The neurotransmitterdopamine is responsible for transmitting signals between the neurons in the brain.  There are several dopamine pathways that areinvolved in playing a role in reward-motivated behaviour, motor control, andhormone release.  One of the earliestexplanations for the causation of schizophrenia is known as the dopamine hypothesis.  The hypothesis is that individuals withschizophrenia have an imbalance of dopamine, which is related to the brainsreward and pleasure pathways.  Aschizophrenic brain experiences an increase in neuron firing which ultimatelyleads to higher levels of dopaminergic stimulation.  The reason this occurs is because individualswith schizophrenia have a higher number of D2 receptors (Carlsson ,Lindqvist, Magnusson, & Waldeck, 1958). In the late 1960’s, Van Rossum conducted research that proved thatneuroleptic drugs possess the ability to block dopamine receptors in thecentral nervous system.  His theory wasthat schizophrenia was due to over active dopamine pathways and his researchprovided evidence supporting that neuroleptic drugs are successful in reducinglevels of dopamine in the brain (Van Rossum, 1966).

  Amphetamines are psychostimulantsresponsible for increasing the presence of dopamine in the brain.  Another study found that amphetamine addicts whoexperienced paranoid psychosis were clinically indistinguishable from paranoid schizophrenics.  And the reason for the indistinguishabilitywas due to excessive dopaminergic stimulation. The findings from this study further supported the hypothesis that anabnormal amount of dopamine is present in a schizophrenic brain (Bell, 1973).When the dopaminehypothesis was first proposed, it was believed that that the nigrostriatalpathways was the main region affected; however, it was later found that the mesolimbicand mesocortical dopamine circuits were identified as being the most importantfor psychoses.  This was supported by evidenceof abnormalities in the frontal cortex and limbic regions in schizophrenicsalong with animal studies that demonstrated the importance of the ventraltegmental area (VTA) and its dopamine projections to nucleus accumbens, limbicand frontal structures for reward mechanisms (Koob & Bloom, 1988).

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Although there is muchevidence for the dopamine hypothesis, there are limitations with this theory.  There is newer evidence suggesting that bothdeficits and excesses of dopamine in the brain can cause the symptomology ofschizophrenia (Abi-Dargham, 2004).  Also,current research has found that other neurotransmitters including glutamate areinvolved in individuals experiencing schizophrenic type symptoms (Gorelick& Balster, 1995).

  This providesevidence that the dopamine hypothesis is not sufficient to explain schizophrenia.  Rather a theory encompassing the idea that severalneurotransmitters and their pathways are responsible for explaining the causationof schizophrenia is more plausible.  

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