EXPLANATION 1: DOPAMINE HYPOTHESIS-DESCRIPTION AO1 Flashcards

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1
Q

How was the link between Dopamine and Schizophrenia first established?

A
  1. Research in the 1950s looked at the role of Dopamine in Parkinson’s disease (a condition that causes tremors and slow, imprecise movements)
  2. They discovered that the drug L-Dopa increased the amount of Dopamine in the brain and reduced Parkinsonian symptoms
  3. However, when people were given L-Dopa, they demonstrated behaviours similar to that of individuals with Schizophrenia
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2
Q

What does the very first Dopamine hypothesis suggest is the cause of Schizophrenia?

A
  1. The very first version of the hypothesis proposed that Schizophrenia was simply caused by an excess of dopamine activity
  2. This caused neurons that use dopamine to fire too often and transmit too many messages
  3. This message overload may produce many of the symptoms of Schizophrenia
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3
Q

What did Delay, Deniker and Harl discover?

A

They discovered Antipsychotic drugs

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4
Q

What did Carlsson and Lindqvist discover?

A

They discovered that Antipsychotic drugs increased the metabolism of Dopamine (made it degrade more rapidly)

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5
Q

What was the last important finding?

A

Several studies showed that Amphetamine increased dopamine and could induce psychotic symptoms and Reserpine (an antipsychotic drug) reduced dopamine and could treat the psychotic symptoms

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6
Q

What did Griffith et al discover after he investigated this finding?

A

Griffith et al induced psychosis in non-schizophrenic volunteers using dextro-amphetamine (a drug that increases the amount of dopamine in the brain). He found out that the volunteers demonstrated a generally abrupt onset of paranoid delusions and demonstrated a cold and detached emotional response.

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7
Q

When was dopamine receptor sites one as a development to the original theory?

A

In the 1970s, the focus moved as researchers acknowledged various dopamine (DA) receptor sites

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8
Q

Why was the D2 receptor important at first?

A

At first, the D2 receptor seemed to be of the most importance as research found a greater volume of them in people with schizophrenia and it was impacted the most by antipsychotics.

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9
Q

Why did the focus move to the D1 receptor?

A

The focus was moved to D1 receptors and they were also found to be important due to their presence in the prefrontal cortex, which is also implicated in schizophrenia.

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10
Q

What receptor sites were discovered?

A

D1-D5

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11
Q

What were Davis et al’s findings?

A

Davis et al proposed that the effects of abnormal dopamine activity could vary by brain region. The levels of dopamine activity in the frontal lobe were low. He suggested that this may account for the negative symptoms of schizophrenia. Furthermore, he argued that the low levels of dopamine activity in the frontal regions of the brain, gave rise to consequent higher levels of dopamine activity in a region of the brain called the striatum. The increased striatal activity was being suggested as the cause of positive symptoms of schizophrenia.

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12
Q

What did Owen find through his autopsy studies?

A

Owen found that people with schizophrenia had excess receptor sites, as well as on the left amygdala.

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13
Q

What did Falkai find through his autopsy studies?

A

Falkai found that the striatal areas had increased dopamine.

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14
Q

What did David et al also suggest about the location of dopamine receptor site abnormalities?

A

Davis et al also suggested that the location of dopamine receptor site abnormalities in the brain would have varied effects. For example, low dopamine activity due to fewer D1 receptors in the prefrontal cortex would cause negative symptoms, and increased dopamine activity due to excess D2 receptors in the striatal areas would cause positive symptoms.

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15
Q

When was a more recent version of the theory developed?

A

In more recent years, the role of Dopamine in the Limbic system has been the main area of study.

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16
Q

Describe the two main dopamine pathways implicated in schizophrenia:

A

Mesolimbic pathway
Mesocortical pathway

17
Q

Mesolimbic pathway:

A

The mesolimbic pathway carries signals from the Ventral tegmental area to the nucleus accumbens. Dopamine is a major neurotransmitter in the mesolimbic pathway. Too much dopamine from neurons that fire too often or too quickly, cause overstimulation and ultimately positive symptoms of schizophrenia.

18
Q

Mesocortical pathway:

A

The mesocortical pathway carries signals from the Ventral tegmental area to the frontal lobe. Kenneth Davis et al notes that too little dopamine is evident in the D1 receptors of the frontal lobe of people with schizophrenia, which lead to the negative symptoms of schizophrenia.

19
Q

What did Frankle and Laurelle find?

A

In the last 20 years, the advancement of imaging studies has allowed researchers to track neurotransmitter function. Frankle and Laruelle have done research which has confirmed that striatal dopamine is elevated in people with schizophrenia and that such elevation is closely linked to the psychotic symptoms. In addition, imaging has also shown that blocking this elevated activity by blocking dopamine release or by blocking the postsynaptic receptors leads to a reduction of these symptoms for most patients.

20
Q

What is the Human Genome project?

A

since the second version of the dopamine hypothesis has come out, the human genome project has been undertaken. This project has successfully mapped every gene in human DNA. Consequently we are almost certain that no single gene codes for schizophrenia. There are likely to be many genes that all have a small effect on the overall picture.

21
Q

What is the Human Genome project?

A

since the second version of the dopamine hypothesis has come out, the human genome project has been undertaken. This project has successfully mapped every gene in human DNA. Consequently we are almost certain that no single gene codes for schizophrenia. There are likely to be many genes that all have a small effect on the overall picture.

22
Q

What did Talkowski et al find?

A

Talkowski et al suggested that four of the top ten genes thought to be involved are directly involved with dopamine activity.