Biological explanation dopamine hypothesis

• Research in the 1950s looked at the role of the neurotransmitter dopamine in Parkinson's disease, a neurological condition which causes tremors and slow, imprecise movements. It was discovered that the drug levodopa (L-DOPA or dihydroxyphenylalanine) increased the amount of dopamine in the brain and reduced Parkinsonian symptoms.
• However what was also observed when people were given L-DOPA were behaviours similar to that of individuals with schizophrenia. As such, a link between dopamine and schizophrenia was established.
• Initially, the dopamine hypothesis was quite a basic concept. It proposed that individuals with schizophrenia simply had too much of the neurotransmitter dopamine, and as such they demonstrated symptoms related to high levels of dopamine.
• The issue with this initial hypothesis was that when drugs were administered to individuals that reduced levels of dopamine, they reduced the positive symptoms that individuals with schizophrenia were displaying but seemed to have little or no effect of the negative symptoms
• This hypothesis was supported by much research, for example in 1968, J.J. Griffith et al. induced psychosis in non-schizophrenic volunteers with the administration of dextroamphetamine (a drug that increases the amount of dopamine in the brain), finding that the volunteers demonstrated a general abrupt onset of paranoid delusions and demonstrated a cold and detached emotional response.
• In more recent years, the role of dopamine in the limbic system has been the main area of study.

  Research has been able to show the impact of antipsychotic drugs on D2 dopamine receptor sites. As D2 receptors are found primarily in subcortical regions, the limbic system became the main focus of the dopamine hypothesis.
• Research (e.g. Seeman and Lee, 1975) had shown the impact of antipsychotic drugs on this specific type of receptor. As D2 receptors are found primarily in subcortical regions, the limbic system became the main focus of the dopamine hypothesis.
• The role of dopamine in the limbic system has been the main area of study in more recent years. The limbic system consists of a variety of subcortical structures that are engaged in many functions, but most notably emotions, memory formation and arousal.
• Nerve pathways leave from the limbic system to many other subcortical structures and also to the cerebral cortex; two of the main pathways associated with schizophrenia include the mesolimbic pathway and mesocortical pathway.
• Mesolimbic pathway Dopamine is a major neurotransmitter in the mesolimbic pathway. This pathway carries signals from the ventral tegmental area to the nucleus accumbens. Too much dopamine, either from neurons that fire too often or too quickly, causes overstimulation and ultimately positive symptoms of schizophrenia such as hallucinations or delusions.
• Antipsychotic drugs reduce dopaminergic neurotransmission and as such reduce dopamine activity in this pathway and ultimately reduce the positive symptoms of many people with schizophrenia.
• Mesocortical pathway Again dopamine is a major neurotransmitter in the mesocortical pathway. This pathway carries signals from the ventral tegmental area to the frontal lobe. This nerve pathway is vital in emotional responses, motivation and cognition. 
• Kenneth Davis et al. (1991) note that too little dopamine ("hypofunction') is evident in D1 receptors of the frontal lobe of many individuals with cognitive impairments and negative symptoms of schizophrenia.