Ofcourse there is strong relation between the schizophrenia disorder and dopamine.

Please check this article

Article Altered dopamine ontogeny in the developmentally vitamin D d...

This is a great chapter discussing this topic:

Guillin O, Abi-Dargham A, Laruelle M (2007) Neurobiology of dopamine in schizophrenia. Int Rev Neurobiol 78:1-39.

See here as well:

http://www.schizophreniaforum.org/for/curr/AbiDargham/

Hi Neil, I think you'll find the attached paper useful in understanding the most recent conceptual framework of the dopamine hypothesis, as well as it's long history

Causal - definitely not. Correlational - yes, but more with positive symptoms or psychosis, not with disease. The dopamine hypothesis has been around for well over 40 years, but it is really only with recent PET imaging data that we have properly begun (and still only begun) to understand the role it has in the symptoms of schizophrenia. Carlsson, back in 1978, said "There is so far no direct support for a primary causative role of dopamine in schizophrenia", and that is as true now as it was then.

Other posters have pointed to a couple of useful reviews, and I'm sure you can find much in the literature to help you answer your questions and put more meat on my answer. Look at work on dopamine and salience, for example. But it is always useful to be sceptical and ask yourself - "is this evidence for changes in (the trait of) schizophrenia, or in (the state of) acute symptoms of the disease?" Also remember that studies of living patients so often overlook the fact that they are receiving antipsychotic drugs, which of course have profound effects on dopaminergic function.

In current understanding there is substantial evidence for a hyperfunction of dopamine in limbic and some striatal regions of the brain in psychosis. However many authors suggest there is also a deficit in dopamine function in the frontal cortex that is associated with negative/cognitive symptoms of the disease. This is an old and attractive hypothesis, but as yet the evidence is circumstantial.

It is arguably more important to address glutamatergic abnormalities and specific GABAergic deficits as "causal", or at least pathophysiological, in the disease. But that is a subject for several further lectures...

The old graph showing the almost perfect correlation between dopamine reactivity and clinical efficacy of a wide range of antipsychotics is the most striking finding in the whole of schizophrenia research. As far as I know, this research has not been challenged, so how Gavin can be so certain that dopamine has no causal role escapes me. Plenty of drugs cause hallucinations, so why not dopamine? I don't think brain scans contribute either way to this debate.

For those who are unsure what Anthony means here, the "old graph" he refers to is the close correlation between the affinity of antipsychotic drugs for dopamine D2 receptors, which is undoubtedly their main mechanism of action, and dose, or plasma concentration, of those drugs in the clinic. This is most definitely not a correlation with clinical efficacy, which varies little between the antipsychotics and is generally poor, with symptoms in a substantial proportion of patients improving only partially or not at all. Putting aside the question of whether clinical dose is truly determined by maximal efficacy, rather than by, say, side effect threshold (an interesting topic for debate), readers will spot the fallacy in the argument that correlation implies causality.

I share Anthony's scepticism about the value of brain scans, but they do provide some support for a disturbance of dopamine in schizophrenia, or at least in psychosis. However most researchers would agree that this is a secondary effect of an underlying pathology in other systems. We have to beware against over-emphasising the importance of antipsychotic drug pharmacology in telling us about pathology, let alone etiology.

Is the argument really much different from saying that as COX2 inhibitors are anti-inflammatory drugs, inflammation is "caused" by COX2 activity. Although PDE5 inhibitors are effective in the treatment of erectile dysfunction, we don't suggest PDE5 activity causes erectile dysfunction!

But perhaps the problem is semantic - by "cause" I assume we mean etiology, or perhaps pathogenesis, rather than a biological correlate.

I agree with Gavin, dopamine certainly has something to do with positive symptoms in schizophrenia, and antipsychotics undoubtedly work by their antagonism of D2 dopamine receptors. However, the aetiology of schizophrenia is far more complicated. You could view dopamine abnormalities as one of the last downstream effects of schizophrenia. There are other theories such as the glutamate hypothesis (see attached document) which actually encompass the most important aspects of the dopamine hypothesis.

Saying that dopamine abnormalities results in schizophrenia would be untrue. But stating that excess limbic and striatal dopamine can cause psychosis is true. It is important to differentiate psychosis from schizophrenia, as schizophrenia encompasses much more than psychosis, including sometimes profound cognitive deficits which persist even when patients aren't psychotic.

If you are interested in the aetiology of schizophrenia, developmental hypotheses based upon neonatal or perinatal stress are important to consider. Multiple types of developmental stressors can lead to schizophrenic phenotypes, including dopamine abnormalities and several potential schizophrenia biomarkers.

Here is an extensive account of the current view on dopamine hypothesis in schizophrenia:

http://www.schizophreniaforum.org/for/curr/AbiDargham/.

The related comments add also to the present understanding of the dopamine role, and interactions with other neurotransmitters.

Because the 'schizophrenias' presumably have a variety of causes, a defect in one of the dopamine pathways may be causal for some schizophrenias.

"a defect in one of the dopamine pathways may be causal for some schizophrenias"

A defect in the dopamine pathways or system may not be needed, rather abnormal amounts of dopamine from exposure to external environmental factors or internal physiological processes that normally make dopamine.

Using a D2 antagonist is only a small part of the management of schizophrenia. Schizophrenia is a far more complex set of physiological and psychological factors than can be addressed by simple 'magic bullet' theories. It can be quite reasonably argued that using a non-specific label such as 'schizophrenia' is itself a hindrance to addressing aetiology.

I agree entirely with Nathaniel that talking about Dopamine abnormalities as being causes of psychosis is far too simplistic.

I look forward to the day when the nature-nurture dichotomy is consigned to the trash.

There is a lot of evidence for differential sensitivity to dopamine among segments of individuals with schizophrenia-type symptoms. Dopamine release is triggered by internal and external events but the sensitivity may be at least partially inborn.