The two main neurotransmitters found to be linked to aggressive behaviour are serotonin and dopamine. High levels of serotonin are said to reduce aggression by inhibiting responses to emotional stimuli that might otherwise lead to aggressive behaviour. Low levels are associated with an increase in impulsive behaviour, aggression and even violent suicide. Evidence supporting the importance of serotonin in aggressive behaviour was found in research using vervet monkeys. Raleigh et al (1991) found that if serotonin levels were reduced by altering their diet, there was an increase in aggressive behaviour whereas an increase in serotonin levels resulted in a decrease in aggressive behaviour suggesting the difference in aggression was due to the serotonin levels.
Alcohol/drugs can increase the level of dopamine (this compensates for the lack of dopamine receptors in individuals with A1 variant of the DRD2 gene). Dopamine stimulates the receptors and thud the behaviour is maintained and the individual relapses.
The hormone cortisol is thought to inhibit aggression. It is thought to do this by having a mediating effect on other hormones related to aggression such as testosterone. High levels of cortisol inhibits testosterone and so inhibits aggression. This may be due to the fact that cortisol increases anxiety and the likelihood of social withdrawal. Olweus found that higher levels of self-reported physical and verbal aggression were associated with higher levels of testosterone.
However, giving elderly people a replacement for dopamine doesn’t seem to help. Although these three neurotransmitters may be involved in depression we do not know how. Researchers investigating the endocrine (hormonal) system have found that the adrenal cortex produces cortisol and cortisone – two hormones involved in metabolism of fats, carbohydrates and proteins. Cortisol production is increased as the individual experiences stress, and this may trigger other psychological responses leading to the experience of depression. Hormonal (oestrogen and progesterone) imbalances are known to be involved in some menstruation-related depression, although the precise involvement is not known.
Many researchers, such as Crow (1985) believe there are two different types of SZ with different underlying pathology. Type 1 SZ is the type of SZ which would be associated with the Dopamine Hypothesis; it involves DA dysfunction, is characterised by positive symptoms and responds well to anti-psychotic medication. Type 2 SZ, however, is the type that is unsupportive of the Dopamine Hypothesis- it is a neurodevelopmental disorder arising from prenatal insults or perinatal insults, characterised by negative symptoms and does not respond well to antipsychotic drugs. The idea of different types of SZ suggests that DA is not the only
Outline and Evaluate the Neural Explanation of Aggression. The Neural Explanation of aggression states that aggression is caused by factors in the brain, such as decreased serotonin levels, increased testosterone, or brain damage, specifically to the frontal lobe. Kim (2002) studied patients with decreased ability to control aggression after a stroke, and found that they showed significant frontal lobe damage. This appears to suggest that people with frontal lobe damage will have a decreased ability to control their aggression; however, this study was done against patients who had recently had a stroke, meaning there are many other areas of the brain affected and different factors to consider. It is always very difficult to isolate brain damage to a specific area of the brain.
If the caudate nucleus is damaged it fails to suppress the signals from the OFC allowing the thalamus to become hyperactive. Additional inherited possibilities include lower levels of the neurotransmitter serotonin and higher levels of dopamine. Low levels of serotonin have been implicated in OCD as it has been found that antidepressant drugs which increase serotonin levels are affective in reducing symptoms of OCD. Higher levels of dopamine as suspected as a possible cause for OCD because in animals higher levels of dopamine can lead to stereotyped movements that resemble the compulsions found in OCD sufferers. Genetic explanations for OCD are supported by family and twin studies.
There are many different types of neurotransmitters. But these are the important ones. Serotonin is the aids in the spread of messages in the brain and the body. It plays a big role in regulation of mood, appetite, memory and learning. A lack of serotonin may result in low self-esteem, depression and aggression.
Support for this theory is the effect of amphetamines. These drugs work by increasing the levels of dopamine. When the drugs given to a non- schizophrenic the individual has been found to develop schizophrenic-like symptoms, this therefore suggests that the increased dopamine levels is likely to be linked to the disorder. Furthermore patients with schizophrenia have been found to have symptoms worsen when they have taken amphetamines. Grilly had found people with Parkinson’s disease (low levels of dopamine) who were taking the drug L-dopa to raise their levels of dopamine were developing schizophrenic type symptoms.
Impaired judgments due to decreased levels of inhibitions can lead to risky sexual activity. As well, those users that use intravenously increase their chances of contracting HEP B or C or HIV/AIDS. Crystal methamphetamine is not necessarily an aphrodisiac, but through increasing the level of dopamine through triggering the release of powerful brain chemicals, it may increase sex drive. Ironically, while desire and stamina are increased, it ultimately decreases the users’ sexual desirability and performance (PBS, n.d.). 6connected with the fact that crystal meth can suppress one’s appetite.