Evaluate Research on the Role of Neurotransmission on BehaviourNeurotransmitters and neurotransmission have been, arguably, one of the most important discoveries to impact research in biological psychology, with their roles in affecting behavior. This essay will be outlining and evaluating the research investigating the role of neurotransmission on human behavior. However, to understand and properly analyze the results, the method and aspects of neurotransmission should first be understood. The process starts with the neuron and nerve cells. When the the nerve cell is stimulated, either from external stimuli, or internally from the body, the neuron fires electrochemical messages to the brain, in order for the body can respond to the stimuli. Neurotransmission is the way by which these messages are sent to the brain, through the nervous system. When the neuron fires, that impulse has to travel up its body, named the axon, to then release the neurotransmitter across to the next neuron, named the synapse. The neurotransmitter is the chemical that is used to transport information from from neuron to neuron, then being absorbed by the reuptake or broken down. The significance of neurotransmitter in the field of psychology related to its adverse effects on human behavior from altering memory and mood, to sexual arousal and even causing mental illnesses. This essay will look at research undertaken to investigate the effects of serotonin and acetylcholine on human behavior.One strength of research on neurotransmission is that it has been used to treat mental disorders and psychological behaviors, such as serotonin based drugs given to patients of depression, as seen in the research done by Caspi et al (2003). Serotonin is the chemical impulse that helps regulate mood, with an imbalance possibly leading to depression. Most research in this area had so far investigated the serotonin-transporter gene 5HTT, chosen because it has been seen to be correlated to the the intake of serotonin by the brain. Caspi aimed to investigate whether the 5HTT gene is linked to a higher or lower risk of depression in an individual. There were 847 participants who were all 26 years old, from New Zealand and they were split into three groups, depending on the length of the alleles on their 5HTT transporter gene. Group 1 – two short alleles, Group 2 – one short and one long allele, Group 3 – two long alleles. Participants were interviewed about stressful life events occurring after the 21st birthday and before the 26th birthday were assessed using a life-history calendar. They were then asked to fill in a “Stressful life events” questionnaire which asked them about the frequency of 14 different events – including financial, health, employment, and problems in their relationships, all occuring between the ages of 21 and 26. They were also assessed for depression. The results were that the participants with two short alleles in the 5HTTPR gene reported more depression symptoms in response to stressful life events than either of the other two groups. Those participants with two long alleles reported fewer depression symptoms. Moreover, participants with childhood trauma showed more signs of depression in adulthood, but only in adults with either one or two short alleles. While there is no direct relation between short alleles on the 5HTT gene and depression, there is a relationship between these and incidences of stress and subsequent depression. The long alleles seem to protect against suffering depression as a result of stress. The effects of the gene adaptation are dependent on environmental exposure to stress. However, this research and procedure had significant limitations, preventing it from coming to any concrete conclusions. The 5HTT gene is highly complex, and actions of other genes could not be controlled. While the stressful life events were standardised as employment, financial, housing, health and relationship, whether or not a participant experienced a certain event as stressful is highly personal. Moreover, the symptoms of depression were self-reported, although one colleague was contacted for each participant in order to verify the symptoms; self-reporting can be unreliable. Furthermore, Caspi’s theory acknowledges the interaction between both biological and environmental factors in depression. There were some participants who did not carry the gene mutation who became depressed, and it cannot be said that the gene alone caused the depression present. However, the question from the research can then be begged: can we assume that all emotion is dictated by chemicals, or is it socio-cultural? Clearly, from Caspi’s results, we can see that either external factors must be at play, or there are additional, untested chemicals affecting the participants’ moods. This renders the study unreliable, and unable to make accurate generalizations about the role of serotonin Another strength is that research has been the accurate methodology, looking at specific demographics as to eliminate any generational or cultural biases. This is shown in the research done by Crockett et al. Crockett investigated the role of serotonin on prosocial behavior, an inhibitory neurotransmitter, meaning that it does not stimulate the brain, produced in Pineal Gland. It is responsible for emotion, sleep, and mental wellbeing. Serotonin was used because it was theorized that link existed with one’s mood, but to affects one’s free will and morality seemed as though it could not be affected by a biological factor. The method used was an interview, including 30 mentally healthy