The nature/nurture debate is a recurring aspect that has been illustrated in a series of studies that have considered how the environment and the role of genes on abnormal brain development. Researchers at John Hopkins University participated in four studies. Their conclusions led them to a greater understanding of nature and nurture and how this interaction can affect the risk of an individual developing schizophrenia. This essay intends to discuss the findings of the aforementioned research and draw on further evidence from biological psychology in relation to the nature/nurture debate.
Our genome or DNA is organized into genes, which pass on genetic information from one generation to the next, activation of a particular gene results in the synthesis of a particular functional protein. The construction of protein is crucial as it influences the effects of itself on cells and ultimately the organs to which they target (as cited in Watson, 2006).
The research conducted surrounding schizophrenia, has suggested this may be influenced by an element of defects within schizophrenia-risk genes and experiences of stressful events in early brain development.
These in conjunction may cause abnormalities in the developmental trajectory (as cited in The Open University 2, 2006) The researchers on Study 1 looked at the interaction of the Disrupted-in-Schizophrenia 1 (DISC1) protein, which is essential to the creation of cells in brain development, and GABA, which is a chemical essential for brain development (The OU 2, 2006).
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They bred ‘Knockout’ mice with a lower level of DISC1 in one type of neuron in the hippocampus region. They found that on a molecular level, the newborn ‘ knockout’ mice had neurons displaying the same characteristics such as size and shape, to those that were normal.
When the GABA was altered to have an opposite effect, the neurons that were newly generated and released at a faster rate, had much longer axonal projections that took indirect routes to their synaptic marks. (The OU 2, 2006) Considering the nature stance, genotypes can be the reason for detrimental alterations to developing neurons. Other genetic diseases can further evidence this, such as Huntington’s disease. Huntington’s disease is a progressive brain disorder caused by a single defective gene.
It is this gene that constructs the defective Huntingtin protein, which is responsible for abnormal development within the brain and the individual’s behavior. Moreover, if the gene is successfully passed on, it is inevitable the disease will develop (as cited in Romero, 2006), regardless of any environmental factor. In contrast to genetic explanations, researchers in study 2, investigated links to changes in the environment and its affects on their development. Newborn mice were separated from their mothers for specific periods.
They considered how this change may present itself in the brain and discovered that GABA ceased to work properly in the hippocampal region. (The OU 2, 2006).
This part of the brain, especially in humans, has an important role in the formation of long-term memory and specific pathways to areas such as the amygdala, which concerns itself with functions such as motivation and emotional response. It has been proposed that a lack of nurturing experience effects brain development. In an observation study by Francis et al (as cited in Watson 2, 2006), results found that rats born to mothers who displayed low-level nursing, displayed the same traits.
However, when pups were fostered from low level nursing mothers to a higher level of nursing dam, they themselves displayed the same traits as the higher nursing foster mother and were also motivated in the environment. Rats nursed by low-level foster caregiver also displayed low level nursing and motivation. This suggests that a nurturing environment, whether it is hereditary or not affects long term behavior. An individuals behavior and brain development is likely to be a product of their environment, however genes also do have a role to play as we have discussed, with diseases such as schizophrenia.
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Study 3 considered how stressful situations affected normal mice and mice with lower levels of DISC1 and what effects it had on the construction of neurons within the brain. What they found in DISC1 mice was larger neurons, less organized and longer axonal projections that were not following the normal trajectory of brain development. Furthermore, genetic studies have found a link between aggression and a mutant Monoamine oxidise A gene (MAOA), which does not produce MAOAP, an enzyme to breakdown neurotransmitters i. e. Serotonin.
Moffitt and Caspi built upon these findings in conjunction with the Dunedin Multidisciplinary Health and Development Study. They tested 442 individuals over 26 years and found that individuals who suffered early maltreatment were more likely to show aggression in later behavior, however that did not follow the course for all individuals. Moreover, those who had the mutant MAOA gene in addition with early maltreatment, were substantially more susceptible to producing aggressive behavior later on in life.
Human relevance to the nature nurture debate surrounding schizophrenia was also a main point for the John Hopkins researchers. They compared the genetic sequences of 2,961 individuals with and without schizophrenia and associated them to their findings from the mice experiments. They found that an individual is 1. 4 times more likely to develop the disease, if they show defective genes alleles that produce an altered DISC1 protein and one that also alters the GABA in the hippocampal region.
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This suggests that Schizophrenia is a product of not only genetics or nature, but also of the environment or nurture. The DISC1 protein in conjunction with altered GABA, not only alters brain development through axonal projections, but also affects long-term memory, emotional regulation and motivation. Another causal factor for this is stressful environments in early childhood. Therefore, the research conducted on mice and individuals with regards to Schizophrenia has contributed to the debate between nature and nurture on biological psychology when explaining potential causes.