Medical What is relation between dopamine and schizophrenia?

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Dopamine plays a complex role in schizophrenia, with evidence indicating an imbalance in dopamine activity across different brain regions rather than a simple chemical imbalance. The prefrontal cortex shows reduced dopamine activity, while excessive activity is noted in subcortical structures, particularly the striatum. The blood-brain barrier is not considered a primary issue in schizophrenia, and the disorder is recognized as an organic brain condition. Current treatments aim to manage symptoms by reducing excessive dopamine activity, but there is no known cure. Ongoing research continues to explore the multifactorial causes of dopamine regulation defects in schizophrenia.
ndung200790
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Please teach me this:
Are there any relation between dopamine and schizophrenia?What is the role of blood-brain barrier in protecting dopamine penetrate into ''system of nervous''(because it is seem to me dopamine cause schizophrenia).If the blood-brain barrier is not in good condition in the protection,how can we improve it?
Thank you very much in advanced.
 
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dopamin is good for healthy people but bad for schizophrenics.
it is not a problem of blood-brain barrier.
schizophrenia is not merely a chemical imbalance in brain. it is an organic brain disorder.
 
New evidence indicates an imbalance in dopamine activity in different parts of the brain. The following link describes reduced activity in the prefrontal cortex and excessive activity in deep brain structures. The prefrontal cortex involves the "highest" level of brain function, including abstract thinking, planning and innovation. It is the part of the brain that is most developed in humans compared to other mammals.

Dopamine is a key neurotransmitter which is essential to normal brain function, so it's not a simple matter of dopamine being "good" or "bad". Schizophrenia can usually be controlled by a variety of medications, but there is no known cure. The disease is still not well understood despite reasonably effective treatments which allow many patients to function. This review suggests that these medications may act by reducing excessive dopamine activity in certain sub-cortical (mesolimbic) structures.

http://ajp.psychiatryonline.org/cgi/content/abstract/148/11/1474
 
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The paper I cited above was published in 1991 and was considered a break-through paper at the time (Version Two). I found a new more current paper which proposes Version Three of the Dopamine Hypothesis. It's fairly technical, but may be of interest to some. As it stands, the basic idea of low dopamine activity in the prefrontal cortex and high activity in the subcortical structures is retained. The focus now seems to be on the striatum, a subcortical structure with connections to the cortex and other deep structures such as the basal ganglia, limbic system and hippocampus. Here,the authors argue. there is a pre-synaptic regulatory defect which is only temporarily addressed by blocking D2 receptors with drugs. In fact this may, in the authors' view, cause upregulation of the dopamine system which results in compensatory hyperactivity when the drugs are withdrawn. It's interesting, but one would expect observable consequences in patients. Withdrawing treatment would leave the patient worse off than if the patient had never been treated. There are certainly such instances, but this does not seem to be a global phenomenon.

The authors also propose that causes of defects in dopamine regulation are multifactoral. This is not a new idea. It was discussed in the 1991 paper. However, the idea that the primary "downstream" defect is in the striatum is new. According to this view, diminished dopamine activity in the prefrontal cortex is secondary to upregulation in the striatum.

http://schizophreniabulletin.oxfordjournals.org/content/35/3/549.full.pdf+html
 
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