Neural explanations for Schizophrenia A01

Question 1

What is Seeman’s (1987) original dopamine hypothesis?

Answer 1

The brain’s neurotransmitters work differently in a patient with Sz

Dopamine is a neurotransmitter which generally has an excitatory effect and is associated with the sensation of pleasure. Unusually high levels as associated with Sz, particularly the positive symptoms.

Messages from neurone that transmit dopamine fire too easily or too often in those with Sz.

They are also thought to have abnormally high levels of D2 receptors on post-synaptic neurons, resulting in more dopamine binding and therefore more neuons firing.

it has been found that an excess of dopamine receptors in subcortical brain areas (i.e Broca’s area) may explain positive symptoms of Sz, E.g hallucinations of voices in the head/mind.

Question 2

What is the updated dopamine hypothesis by Davis (1991)?

Answer 2

High levels of dopamine are not found in all schizophrenics and the modern antipsychotic drug Clozapine with very little dopamine blocking activity, works effectively against Sz

The new hypothesis suggests that hypodopaminergia (too low dopamine) in the cortical areas of the brain, specifically the prefrontal cortex can explain negative symptoms of Sz (such as issues with cognition E.g avolition)

Therefore, one can propose that both too high (hyper) and too low (hypo) levels of dopamine in different brain areas are associated with positive symptoms of Sz.

It has also been suggested that cortical hypodopaminergia leads to subcortical hyperdopamingeria

Question 3

What does too low dopamine levels (hypodopaminergia) lead to?

Answer 3

Avolition

This is due to the prefrontal cortex being responsible for rational thinking and decision making.

Question 4

What does too high dopamine levels (hyperdopaminergia) lead to?

Answer 4

Auditory hallucinations

This is due to the Sub-cortical areas such as the Broca’s area being responsible for motor speech and speech perception/production.