Schizophrenia: The Dopamine Hypothesis Flashcards Preview

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Flashcards in Schizophrenia: The Dopamine Hypothesis Deck (16)
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1
Q

Define ‘neurons’.

A

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

2
Q

Define ‘neurotransmitter’.

A

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

3
Q

How does neurotransmitter relate to mental disorders?

A

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

4
Q

Briefly describe synaptic transmission, using 5 points.

A

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

5
Q

What is the rationale behind a biological theory for schizophrenia?

A

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

6
Q

What does the ‘dopamine hypothesis’ state about schizophrenia?

A

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

7
Q

What 3 ways can excess dopamine activity be explained?

A

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

8
Q

Describe the dopamine hypothesis using the 3 explanations.

A
  • 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
9
Q

How would drugs explain development of schizophrenia?

A

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

10
Q

How might amphetamines link to schizophrenia?

A

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

11
Q

How might Parkinsons’s disease link to schizophrenia?

A

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

12
Q

How might L-DOPA link to schizophrenia?

A

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.

13
Q

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

A

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

14
Q

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

A

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

15
Q

Are there any applications?

A

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

16
Q

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

A

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