Paper 4: Clinical Content- Depression (AJW)



|Neurochemical hypotheses |AO2 SUPPORT |AO2 AGAINST |

|The Catecholamine Hypothesis | | |

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|The Permissive Amine | | |

|Hypothesis | | |

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|The Dopamine Hypothesis | | |

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Biological Explanation of Uni-Polar Depression: Neuro-chemical hypotheses

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|The drug reserpine (used reduce high blood pressure) reduces| | | |

|availability of noradrenaline. When given to treat patients | |Unmedicated depressed patients do not get any |Post mortems of depressed people have not |

|with high blood pressure it has side effects of depression |Dopamine levels diminish significantly over the |worse when given drugs to reduce 5HT and |revealed any abnormality of noradrenaline |

|and suicidal tendencies. |age of 45. |noradrenaline, |concentration |

| | |(Delgado, 2000). |(Cooper, 1988) |

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| | |Using PET brain imaging it is possible to measure|Specific Serotonin Reuptake Inhibitors (SRRIs) |

| |Non-depressed Pps who have been given drugs that |the action of neurotransmitters; this technique |(e.g. Prozac) raise levels of serotonin and have |

|L Dopa is a drug which replicates the action of dopamine in |reduce 5HT levels and noradrenaline do not become|was used by Mann (1996) who was able to |a well-established antidepressant effect. |

|the brain but it has no anti-depressant effect. |depressed, (Claridge and Davis, 2003) |demonstrate that people with depression did have | |

| | |impaired serotonergic transmission. | |

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|Tricyclics increase availability of serotonin, noradrenalin |MAOIs prevent the enzyme monoamine oxidase (MAO) | | |

|and dopamine. They work by preventing the reuptake of |from breaking down the neurotransmitters and this| | |

|noradrenaline and serotonin leaving more of the transmitter |increases the levels of serotonin and | | |

|in the synaptic gap, making transmission of the next nerve |noradrenaline; it compensates for low levels of | | |

|impulse easier. They are effective in overcoming depressive |these neurotransmitters in people with depression| | |

|symptoms. |and has an anti-depressant effect. | | |

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|Post mortem studies have found increased density of |Tryptophan is a substance found in starchy foods |Antidepressants often take up to 2 weeks to start |Not everyone with depression experiences relief from|

|noradrenaline receptors in the brains of depressed |which increase serotonin levels; Delgado found that |working despite raising the levels of |serotonin-based medications. |

|suicide victims – (when neurotransmitter molecules |medicated depressive patients whose tryptophan |neurotransmitter almost immediately; therefore the | |

|are very scare, the post synaptic cell may expand |levels were reduced through diet experienced a |ways they work must be more complex than it first | |

|the number of receptor sites in order to improve |return of their symptoms. |appears, e.g. they may work by altering the | |

|chances of picking up whatever signal is available) | |sensitivity of the post-synaptic receptors, | |

| | |(Kennett, 1999) | |

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| | |Martin et al (2001) compared levels of serotonin and| |

|Not everyone with low levels of serotonin and |Noradrenaline levels were lower in Seligman’s dogs |noradrenaline in depressed Pps following either | |

|noradrenaline is depressed. |after the learnt helplessness trials but not before,|antidepressant medication or interpersonal therapy; | |

| |(Miller 1977) |therapy was as effective at increasing levels of | |

| | |neurotransmitters. | |

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