Although Dopamine and Norepinephrine are structurally the same, they only differ by an extra –OH group on the Norepinephrine molecule. The nerve cells that benefit from Norepinephrine have the exact enzyme which joins the –OH group to Dopamine.
Schizophrenia has been a topic of debate that has been widely critized by all different approaches in psychology. However, the Biological implications tend to concentrate on the abnormalities of a behaviour, and how it can happen, referring to the medical model manual as a backup. But, assuming to this model most disorders are based on physical causes, as Kraepelin (1883) stated. Also in (1896) Kraepelin implied that there are major groups of serious mental diseases, and they are Dimentia Praecox (1st terminology for Schizophrenia) caused by a chemical imbalance of the brain, and Manic- Depressive Psychosis, which is caused by a faulty metabolism.
In identifying Schizophrenia biologically, their have been hundreds of studies, and what they have discovered was a general predisposition for Schizophrenia. Especially when studying Schizophrenics and their family members. Suggested by Nicol& Gottesman (1983) and Geishon & Reider (1982). They concluded that for relatives who have individuals with Schizophrenia their was an indication of a greater genetic risk. There is also a weakness in these findings of genetic relationships. As their have been identical twin studies reared together, showing a concordance rate of 50%. Suggesting their may be more than genetic issues involved. Nicol & Gottesman (1983) noted that their were very few cases of identical twins with Schizophrenia that were separated. Showing that this was a poor assumption as a representation of the general public. Even though genetic factors have been applied, no one knows exactly what they are after, after many years of trying.
The Biochemical explanation, has created the most rewarding outcome in recent years towards the diagnosis of Schizophrenia, and this happens to be the Dopamine Hypothesis. Which refers to the over activity in the neural pathways. Due to an excess of the Dopamine neurotransmitter. There is evidence to support such a prognosis e.g. in certain postmortems carried out on Schizophrenics, resulted in un-usually high levels of Dopamine in the limbic system .Iverson (1979). Secondly there are the anti-schizophrenic drugs (chlorpromazine) which are predicted to work by binding the receptor sites which contain Dopamine, suggesting that they restrain the ability of the Dopamine receptors to react, concluding with their being less Dopamine activity. There is also evidence to suggest that high levels of Amphetamines and L-dopa, can actually increase the activity of Dopamine, producing disorders that are similarly found within certain cases of Schizophrenia. These Dopamine neurons are found within the basil ganglia, and frontal cortex of the brain. Which happen to control the initiation of movement etc.
Lavender (2000) stated… ‘if Schizophrenia is not a clearly identifiable syndrome but an umbrella term covering a range of symptoms with unclear onset, course, and outcome, then it is obvious that much of the work investigating a specific biological basis will be inevitably be inconclusive’… Gross, (2001) pg 654.
We have to look at the evidence, and decide whether or not the biochemical approach is right at implying that it is the neurotransmitters that implicate the onset of such a prognosis as Schizophrenia. But, there is evidence to suggest otherwise.
Joanne Marchant (2001) in the US. Stated that some cases of Schizophrenia may have been activated by a viral DNA lurking within our genome. These US researchers claim that if so, it may be possible to treat such a disease as Schizophrenia with anti viral drugs. Apparently we all carry around retroviral DNA from viruses that have incorporated themselves into our Human genome millions of years ago. The retroviral genes (endogenous) are similar to those that are established with HIV, but they are usually inactive, and do not cause such problems like those ones within HIV.
David Yolken at the J,H University of Baltimore, and some of his colleagues. Have discovered some of the endogenous retroviruses in the cerebrospinal fluid of 10 patients out of 35, recently diagnosed with acute Schizophrenia. A control group in this study showed no signs at all of such genes. Yolken stated …’he thought retroviruses might be involved, because Schizophrenia seems to depend on environmental factors and genetic factors’. He also stated…’that such infectious agents are acting in the presence of a genetic disposition’. Academy Of Science Vol 98 Pg 4634.
Again another statement against such a suggestion of neurotransmitters implicating the onset of Schizophrenia. Are that of Greenough (2002) he suggested that Schizophrenia Could be the result of the differences in the structures that connect neurons together. In his theory he suggests that the differences are discovered in the spiny structures found at the synapse. A complete different theory to the Dopamine Hypothesis. Greenough (2002) discovered the spines in the brains of people suffering from Schizophrenia were much smaller and abnormally shaped. Losing what they call characteristic head & tail morphology. In favour of simply a tail or cylindrical structure. This research was carried out in the University of Illinois, US.
There has already been previous work that have suggested that there are some general structural differences within the brains of Schizophrenics, and that they have a reduction in the volume of the cortex, especially within the pre frontal cortex, with an enlargement of the ventricles. Greenough whom was a member of the above study, concluded that there is a large scale difference in the structure of the synapses. Stating that it is a maladaptive change that would alter the way neurons communicate.
In conclusion the diagnosis of Schizophrenia is not as clear cut as first thought. As looking back at some of the empirical evidence, suggests that there can be a number of different aspects that can effect the prognosis of such a disease as Schizophrenia. We have looked at the evidence that suggests that neurotransmitters can cause a Dopamine chemical reaction which indicates to that of the Dopamine Hypothesis. Yet, there still seems to be a lack of understanding whether it is infact biological or environmental factors that bring on the onset of such a disease.
REFERENCES:
Geishon & Reider (1982) Schizophrenia. R, Gross (2001) 4th ed. Psychology The Science Of Mind & Behaviour.
London: Hodden & Stoughton.
Kraepelin (1883)& (1896) Schizophrenia. R, Gross (2001) 4th ed. Psychology The science Of Mind & Behaviour.
London: Hodden & Stoughton.
Lavender (2000) Schizophrenia. R, Gross (2001) 4th ed. Psychology The Science Of mind & Behaviour.
London: Hodden & Stoughton.
Nicol & Gottesman (1983) Schizophrenia. R, Gross (2001) 4th ed. Psychology The Science Of Mind & Behaviour.
London: Hodden & Stoughton.
J, Marchant (2001) National Academy Of Science. Volume 98…Pg 4634. .
D, Yolken (2002) National Academy Of Science. Volume 98…Pg 4634
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