The paranoid psychosis were clinically indistinguishable from

The neurotransmitter
dopamine is responsible for transmitting signals between the neurons in the brain.  There are several dopamine pathways that are
involved in playing a role in reward-motivated behaviour, motor control, and
hormone release. 

One of the earliest
explanations for the causation of schizophrenia is known as the dopamine hypothesis.  The hypothesis is that individuals with
schizophrenia have an imbalance of dopamine, which is related to the brains
reward and pleasure pathways.  A
schizophrenic brain experiences an increase in neuron firing which ultimately
leads to higher levels of dopaminergic stimulation.  The reason this occurs is because individuals
with schizophrenia have a higher number of D2 receptors (Carlsson ,
Lindqvist, Magnusson, & Waldeck, 1958). 
In the late 1960’s, Van Rossum conducted research that proved that
neuroleptic drugs possess the ability to block dopamine receptors in the
central nervous system.  His theory was
that schizophrenia was due to over active dopamine pathways and his research
provided evidence supporting that neuroleptic drugs are successful in reducing
levels of dopamine in the brain (Van Rossum, 1966). 

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Amphetamines are psychostimulants
responsible for increasing the presence of dopamine in the brain.  Another study found that amphetamine addicts who
experienced paranoid psychosis were clinically indistinguishable from paranoid schizophrenics.  And the reason for the indistinguishability
was due to excessive dopaminergic stimulation. 
The findings from this study further supported the hypothesis that an
abnormal amount of dopamine is present in a schizophrenic brain (Bell, 1973).

When the dopamine
hypothesis was first proposed, it was believed that that the nigrostriatal
pathways was the main region affected; however, it was later found that the mesolimbic
and mesocortical dopamine circuits were identified as being the most important
for psychoses.  This was supported by evidence
of abnormalities in the frontal cortex and limbic regions in schizophrenics
along with animal studies that demonstrated the importance of the ventral
tegmental area (VTA) and its dopamine projections to nucleus accumbens, limbic
and frontal structures for reward mechanisms (Koob & Bloom, 1988).

Although there is much
evidence for the dopamine hypothesis, there are limitations with this theory.  There is newer evidence suggesting that both
deficits and excesses of dopamine in the brain can cause the symptomology of
schizophrenia (Abi-Dargham, 2004).  Also,
current research has found that other neurotransmitters including glutamate are
involved in individuals experiencing schizophrenic type symptoms (Gorelick
& Balster, 1995).  This provides
evidence that the dopamine hypothesis is not sufficient to explain schizophrenia.  Rather a theory encompassing the idea that several
neurotransmitters and their pathways are responsible for explaining the causation
of schizophrenia is more plausible.