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Critique of the Dopamine Hypothesis of Schizophrenia

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Recent scientific discoveries have proofed that the etiology of schizophrenia has various links to the dopaminergic over activity. For instance drugs such as amphetamines have been known to increase the levels of dopamine; in addition, they also increase the psychotic symptoms of schizophrenia. (Abi-Dargham, 2004). Despite the ignorance in its underlying neuronal correlations, the key feature to psychosis distortion are mainly characterized by delusions and hallucinations, However, a study on schizophrenic patients has enriched “the reality of auditory verbal hallucinations(AVH) during functional magnetic resonance imaging (fMRI)” (Nature, June 24, 1976). Binding studies on the dopamine receptors through the positron emission tomography(PET scans) and Postmortem studies have led to conclusions that a disturbance of centralD1 dopamine receptor does exist in schizophrenia. Karlsson et al., (May 2002) on their study, using PET scans, to compare how D1 receptor function between, schizophreniapatients and healthy subjects, concluded that; “binding to D1 receptors did not differ significantlybetween subjects with schizophrenia and healthy subjects inany of the brain regions or for any of the binding measuresstudied.”  Their results therefore concluded that there was no major replication to previous postmortem and PET findings which had involved altered central dopamineD1 receptor binding in schizophrenia. Moreover, their findings motivatefurther D1 ligand studies with higher signals in the corticalregions.

Besides, dopamine hypothesis on amphetamine initiated psychosis had long been recognized,that the use of amphetamines or other central dopamine agonistscan mimic the active symptoms of schizophrenia during the acuteintoxication phase, even among individuals without a geneticdiathesis for schizophrenia. (Connell, 1958, Bell, 1973).  Therefore, investigations inboth animals and humans study models, on the acute behavioral effects which thesedrugs induce, has been a cornerstone of the dopamine hypothesis ofschizophrenia. (Snyder, 1974).  Astudy onPCP by Hajszan (2006) and Kehrer et al. (2008) in animal modelsof Schizophrenia, and other PCP-like compounds as an alternative treatment of brain ischemia further cited the fact that PCP produces a syndrome that is similar to schizophrenia. Besides, PCP being an N -methyl-D-aspartate (NMDA) antagonist “can worsen the psychotic symptoms in schizophrenic people. This implies that PCP blocks the action of glutamate and aspartate, excitatory amino acid CNS neurotransmitters. This argument therefore clarifies that PCP does not act on dopamine. Besides, they also found out that PCP is highly anticholinergic in nature.

The National Institute of Mental Health has concluded from their mice model studies that, recurrent genetic etiology of schizophrenia impairs communications between the brain's memory and decision-making hubs this lead deficits in working memory. The Institute’s research further showed that, neuroimaging studies had discovered “abnormal connections between the prefrontal cortex, the executive hub, hippocampus and the memory hub, having been linked to impaired working memory.” (Sigurdsson, 2010).  The Institute has further showed that molecular abnormalities result in schizophrenic brain. This has been achieved through studying the connections of the cortical-striatal circuitry and the hippocampal-entrohinal in humans.  Data analysis on the molecular changes has also been determined showing neonatal damage of the hippocampus or prefrontal cortex in animal models of schizophrenia. A further finding by Pearlson et al on Nervous and Mental diseaseexplains that data obtained from the Computer axial Tomography (CT scans), Positron Emission Topography (PET scans) and Magnetic Resonance Imaging (MRI) show that defects in the morphology of the brain and its physiology are associated with the development of schizophrenia. PET scan studies have further discovered an increased number of neuronal receptors for dopamine in some areas of the brains of people with schizophrenia.  Prior, work done earlier by Rapoport et al. (1999) revealed prospective longitudinal brain (MRI) studies of the NIMH COS population as having showed an increasing ventricular volume while on the other hand a decreasing total cortical, frontal, medial temporal and parietal GM volumes at 2- to 6-year follow-up” during adolescent years, as they later confirmed in New perspectives for child psychiatry, (2001).

Both Creese and Seeman (1972) had commented on the move to prescribe Dopamine-D2 by psychiatrists in addition to other blockingdrugs so as to alleviate the positive symptoms of schizophrenia discussed above, hallucinations and delusions.  But despite such blockers diminishing most psychotic symptoms, Hyman (1995) remarked that they caused side effects such as stiffness and otherneuromotor effects. This further questions the dopamine hypothesis as in its blocking mechanisms. In the ‘90s, four new antipsychotic drugs, olanzapine, quetiapine, clozapine and risperidone, were introduced. These drugs alleviated positivesymptoms of schizophrenia, without causing the neurological side effects associatedwith the former drugs. To explain the positive symptoms, Arnold et al proposed that positive patients have two defects: One, defect in a schizophrenia gene which is involved in regulating the activity of the dopaminergic compensatory system cannot turn itself down but by pharmacologically neuroleptics. Two, Negative-symptom patients get little benefit from neuroleptics, since their dopaminergic system can reduce itself spontaneously. This therefore implicates that typical neuroleptics have minimal effects. Earlier results by America psychiatrists had that these positive symptoms were related to positive schizotypy,social dysfunction, and BPD symptoms. This indicates that schizophrenia etiologically may be related to severityof illness, rather than specific symptom dimensions. This may explain the reason behind the delayed effects of neuroleptics by the dopamine blockers. The information which is emerging from new scientific studies, is therefore proofing that other non-dopamine hypothesis and explanations play a crucial etiological role in schizophrenia: showing that the dopamine hypothesis may not be very relevant today given that most research findings are proofing contradictory evidence in relation to the once domineering dopamine theory of schizophrenia

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