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Many brain regions such as the prefrontal cortex, basil ganglia, and the cerebellum have been implicated as potential sources of schizophrenia’s affects (103 lecture). It has been hypothesized that the medications used to treat Schizophrenia work to restore the neural conductivity and activity to the region of affect by restoring proper neurotransmitter function. Current treatment of Schizophrenia utilizes atypical antipsychotics, such as Aripiprazole (Abilify), Clozaril (Clozapine), and Risperdal (Resperidone) (Schizophrenia.com). These medications have contributed significantly to the study of Schizophrenia and are now the primary basis by which researchers study the neurological effects of the disease. Many major neurotransmitter systems such as Serotonin (5-HT), Dopamine (DA), and Glutamate (NMDA) have now been implicated in Schizophrenia and it is possible that complex interactions between these systems lead to the neurological effects of the disease. This paper will primarily focus on the Serotonin neurotransmitter system, with respect to the 5-HT2A receptors in the brain.
The 5-HT2a Receptor
While the cause of schizophrenia is largely unknown there is evidence that it is a result of abnormal brain pharmacology. The role of the 5-HT receptors in schizophrenia has come to light in the past few decades when it was found that the new generation of antipsychotics (referred to as atypical antipsychotics) act as potent 5-HT2a receptor antagonists relative to the antagonistic effect on dopamine receptors (Herbert Y.
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