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Schizophrenia is classified as a long term mental disorder that causes both positive symptoms such as hallucinations and delusions, negative symptoms such as disorder also creates cognitive symptoms that may cause changes in memory, or issues with thinking. This essay will explore biological explanations of schizophrenia, such as the ‘dopamine hypothesis’, where an increase in dopamine in the brain can cause schizophrenic symptoms as suggested by Carlsson and Lindqvit (1963). After, inheritance of genes found amongst biological families will be discussed, as this has been found to be linked to schizophrenia, however, genetics combined with environmental factors may play a role. Along with this, social factors may play a part in the development of schizophrenia, such as family dysfunction, where parents may show conflicting and contradictory emotions towards a child, leading them to become confused, and showing negative symptoms. Lastly, sociocultural factors such as the ‘urban effect’, where it has been found that schizophrenia patients are more common in more built-up areas, as oppose to rural areas. The ‘dopamine hypothesis’ first proposed by Carlsson and Lindqvit emerged as a result of antipsychotic drugs such as cocaine, that increased the …show more content…
In a review by Gottesman and Shields (1972), the pair looked at adopted and twin studies between 1967-1976, and found a concordance rate of 58% in identical twins, and 12% for non-identical twins. Therefore, due to the concordance rates not being 100%, similarly like the dopamine hypothesis, environmental factors such as rearing patterns will influence the development of schizophrenia. However, this explanation shows that the closer one is genetically similar to another family member, they are at a higher risk of showing schizophrenic
The Role of Dopamine Receptors in Schizophrenia. Retrieved March 3, 2005, From Stanford University, Chemistry department web site, http://www.chem.csustan.edu/chem44x0/SJBR/Mann.htm Naheed, M., & Green, B. (2000). Focus on Clozapine. Retrieved February 7, 2005. From http://www.priory.com/focus14.htm Waddinton, J.L., & Buckley, P.F. (1996).
Van Den Berg, S. M. and Others. 2012. Genetic analysis of rare disorders: bayesian estimation of twin concordance rates. Behavior genetics, 42 (5), pp. 857-865.
Wang, G., Smith, L., Volkow, N., Telang, F., Logan, J., Tomasi, D., & ... Fowler, J. (2012). Decreased dopamine activity predicts relapse in methamphetamine abusers. Molecular Psychiatry, 17(9), 918-925. doi:10.1038/mp.2011.86
Cocaine. National Institute of Drug Abuse: The science of drug abuse and addiction, Retrieved from http://www.drugabuse.gov/about-nida/directors-page Holman, B. (1994) The 'Secondary' of the 'Secondary' of the 'Secondary' of the 'Secondary' of the 'Secondary' of the 'Secondary' of the 'Secondary' of the 'Secondary Biological effects of central nervous system stimulants. Retrieved from http://web.a.ebscohost.com.subzero.lib.uoguelph.ca/ehost/pdfviewer/pd fviewer?sid=118723c1-a0ab-413a-ace1.
Schizophrenia is a disease that has plagued societies around the world for centuries, although it was not given its formal name until 1911. It is characterized by the presence of positive and negative symptoms. Positive symptoms are so named because of the presence of altered behaviors, such as delusions, hallucinations (usually auditory), extreme emotions, excited motor activity, and incoherent thoughts and speech. (1,2) In contrast, negative symptoms are described as a lack of behaviors, such as emotion, speech, social interaction, and action. (1,2) These symptoms are by no means concrete. Not all schizophrenic patients will exhibit all or even a majority of these symptoms, and there is some disagreement in the psychiatric community as to the exact diagnostic criteria. In addition, there is a great deal of debate as to the causes of the disease. While some proposed causes have been proven false, such as bad parenting and poor will power (2), there are many theories that remain. One of the most famous and most debatable is the dopamine hypothesis. The proposed hypothesis states that the brain of schizophrenic patients produces more dopamine than normal brains. It is this increased dopamine that is believed to be responsible for the symptoms of the disease. However, the is much debate in the scientific community as to the exact mechanism by which altered dopamine levels, especially in the prefrontal cortex, striatum, and limbic system, produce schizophrenia. There is much clinical evidense that provides support for the dopamine hypothesis. The first evidense that dopamine may be involved in schizophrenia came from amphetamine users. Amphetamines work by causing the brain to produce mo...
