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Example research essay topic: Prefrontal Cortex Identical Twins - 1,269 words

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Schizophrenia is a disease that has plagued societies around the world for centuries. It is characterized by the presence of both positive and negative symptoms. (Positive symptoms-altered behaviors ie excited motor activity, hallucinations, incoherent thoughts and speech, negative symptoms - the lack of behavior ie emotion lack of speech, and lack of emotion. Not all schizophrenic patients will exhibit all of these symptoms. There has been much debate as to the causes of schizophrenia. While some proposed causes that exist today have been proven false ie bad parenting, many still remain. One of the most famous and most debatable is the dopamine hypothesis.

Kendler & Gruenbert (1984) and Rosenthal et al. , (1980) found that although 1 % of the population develops sch an individual has a 10 % chance of sch occurring if they have the illness in their family (ie parent, child, or sibling) even if a healthy family adopted the relative shortly after birth. Holman & Matthysse (1990) also show that the concordance rates for sch are higher in identical twins (45 %) than fraternal twins (10 %). However the fact that these concordance rates for sch in identical twins is very low lends more weight on individual experience among people may provoke the development of sch. The current view among researchers is that some individuals inherit the potential for sch which may be activated by experience (Gottesman & Bertelsen, 1989). Norman & Malla (1993) found that stress may be play a major role in this activation of schizophrenic symptoms among people with this susceptibility. They found thro several studies that exposure to stressors is common prior to a schizophrenic attack.

In the 1950 s the anti-schizophrenic drug, chlorpromazine, was accidentally found. Initially it was developed as an antihistamine however scientific study showed that it had a calming effect when it was administered before surgery. It was then suggested that it might have the same calming effect when administered to psychotic patients. This was not the case, moreover it was found to help schizophrenic symptoms, allowing many institutionalized patients to be discharged. About the same time scientists discovered Reserpine which comes from the snakeroot plant and was used in India for centuries to help those with mental illness. Reserpine was also found to have an anti-schizophrenic effect when administered to patients.

Chlorpromazine and reserpine both produced the anti schizophrenic effect in two ways. 1. The effects of both became apparent only after 2 / 3 weeks of taking the drug. 2. Secondly the anti-schizophrenic effect of both drugs related to motor effects similar to the symptoms of Parkinsons disease ie tremors at rest and muscular rigidity. These similarities let scientists to believe that both drugs acted through the same mechanism that was related to Parkinsons disease. From research on Park disease in 1960 it was reported that the striatum of an individual dying of park disease had been depleted of dopamine (Whringer & Hornykiewicz, 1960). This suggested that the disruption of dopaminergic transmission might produce park disease and in turn the anti-schizophrenic effects of chlorpromazine and Reserpine may be prod in the same way.

The dopamine hypothesis suggests that such is caused by too much dopamine and the anti-schizophrenic drugs exert their effects by decreasing dopamine levels. Support: 1. Reserpine was known to deplete the brain of dopamine and other monoamine's by breaking down their synaptic vesicles. 2. Amphetamines and cocaine, which trigger schizophrenic episodes in normal subjects, increase the extra cellular levels of dopamine and other monoamine's in the brain.

REVISION NUMBER 1: Unlike Reserpine, chlorpromazine didnt deplete the brain of dopamine. The extra cellular levels of dopamine were unchanged. Carlsson & Lindqvist (1963) concluded that these two drugs antagonize the transmission at dopamine synapses in 2 different ways. 1. Reserpine depletes the brain of dopamine 2.

Chlorpromazine binds to the dopamine receptors. However they argued that chlorpromazine binds to dopamine receptors without activating them thus keeping dopamine form activating them therefore making it a false transmitter. They further explained that the lack of activity at postsynaptic dopamine receptors sent signals to presynaptic cells that increase release of dopamine due to stressors which activates such episodes. This explains why dopaminergic activity was reduced while dopamine levels stayed the same and the extra cellular levels of its metabolites were increased.

Carlsson & Lindqvists finding led to a revision of the dopamine hypothesis. It suggested that it is not high levels of dopamine that is the main factor in sch it is the high levels of activity at the dopamine receptors. REVISION NUMBER 2 In the 1970 s Snyder and his colleagues assessed the degree to which various anti-schizophrenic drugs bind to dopamine receptors. They found that chlorpromazine and other effective drugs had a high affinity for dopamine receptors, however there were several exceptions.

Haloperidol was one of these exceptions. This drug was one of the most potent anti-schizophrenic drugs at that time but had a very low affinity to bind to dopamine receptors. This finding led to the discovery of more than one dopamine receptor subtype. Chlorpromazine and other anti-schizophrenic drugs in its chemical class (phenothiazines) all bind effectively to both D 1 & D 2 receptors. Haloperidol and other anti-schizophrenic drugs in its chemical class (butyrophenones) all bind effectively to D 2 receptors but not D 1 receptors. The selective binding of butyrophenones to D 2 receptors led to a second revision of the dopamine hypothesis: it claims that such is caused by hyperactivity mainly at D 2 receptors as opposed to dopamine receptors in general.

Support: Snyder (1978) supported this revision by showing how the Butyrophenone, spiroperidol had the greatest affinity to bind to D 2 receptors and had the most potent schizophrenic effect. Within the category of D 2 receptors there are three subtypes PET scan analysis of dopamine usage in the brain and post-modem molecular analysis of brain tissue were able to examine the relative levels of dopamine receptors between patients suffering from sch and non-schizophrenic patients. These analyses indicate that the striatum, limbic system and the cortex have more receptors that the rest of the brain. Support: Research into the prefrontal cortex of schizophrenic patients shows decreased levels of D 1, D 3, & D 4 receptors. NEW RESEARCH: Also research has shown that the neurotransmitter NMDA seems to have some regulatory control over the production of dopamine mRNAs. Another researcher found that by using an NMDA antagonist the level of D 4 production was decreased and the level of D 3 production was increased.

This produced episodes similar to those of such in non-schizophrenic subjects. The drug PCP that inhibits NMDA has been shown to produce effects similar to both the negative and positive symptoms of sch. It remains unclear however to what extent dopamine is involved in the production of the symptoms of such. CRITICISMS: Positive symptoms of such can be related to increased levels of dopamine in the striatum however it has been suggested that the prefrontal cortex may be involved in the activation of these positive symptoms. This seems the case as the prefrontal cortex controls and organized the information that passed thro to and from the cortex, therefore a decrease in the activity in this region of the brain may result in a decrease of organization of thought processes and individual perception. This transmitter disorder may result in the hallucinations and thoughts that can be experienced by individuals suffering from such.

There is also a high instance of head injury during childhood among schizophrenic patients, which may also explain why such becomes apparent during late adolescence, as this is when the prefrontal cortex becomes fully developed.


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Research essay sample on Prefrontal Cortex Identical Twins

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