Neurotransmitters (20)

• intro: Neurotransmitters are electrochemical messengers that transmit nerve impulses across a synapse during synaptic transmission. Excitatory NTs ensure there is a positive charge and makes the neuron more likely to fire. Inhibitory NTs have a more negative charge, meaning the neuron is less likely to fire.
• 1; AO1:

  •  original dopamine hypothesis = hyperactivity of dopamine transmission which led to positive symptoms of schizophrenia such as hallucinations
  •  post mortem examinations show that Sz brains have a higher density of dopamine receptors in the cerebral cortex compared to non schizophrenics, suggesting that those with Sz are more sensitive to dopamine
  •  Hypersensitivity of D2 receptors in the brain means that the patient may have an increased response to the presence of the NT
• 1; AO3:

  •  strength: Lieberman stated that around 75% of patients show new symptoms or an increase in symptoms after using drugs which mimic dopamine activity, such as amphetamine, this suggests that excess dopamine and hypersensitivity of dopamine receptors results in symptoms of psychosis, providing an explanation for Sz because having more receptors gives a greater opportunity for dopamine to stimulate these and cause subsequent reactions
• 1; AO3:

  •  weakness: explanation is limited, only a small proportion of those regularly using these drugs suffer from psychotic symptoms, this demonstrates that there must be differences in how peoples’ brains react to dopamine and the dopamine hypothesis is not a complete explanation
• 2; AO1:

  •  revised dopamine hypothesis = positive symptoms are caused by excess dopamine in mesolimbic pathways whilst negative symptoms are caused by a dopamine deficit in the mesocortical pathways
  •  Reduced dopaminergic activity in one area may mean that excess receptor sites develop in another area, a lack of receptors in the PFC & limbic system may lead to a lack of inhibition of receptor production in the striatum.
• 2; AO3:

  •  strength: antipsychotics alleviate the symptoms, dopamine antagonists block dopamine receptors & reduce stimulation, eliminates positive symptoms such as delusions and hallucinations, this strengthens the case for dopamine being a significant contributing factor to Sz development
  •  weakness: Alpert and Friedhoff - some patients showed no improvement after taking a dopamine antagonist, this suggests that people’s brains respond differently to dopamine and the cause of Sz may be different for different people
• 3; AO1:

  •  mesocortical pathway is the VTA to the prefrontal cortex. Its role is in motivation, emotion and executive functioning, a dopamine deficit leads to negative & cognitive symptoms such as low mood or social withdrawal
  •  mesolimbic pathway is the VTA to the basal ganglia. Its role is in decision making, attention, reward & motivation. Excess dopamine in the mesolimbic pathway leads to positive symptoms such as auditory hallucinations and delusions of grandeur.
• 3; AO3:

  •  strength: successfully explains negative symptoms, by suggesting that reduction of dopamine activity in the mesocortical pathway leads to social withdrawal & flattened emotions, strengthens the theory of neurotransmitters explaining Sz, as other explanations struggle to account for this
  •  weakness: could be reductionist, it ignores social or environmental factors & attempts to explain a complex illness using 1 small unit; excess dopamine
• 4; AO1:

  •  Glutamate - neurotransmitter which binds to NMDA receptors, regulates dopamine and is associated with positive and negative symptoms; failure in the cerebral cortex leads to negative symptoms and failure in the basal ganglia leads to positive, its role is in cognition, mood regulation & brain development so a lack of glutamate explains issues in attention, speech poverty and cognitive control
  •  Serotonin is associated with mood regulation, sleep wake cycle & body temperature. It balances dopamine levels in the mesolimbic pathway so low levels can result in positive symptoms.
• 4;AO3:

  •  strength: Lindstroem et al, a chemical used by the brain to produce dopamine - L DOPA - was administered to 10 untreated Sz patients & PET scans were used to measure activity compared to controls. They found that L DOPA was taken up more quickly in Sz patients, this suggests that people with Sz have an excess of dopamine compared to non Sz people so receptors are hypersensitive, producing an overreaction which leads to symptoms.
• 4; AO3:

  •  weakness: research is correlational, none of the research into the dopamine hypothesis has been able to establish a cause and effect between increased dopamine activity and schizophrenia, it is hard to determine whether high levels of dopamine cause Sz or whether Sz causes high dopamine levels, reducing the internal validity of the research.
• alternate and application:

  1. An alternate theory is the stress diathesis model. This may be a better explanation to neurotransmitters as it is a combination of environmental & biological factors. It suggests that environmental factors are thought to act as a trigger for a biological predisposition like increased D2 receptors. Therefore, it is a more detailed & less reductionist explanation of how Sz is caused.
• alternate and application: However, the explanation has useful applications. It suggests that if Sz is caused by a chemical imbalance, this can be treated with antipsychotic drugs which block dopamine receptors to reduce stimulation. Therefore, treatment plans can be easily formulated & this improves the individual’s quality of life & allows them to maintain stability.