participants with a mean age of 26. The experiment was done twice with two different conditions. In the first test, participants were given a dose of citalopram, and drug that blocks the rebuke of natural serotonin in one’s body, boosting its concentration. The second condition was a control test, where the participants were given a placebo with no biological effects. This was a double blind study, meaning neither the participants nor the researchers taking the results knew which test was under which condition. After all the participants had taken the dose, they were given a series of moral dilemmas in which they had to choose whether to sacrifice one live to save five. These were categorized as personal, meaning weather participant would agree to actively push someone into a train to save a group of people, or impersonal, only needing to pull a lever to make their decision. Findings showed that responses in the impersonal version were not influenced by citalopram. However, after receiving a dose of citalopram participants were less likely to push the man into the train in the personal scenarios. However, the impersonal scenarios were unaffected by the increase in serotonin. The researchers thus concluded that a boost of serotonin would only deter participants from killing another person, even if to save five others. It makes it seem only more socially unacceptable than before, and actually encourages prosocial behavior. However the method used is very likely to yield inaccurate results. AS previously stated, the method used was an interview, meaning the participants have a bias to present themselves as socially desirable, and would be more likely to showcase their morality by not actively killing the man to save the others in the personal dilemma. Another weakness is that these results could vary from culture to culture, as different societies have different views on death and justice. it is difficult to argue that only a single neurotransmitter is responsible for the behaviour. It is more likely that the neurotransmitter is only part of a more complex explanation of the behaviour, perhaps also involving cultural influences. This then poses the question: is morality dictated by neurotransmitters like serotonin, or are there sociocultural factors? Another strength is that researchers have been able to find a direct cause- effect relationship between a specific behavior and a neurotransmitter. In the case of Martinez and Kesner (1991), acetylcholine was tested. Acetylcholine is known for signaling the muscles to start or stop physical movement, and also heavily promotes learning and pattern recognition in the brain. Martinez and Kesner aimed to determine role of acetylcholine on memory, specifically memory formation. The researchers used rats as test subjects. Rats were trained to go through maze and get to the end where they received food. After they were proven to abe capable of this, Kesner injected the first group with scopolamine, which decreases the amount of acetylcholine by blocking the receptor sites. The second group was injected with physostigmine which blocks production of cholinesterase, an enzyme responsible for breaking down acetylcholine, thus increasing its amount. The third group was a control group used to measure how the rats would operate under unaltered conditions. The results showed that the first group were slower at finding their way around maze and made more errors than either the control or second group. The group injected with physostigmine both were quicker and more accurate than the other two groups. The study shows that acetylcholine affects memory, and subsequently, behavior, with memory significantly improving with and increase of acetylcholine, and a decrease severely limiting memory. One of the main strengths of Martinez and Kesner was its experimental design and application. The use of a proper experimental method with a control group made it possible to establish cause and effect relationship between levels of acetylcholine and memory. However, there were several prevalent limitations, including the ethical implications of animal drug testing. For a research to be ethically sound, the participants must confirm that they are willing to participate after being completely debriefed on the experiment, something that remains impossible when using animal test subjects, like rats. The rights of animals compared to humans can also be called into question. An acetylcholine deficiency is known to cause a decrease in normal memory function, and slow down thinking. Showing that the rats suffered psychological trauma from the researchers’ procedure would make their methods unethical. Furthermore, as to what extent these findings can be generalized to humans? Martinez and Kesner assumes that memory processes are the same for all animals, humans and rats alike. If the findings are only rat-specific, then none of the findings can be inferred for human behavior. In conclusion, from evaluating research done investigating neurotransmitters such as serotonin and acetylcholine and their effects on specific human behaviours such as mood and memory, it can be seen that neurotransmitters have a variety of effects on human behavior. However, implications of neurotransmission controlling functions such as emotion, memory, and morality exist, and should be considered when looking at research done on neurotransmission. There are also implications of applying findings of animal testing (in this case rats were used) to humans, as well as treatment of animal test subjects that could render the research unethical.