Schizophrenia: The Dopamine Hypothesis

Question 1

Define ‘neurons’.

Answer 1

Brain cells that transmit and receive messages through communication with neurotransmitters.

Question 2

Define ‘neurotransmitter’.

Answer 2

A chemical substance that transfers an electrical impulse by diffusion at the synapse.

Question 3

How does neurotransmitter relate to mental disorders?

Answer 3

One theory states that mental disorders are caused through imbalance of neurotransmitters.

Question 4

Briefly describe synaptic transmission, using 5 points.

Answer 4

1) The electrical impulse travels down the axon terminal and stimulates the vesicles full of neurotransmitters
2) The vesicles then move down the pre-synaptic neuron to fuse with the pre-synaptic membrane
3) The neurotransmitters are then released as chemical messengers and diffuse across the synaptic gap
4) They attach to the corresponding receptor on the dendrite of the post-synaptic neuron and will then be absorbed
5) Any neurotransmitters that are not absorbed will get reabsorbed by the pre-synaptic neuron in the process of reuptake through the transporters

Question 5

What is the rationale behind a biological theory for schizophrenia?

Answer 5

If schizophrenia can be inherited genetically then bio-chemical abnormalities should be detectable.

Question 6

What does the ‘dopamine hypothesis’ state about schizophrenia?

Answer 6

Chemical imbalance through excess dopamine in the brain causes schizophrenic symptoms.

Question 7

What 3 ways can excess dopamine activity be explained?

Answer 7

1) Through excess release by the axon
2) Having too many dopamine receptors
3) Over-sensitivity of the receptors

Question 8

Describe the dopamine hypothesis using the 3 explanations.

Answer 8

• Patients having more D2 receptors means more dopamine can bind to them which could lead to over-sensitivity that can occur through genetic inheritance
• Positive symptoms, such as paranoia, are therefore caused by over-activation of the D2 receptors
• The meso-limbic pathway is the reward and fear pathway that can contribute to positive symptoms when there is an excess of dopamine that causes intensified emotions
• The meso-cortical pathway is essential for normal cognitive function and so abnormalities here such as flooding of dopamine may lead to negative symptoms
• Some research suggests a lack of dopaminergic activity in one area of the brain could cause a spike in another such as the pre-front cortex which could be indirectly linked with schizophrenia
• low levels of beta-hydroxalase

Question 9

How would drugs explain development of schizophrenia?

Answer 9

They change the neurochemicals within the brain and so may cause and imbalance.

Question 10

How might amphetamines link to schizophrenia?

Answer 10

They give similar symptoms to those of excess dopamine through flooding the synapse with this neurotransmitter which can cause psychosis.

Question 11

How might Parkinsons’s disease link to schizophrenia?

Answer 11

These people suffer from low levels of dopamine whereby they take drugs to increase activity that correlate to developing schizophrenic symptoms.

Question 12

How might L-DOPA link to schizophrenia?

Answer 12

L-DOPA is a chemical that the brain uses to produce dopamine therefore taking drugs that use this chemical may cause an onset of schizophrenia.

Question 13

Using the acronym ‘EACH’, evaluate 2 ‘evidence’ points.

Answer 13

P - Lindstroem et al (1999) supports
E - He used PET scans to compare L-DOPA uptake of people with and without schizophrenia and found that those with schizophrenia took it up quicker
E - This therefore suggests that people with schizophrenia have more D2 receptors
P - Falkai (1988) supports
E - He found that there was an increased amount of dopamine activity in schizophrenia patients when conducting post-mortems
E - Therefore showing that higher levels of dopamine activity correlates with schizophrenic symptoms

Question 14

Using the acronym ‘EACH’, evaluate 2 ‘how’ points.

Answer 14

P - Lindstroem et al (1999) has high reliability
E - He used PET scans to trace the chemical L-DOPA which produce scientific and objective data
E - This can be replicated and compared easily
P - Can’t establish cause and effect
E - No research into the dopamine hypothesis has been able to establish whether schizophrenia is the consequence or cause of increased dopamine activity
E - Therefore it’s difficult to establish whether increased dopamine activity causes schizophrenia or is a result of it

Question 15

Are there any applications?

Answer 15

P - Yes
E - It states that increased dopamine activity could be an explanation of schizophrenia
E - Therefore medication can be used to combat this or further research can be done to establish finality on whether or not dopamine affects schizophrenia

Question 16

Using the acronym ‘EACH’, evaluate 2 ‘criticisms’ points.

Answer 16

P - Some research uses animal studies
E - Animals such as rats have qualitative differences in the brain
E - Therefore results cannot be fully generalised as human brains are more complex with added features
P - Reductionist
E - Faustman et al (1999) found low levels of the neurotransmitter glutamate in patients with schizophrenia
E - Therefore it only focuses on dopamine which disregards other neurotransmitters and social factors that could cause development of schizophrenia