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Schizophrenia is a degenerative mental disorder that affects millions of people worldwide. The term schizophrenia comes from the Greek roots schizen “to split” and phren “mind” so it is referred to as a as a “split-mind disease.” Eugen Bleuler diagnosed the first case of schizophrenia in 1908, but Auguste Morel had characterized the disease over 40 years earlier in 1860 (Wikipedia 109). Characteristics of schizophrenia include positive and negative symptoms that manifest in very different ways. The positive symptoms include psychotic behavior such as auditory hallucinations and delusions as well as disorganized characteristics such as paranoid affect and a disordered thought process. On the other hand, negative symptoms signify a loss of normal activity and can include social withdrawal, flat affect, and psychomotor retardation (103 lecture). Having schizophrenia can result in average decrease in life expectancy of 12-15 years (due to its association with secondary side affects (wiki 2). Studies now show that schizophrenia has a global lifetime prevalence of around 1-2%, and accounts for up to half of all psychiatric inpatients (103 lecture). The debilitating effects of Schizophrenia usually results in a poor quality of life for the millions of people who suffer from the disease, so it is of the utmost importance to investigate its causes and potential treatments.
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) ( 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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Meltzer, 1999). Before this finding it was thought that dopamine was the main neurotransmitter system involved in schizophrenia (Seeman, 2002). For example in a study done by Seeman and colleagues in 2002 they found that out “of the 31 antipsychotics examined, the older traditional antipsychotics such as trifluperazine, pimozide, chlorpromazine, fluphenazine, haloperidol, and flupenthixol bind more tightly than dopamine itself to the dopamine D2 receptor, with dissociation constants that are lower than that for dopamine. The newer, atypical antipsychotics such as quetiapine, remoxipride, clozapine, olanzapine, sertindole, ziprasidone, and amisulpride all bind more loosely than dopamine to the dopamine D2 receptor and have dissociation constants higher than that for dopamine.” It was Doctor Meltzer who first proposed that the pharmacology of both serotonin and dopamine contributed to the neuropharmacological effect of the new atypical antipsychotics by using Clozapine as a model drug. The notion that these atypical antipsychotics bind more tightly to the serotonin 5-HT2a receptor than to the dopamine D2 receptor was a revolutionary concept and has generated much more research into this topic.
The 5-HT2a receptors are found throughout the brain but have a greater concentration in the cortex (Hoyer et al., 1986). The receptors themselves are found on pyramidal glutamatergic neurons (Hirose et al., 1990) as well as on GABAergic interneurons, which has major implications as to their role in the brain (Willins et al., 1997). The new generation of atypical antipsychotic drugs used to treat schizophrenia have reduced extra pyramidal symptoms (EPS) such as akinesia (inability to initiate movement) and akathisia (inability to remain motionless), compared to the typical antipsychotics. The reduced side effects of the atypical drugs is thought to be due to the increased antagonism of serotonin receptors and the decrease in antagonism of dopamine receptors (Meltzer et al. 2003). The receptors on the GABAergic neurons have been implicated in the control of GABA release, which would have an important regulatory effect on neural activity ([Cozzi and Nichols, 1996 and Abi-Saab et al. 1999) (Serotonin receptors). On the other hand, the receptors on the glutamatergic neurons are thought to have an excitatory affect on neural activity (Meltzer et al. 2003). It is clear that the role of antipsychotics on serotonin receptors is more complicated than initially thought. It has also been found that there is a significant reduction in the levels of 5-HT2a receptors in the cortex of post mortem patients that had schizophrenia, which strengthens the link between serotonin and schizophrenia (Meltzer et al. 2003). However, in 2000 Okubo et al. found that “PET studys failed to find a decrease in 5-HT2A receptors in the cortex of 10 unmedicated patients with schizophrenia.” There are a few theories that predict why this may be the case, one such theory hypothesizes that it is the antipsychotic drugs that down regulate the 5-HT2a receptor in the cortex of schizophrenic patients ([Meltzer et al., 1989). In order to help test these hypotheses researchers have come up with animal models for schizophrenia that mimic the disease and can be used to study the individual effects of serotonin receptor antagonism and the neurological effects of potential new antipsychotic drugs.

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