Biological Explanations of Schizophrenia: Dopamine Hypothesis

Dopamine

Dopamine is a neurotransmitter. Your body makes it, and your nervous system uses it to send messages between nerve cells, enhancing communication between neurons.

It can be both excitatory and inhibitory, depending on where in the brain and at what receptor site it binds t.

There are 5 dopamine receptors sites identified; D1 - D5. It has a range of effects:

It helps with focus, it is responsible for our drive and motivation, it is also central to reward system and affects movement.

The Original Hypothesis - HypERopaminergia in subcortex

The original hyp states that schizophrenic patients release more dopamine into the synapse than occurs in normal individuals.

This causes neurons that use the transmitter ‘dopamine’ to fire too often and transmit too many messages.

Schizophrenics were initially thought to have abnormally high numbers of D2 receptors on receiving neurons in the subcortex (central area’s such as Broca’s area potentially explaining speech poverty/ or auditory hallucinations)

Result is more dopamine binding to the post-synaptic neuron and therefore more neurons firing.

Certain D2 receptors are known to play a key role in guiding attention which would explain problems in perception and thoughts in schizophrenics.

The updated Hypothesis - HyPOdopaminergia in cortex

The Dopamine hypothesis was updated by Davis et al (1991) because high levels of dopamine are not found in all schizophrenics and because the modern drug clozapine only blocks dopamine a little but works effectively against the disorder.

The original hypothesis focused on high levels of dopamine in the subcortex, specifically the limbic system (central areas of the brain) which are associated with positive symptoms.

But low levels of dopamine have been found in the pre-frontal cortex (area responsible for thinking and decision-making) which in only contains D1 receptors. Therefore Davis maintains that reduced dopamine in frontal areas causes the negative symptoms on sz.

Evidence: Anti-Psychotics

• (dopamine antagonists) block (lower) dopamine activity and have high success rates in treating positive symptoms of sz.

Evidence: L-Dopa

• People who suffer from Parkinson, have low levels of dopamine

• L-Dopa is a drug given to raise dopamine activity

• People with Parkinson’s develop schizophrenia symptoms if their L-Dopa level is set too high.

Evidende: amphetamines

• Such as speed, cocaine, crystal meth are dopamine agonists causing the snaps to be flooded with dopamine.

• large doses lead to delusions and hallucinations in non-schizophrenics and heightens symptoms in sz sufferers.

Evidence: researchers

Patel et al 2010: using PET scans assessed dopamine levels in sz and normal individuals finding lower levels of dopamine in PFC of sz compared to controls - supporting the updated theory.

Wang & Deutch 2008: found cognitive impairment in the PFC of rats upon whom they had depleted dopamine

AO3: +/-Research evidence

• Studies indicated that there is an important role for Dopamine but the evidence is mixed. Therefore there many be other neurotransmitter involved: Drugs implicate Serotonin’s involvement too.

• Barlow & Durand (95) argue both neurotransmitters are involved (dopamine and serotonin) - clozapine blocks both of these, the earlier neuroleptics dont.

• Recent attention has been given to raised levels of the neurotransmitter glutamate (which helps send signals to other cells and is important for learning, memory and plasticity).

• Javitt et al 2000 found and highlighted the importance of glutamate interactions with dopamine.

• Also, several candidate genes for sz are believed to be involved in glutamate production.

-Doesn’t explain why sufferers only recover slowly

The theory cannot explain why sufferers only recover slowly when given neuroleptic drugs (often takes 4 weeks to see any sign they are working) - as the mediation has an instant effect on dopamine levels.

Lloyd et al (84) → believe dopamine levels may be mediated through environmental factors, as abnormal family circumstances or social isolation can lead to high levels of dopamine.

AO3: Which came first: Schizophrenia or Faulty Chemicals?

• Dopamine theory is correlational - it only emerged after it was discovered anti-psychotics lessen the symptoms.

• This suggests we must be cautious in presuming a cause and effect relationships.

• This relationship may exist due to backward causation: High dopamine may cause SZ, but SZ also may lead to high levels of dopamine production

Explain the differences between the orgincal dopamine hypothesis and the updated dopamine hypothesis

The original dopamine hypothesis suggests that symptoms of sz results from abnormally high levels of dopamine (leading to positive symptoms), whereas the updated dopamine hypothesis considers how some sz patients may also have abnormally low levels of dopamine, which contribute to negative symptoms.

Antipsychotic drugs are commonly used to treat sz. Using your knowledge of biological explanations, explain why these drugs may reduce positive symptoms

The dopamine hypothesis suggests sz patients have hyperdopaminergia, which means they have abnormally high levels of dopamine, and this leads to positive symptoms. Antipsychotic drugs reduce the level of dopamine (dopamine antagonist), and in turn reduce the experience of positive symptoms.