Dopamine Hypothesis Flashcards

1
Q

What is dopamine?

A
  • In the brain, dopamine functions as a neurotransmitter–a chemical released by neurons (nerve cells) to send signals to other nerve cells.
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2
Q

NEUROTRANSMISSION

A
  • Neurones are brain cells which transmit and receive messages.
  • They communicate with each other via chemical messengers called neurotransmitters.
    One theory about the causes of mental disorders is that there an imbalance.
  • Neurotransmitter molecules are released from the end of the presynaptic cell (the axon) into the space between the two nerve cells (the synapse).
  • Having travelled across the synaptic gap or cleft, molecules may then be ‘taken up’ by specially shaped receptor sites on the postsynaptic nerve cell (the dendrite) and so the chemical message is passed
    on.
  • The relationship between the neurotransmitter molecule and the receptor site is like a lock and key, molecules will only fit certain receptor sites.
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3
Q

What does the dopamine hypothesis suggest?

A
  • The dopamine hypothesis, a bio-chemical explanation of schizophrenia, suggests that an EXCESS of the neurotransmitter dopamine may be responsible for schizophrenia.
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4
Q

How did this come about?

A
  • During early research into this area, it was found that patients who abused large doses of the drug amphetamine, which mimics the action of dopamine in the brain, often showed positive symptoms of psychosis, such as hallucinations and delusions.
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5
Q

Randrup and Munkvad (1966)

A
  • Randrup and Munkvad (1966) raised the dopamine levels of rats by injecting them with amphetamines (they too showed psychotic-type behaviour). This soon became coined ‘The Dopamine Hypothesis’.
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6
Q

Lieberman et al. (1987)

A
  • Lieberman et al. (1987) states that 75% of patients with schizophrenia show new symptoms or an increase in psychosis after taking drugs such amphetamine and methylphenidate, which mimic the action of dopamine in the brain
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7
Q

EXCESS DOPAMINE - HYPERDOPAMINERGIA

A
  • In the 1950’s, two antipsychotic drugs (chlorpromazine and reserpine) were found to help reduce symptoms of schizophrenia. However, both caused tremors and muscle rigidity (which are symptoms of Parkinson’s disease, a condition caused by low levels of dopamine).
  • It was therefore argued that schizophrenia may be caused by high levels of dopamine.
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8
Q

TWO EXPLANATIONS - HYPERDOPAMINERGIA

A
  • Low levels of beta hydrolyxse, an enzyme which breaks down dopamine.
  • Certain dopamine receptors (D2 receptors) may be hypersensitive to the presence of the neurotransmitter
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9
Q

DOPAMINE DEFICIENCY - HYPODOPAMINERGIA - What causes positive symptoms

A
  • Due to excess dopamine in the mesolimibic pathway
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10
Q

DOPAMINE DEFICIENCY - HYPODOPAMINERGIA - What causes negative symptoms?

A
  • May be caused by a lack of dopaminergic activity in the mesocortical pathway
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11
Q

SEROTONIN AND NEGATIVE SYMPTOMS

A
  • Clozapine (an antipsychotic drug) binds to D1 and DA dopamine receptors, but only weakly to D2
    receptors. As clozapine binds to serotonin receptors and reduces both positive and negative symptoms, it may be that irregular serotonergic activity causes schizophrenia. However, serotonin
    does regulate dopamine levels in areas such as the mesolimbic pathway.
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12
Q

Howes and Kapur (2009)

A
  • Howes and Kapur (2009) - A more recent version of the dopamine hypothesis suggests that
    dopamine dysregulation in the stratum as the common pathway to psychosis. These researchers
    suggested that attention should be paid to high presynaptic dopamine as opposed to irregularities of
    dopamine receptors. They focus on interactions between genetic, environmental and sociocultural
    factors and believe the dopamine hypothesis should be softened and viewed as an explanation of
    ‘psychosis proneness’ rather than an explanation of schizophrenia.
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13
Q

MESOLIMIBIC PATHWAY

A
  • Brain pathway
  • pleasurebale stimulus is experienced
  • the meso-limibic pathway is activated causing the nucleus to release dopamine
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14
Q

MESORTICAL PATHWAY

A
  • Linked with the reward-seeking and motivated behaviours
  • links to the prefrontal cortex
  • lack of activation is attributed to low levels of dopamine
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