Schizophrenia has been defined as a mental disorder characterized by a breakdown in mental thinking and a poor emotional response. This disorganization hasn’t till now acquired a clear understanding of the mechanisms that lie behind (Harrison 1999) but researchers suggest an increase in the dopaminergic transmission in the prefrontal cortex coupled to an inhibition of the glutamatergic pathways, majorly at the level of NMDA receptors (Wen-Jun Gao). For more than 50 years, the dopamine hypothesis had been considered the mother of the theories of schizophrenia. Van Rossum first proposed it in 1966 suggesting that a hyperactivity occurring at the level of the mesolimbic dopamine pathway is the mediator of positive symptoms of schizophrenia (Seeman 1987). More research has flaunted a hypoactivity in the mesocortical dopamine pathway, which has been hypothesized to mediate the negative, cognitive, and affective symptoms of schizophrenia (Knable & Weinberg 1997; Tzschentke 2001). However, in the past two decades, hypotheses of schizophrenia focused less on the already established facts of the hyperactivity of mesolimbic dopamine neurons and under-activity of the mesocortical dopamine neurons. A major hypothesis of schizophrenia digging, to a certain extent, far from dopamine proposes that a combination of genetic factors converge on the N-methyl-D-aspartate (NMDA) receptor of the excitatory neurotransmitter glutamate, leading to neurodevelopmental abnormalities in glutamate synapse formation and ultimately resulting in the observed hypofunction at the level of NMDA receptors. Knowing that NMDA receptors regulate dopaminergic neurons, the decreased activity of NMDA receptors may be involved in the abnormal dopamine activity associated ...
There are many disorders throughout the world that affect people on a daily basis. They are life altering and life changing. They affect how a person can function on a normal level of life. This, in itself, is an interesting way of viewing the disorder, but it truly is the way that schizophrenia is viewed. The term normal is in its self a complex concept, but to understand that for the purpose of schizophrenia; normal is anything that deviates from the socially accepted way of conducting one’s self. The person affected by this disorder is drifting away from reality and, at the same time, drifting away from who they have been their whole life.
There is a definite biological basis for this disease, although it is not totally understood. For a long time schizophrenia was a mystery to doctors and scientists. Virtually any patient with a psychological disorder used to be placed under the expansive umbrella that defined the disease. Poor parenting was a misleading, early excuse for the troubles caused by what is now known to be substantially based in genetics. The most current idea of origin is that this disorder occurs during the crucial beginning months of life, those spent within the womb. Neither ...
...hizophrenia; seeing that dopamine does not trigger any negative symptoms. They state that dopamine dysfunction is purely a secondary cause of schizophrenia. In the view of these studies, schizophrenia aetiology needs further research in order to understand it better.
A study done by Puig and colleagues (2012) compared the effects of intermittent (once daily) and binge (three times a day) cocaine treatment for 1 and 14 days after the last cocaine injection on spontaneous locomotor activity and dopamine levels in the NAc in rats. The intermittent treatment led to a spontaneous increase in dopamine and in locomotor activity at the exact hour which rats were habituated to receive a cocaine injection (Puig, Noble & Benturquia, 2012). The binge treatment led to sensitization of locomotor effects of cocaine, associated to a dopamine release sensitization in the NAc (Puig, Noble & Benturquia, 2012). These results show the addictive nature of cocaine and the behavioural and sensitization effects it has on the animal, which can be related to the effects it can possibly have on humans (Puig, Noble & Benturquia,
Drug addiction is often characterized as being a complex brain disease that causes compulsive, uncontrollable, drug craving, seeking and use without any regards to the consequences they may bring upon themselves, or society. As long as the brain is exposed to these large amounts of dopamine on the reward system, it will inevitably develop a tolerance to the current dopamine levels, which it is receiving, lessening the pleasure the user will experience. In order to satisfy the brains “reward...
Drugs seem to cause surges in dopamine neurotransmitters and other pleasure brain messengers. However, the brain quickly adapts and these circuits desensitize, which allows for withdrawal symptoms to occur (3). Drug addiction works on some of the same neurobiological mechanisms that aid in learning and memories (3). "This new view of dopamine as an aid to learning rather than a pleasure mediator may help explain why many addictive drugs, which unleash massive surges of the neurotransmitter in the brain, can drive continued use without producing pleasure-as when cocaine addicts continue to take hits long after the euphoric effects of the drug have worn off or when smokers smoke after cigarettes become distasteful." (4)
Schmied, L. A., Steinberg, H., & Sykes, E. A. B. (2006). Psychopharmacology's debt to experimental psychology. History of Psychology, 9, 144-157.
and its constituents may suggest that it is multifarious in its origin (Kolb & Whishaw, 2011).
Cocaine and the Nervous System. [online] Available at: http://serendip.bryanmawr.edu/exchange.node/1739 [Accessed: 2 Oct 2013]. Donaghy, M. 2005. "The Species of Neurology.