Schizophrenia is a complex psychological disorder with neurological components. First described in 1887 as dementia praecox by German physician Emil Kraepelin, schizophrenia consists of both positive and negative symptoms. The positive symptoms of schizophrenia are those that involve an exaggeration or distortion of normal thoughts, emotions and behavior, such as delusions and hallucinations. The negative symptoms of the condition are those that involve a reduction or absence of normal thoughts, emotions and behavior, such as flat affect, or a lack of emotional reaction; an inability to connect with others; and a tendency toward social isolation. Given the serious nature of this disease, much research has been conducted over the past century to better understand schizophrenia. One area of intense research involves understanding how chemicals in the brain, such as dopamine and glutamate, impact schizophrenia.
The Dopamine Hypothesis
The dopamine theory of schizophrenia is based on knowledge of antipsychotic medications, as well as the effects of illicit substances such as amphetamines. One of the side effects of antipsychotic medications is Parkinson's-type tremors. Scientists know that Parkinson's disease is caused by low levels of dopamine in certain areas of the brain. Since the medications used to treat schizophrenia work to decrease excessive levels of the neurotransmitter, researchers began to wonder about dopamine levels in the brains of schizophrenia. Additional information regarding this theory came from observing individuals using amphetamine. Amphetamine-induced psychosis closely resembles paranoid schizophrenia. When under the influence of amphetamine, the brain is flooded with dopamine and norepinephrine. Using these facts as a starting point, scientists eventually figured out that patients with schizophrenia have excessive dopamine receptors in specific brain regions.
Glutamate and Schizophrenia
Dopamine is just one of the neurotransmitters involved in schizophrenia. Glutamate, a transmitter that is widespread in the human brain, may also play a role. As with dopamine, notes on the effects of illicit drug use led to interest in glutamate. The drug phencyclidine, or PCP, can induce psychosis, as well as some of the negative symptoms of schizophrenia. PCP produces its effects by interfering with glutamate receptors in various brain regions, including the prefrontal cortex, which is the seat of executive functioning -- the umbrella term to describe the activities responsible for attention, short term memory and general processing of new information -- and some aspects of reasoning.
The Prefrontal Cortex and Schizophrenia
The prefrontal cortex is implicated in schizophrenia because this region is where a great deal of dopamine, glutamate and other neurotransmitter activity takes place. To further examine the role of the prefrontal cortex in schizophrenia, researchers at Albany Medical College in New York conducted a study in 2007 that was published in the journal "Biological Psychiatry." The researchers investigated the behaviors of rats with prefrontal cortex damage and found that damage here led to a disruption in dopamine-glutamate activity. Once this disruption occurred, the rats began exhibiting schizophrenic behavior. From these outcomes, the researchers hypothesized that a disruption of prefrontal cortex dopamine-glutamate interactions might contribute to the manifestation of schizophrenia-like symptoms.
Neurotransmitters and Cognition
Researchers are starting to better understand the role of dopamine and glutamate in the psychosis of schizophrenia. New research published in the journal of "Current Medicinal Chemistry" examined dopamine and glutamate in the cognitive disruptions of the disease. Scientists at the Neuropsychiatric Research Institute in Sweden used mouse models to look at whether dopamine could be implicated in diminished cognition. They tested traditional neuroleptics and new generation antipsychotics, which tend to focus more on dopamine, and found that the dopamine compounds led to better mental stabilization.
References
- "Abnormal Psychology With Cases, 9th Edition;" Gerald Davison, et al.; 2004
- "Biological Psychiatry"; Post-Pubertal Disruption of Medial Prefrontal Cortical Dopamine-Glutamate Interactions in a Developmental Animal Model of Schizophrenia; K. Y. Tseng, et al.; January 2007
- "Current Medicinal Chemistry"; Schizophrenia: From Dopamine to Glutamate and Back; M. L. Carlsson, et al.; November 2004
