Biological explanations of schizophrenia: Dopamine Hypothesis

The original hypothesis

HypERdopaminergia in sub cortex

• the original hypothesis states that schizophrenic patients release more dopamine into the synapse than occurs in normal individuals

• This causes neuron’s that use the transmitter ‘dopamine ‘ to fire too often transmit too many messages

• Schizophrenics were initially thought to have abnormally high numbers of D2. Receptors on receiving neuron’s in the sub cortex (central areas such as Broca’s area)

• Result is more dopamine binding to the post synaptic neuron’s and therefore more neuron’s 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 Davi’s er al 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 sub cortex specifically the limbic system which are associated with positive symptoms

• But low levels of dopamine have been found in the prefrontal cortex which only contains D1 receptors. Therefore Davi’s maintains areas causes the negative symptoms of SZ

Evidence

1. Anti psychotics

Anti psychotic drugs ( dopamine antagonist) block (lower) dopamine activity and have higher success rates in treating positive symptoms

2. L-dopa

Parkinson’s suffers have low levels of dopamine

L-dopa is a drug given to raise dopamine activity

People with Parkinson’s develop SZ symptoms if their L- dopa level is set top high

3. Amphetamines

Amphetamines such as speed, cocaine, crystal meth are dopamine agonists causing the synapse to be flooded with dopamine

Large doses lead to delusions and hallucinations in non-SZ and heighten symptoms in SZ sufferers

Evidence is mixed

P. Indicate that there is an important role fro dopamine but the evidence is mixed

E. Therefore there may be other neurotransmitters involved, drugs implicated serotonins involvement too.

E. Barlow and Durand argue both neurotransmitters are involved - clozapine blocks both of these, the earlier neuroleptics don’t.

L. Recent attention has been given to other cells and is important for learning, memory and plasticity.

Cannot explain why sufferers only recover slowly

The theory cannot explain why sufferers only recover slowly when given neuroleptic drugs as the medication (often takes 4 weeks to see any sign they are working) as the medication has an instant effect on dopamine levels. Lloyd et al believe dopamine levels may be medicated through environmental as abnormal family circumstances or social isolation can lead to high levels of dopamine.

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 relationship

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