturbances and disorganized thought and behavior. Dopamine was the first neurotransmitter to be implicated in the disease, and though no longer the only suspect in schizophrenia pathophysiology, it obviously plays an important role. The basal ganglia are the site of most of the dopamine neurons in the brain and the target of anti-psychotic drugs. In this review, we will start with an overview of basal ganglia anatomy emphasizing dopamine circuitry. Then, we will review the major deficits in dopamine function in schizophrenia, emphasizing the role of excessive dopamine in the basal ganglia and the link to psychosis.