Dopamine and neural correlates

• Dopamine hypothesis of schizophrenia


  Abnormalities in the dopamine systems involved in movement and attention are responsible for schizophrenia
• Increase in dopamine activity (hyperdopaminergia) in the subcortex


  Linked to positive symptoms of schizophrenia
• Cause of increased dopamine activity


  • Abnormally high levels of D2 receptors on receiving neurons results in more dopamine binding and therefore more neurons firing
  • If this increased activity occurs in Broca's area (responsible for speech production) this could lead to auditory hallucinations and speech difficulties (such as word salad) which are symptoms of paranoid and disorganised schizophrenia
• Decrease in dopamine activity (hypodopaminergia) in the cortex


  Linked to negative symptoms of schizophrenia
• Effects of decreased dopamine activity


  • Decreased activity in the prefrontal cortex which is responsible for thinking and decision making can be linked to cognitive deficits (such as derailment) which characterise disorganised schizophrenia
• Typical antipsychotic drugs


  Have an antagonistic effect by blocking dopamine receptors
• Typical antipsychotic drugs


  • Chlorpromazine
• Thornley et al. (2003) reviewed 13 trials (1121 participants) and found that chlorpromazine was associated with better overall functioning and reduced symptom severity
• The fact that other neurotransmitters may be involved in schizophrenia has led to the evidence for the role of dopamine being inconclusive
• Noll (2009) claims antipsychotic drugs only help alleviate symptoms such as hallucinations in one-third of cases
• Some people experience such symptoms despite having normal levels of dopamine activity
• Dopamine may be just one of many causal factors involved in schizophrenia
• Strength of understanding the neurochemical processes involved in schizophrenia


  • Practical application of developing psychoactive drugs that alter levels of dopamine
  • The theory that hallucinations may be caused by excessive dopamine activity has led to the development of antagonistic drugs that decrease these levels of activity and ultimately the symptoms of schizophrenia
  • Such applications can help individuals suffering with schizophrenia to have a better quality of life
• The dopamine hypothesis is reductionistic as it can be criticised for over simplifying the complex causes of schizophrenia down to the sole action of dopamine
• There are many other neurotransmitters that have been implicated in the causes of schizophrenia other than just dopamine, for example, current research has shifted towards the role of glutamate
• The presence of psychological factors can influence the extent to which levels of dopamine affect schizophrenic symptoms for an individual
• A particular level of dopamine activity is therefore just one of a number of interacting factors and may not therefore be a complete explanation of schizophrenia
• Neural correlates of schizophrenia


  Abnormalities in structural or functional features of the brain which link to particular schizophrenic experiences
• Reduced density and volume of grey matter (neuron cell bodies) in the left temporal lobe


  • Linked to the positive symptom of auditory hallucinations
  • The upper part of the temporal lobe (superior temporal gyrus) contains the auditory cortex which is involved in perceiving and interpreting speech-based information
  • Decreased connectivity affects the ability of an individual to realise that internally generated speech is their own 'inner voice' and misattribute this to someone else, giving rise to the experience of 'hearing voices'
• Enlarged ventricles (fluid-filled gaps between brain areas)


  • Increase in size because of shrinkage or damage to the surrounding brain matter
  • Enlarged ventricles in central brain areas and the prefrontal cortex have been linked to negative symptoms of schizophrenia such as disorganised thinking and avolition
• Milev et al. (2003) found smaller temporal lobe grey matter volume was negatively correlated (as the volume of grey matter decreases, persistence of hallucinations increases) with persistence of hallucinations during follow-up, suggesting that hallucinations may have a neurological basis
• Ho et al. (2003) found that negative symptom severity was positively correlated (as ventricles increase, negative symptom severity also increases) with enlargement in frontal lobe cerebrospinal fluid volume (Pearson r = 0.44; n = 70; p<0.001), suggesting a link between schizophrenic symptoms and neurological structures
• A limitation of research into neural correlates is that it is difficult to establishing causality as it is problematic to establish an initial neural cause of schizophrenia
• Research into neural correlates fulfils scientific criteria as it uses imaging techniques like MRI and PET scans to produce objective comparisons between schizophrenic and non-schizophrenic brains
• Brain scans cannot provide a full explanation of schizophrenia and casts doubt on whether solely scientific methods can be used