Monoamine theory of Depression Flashcards

1
Q

Fava+ Kendler (2000)

A

reserpine
leaky vesicles
reduce neuronal store of 5-HT and NA
indicated involvement of these in depression

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2
Q

Vetulani+ Nalepa (2000)

A

higher levels of MPHG+ 5-HIAA in blood/ urine

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3
Q

Maas (1975)

A

increased/ normal levels of NA

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4
Q

Asberg (1976)

A

increased/ normal levels of 5-HT

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5
Q

Spillman (2001)

A

blocking NA/5-HT receptors induces depression in remitted patients

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6
Q

Vetulani+ Nalepa (2000)

A

1st gen (MAOI/TCAs) work my increasing monoamine levels

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7
Q

Van Praag (1997)

A

amitryptilline (5-HT) good for normal NA
desipramine (NA) good for low NA
therefore 2 biological mechanisms/ subtypes

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8
Q

Pringle (2013)

A
2nd gen (SSRIs/ NSRIs) work
SNRIs= most effective
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9
Q

Caspi (2003)

A

short 5-HTT gene increases risk of MDD

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10
Q

Schloss+ Henn (2004)

A

symptoms of depression
explain therapeutic delay
-normally hypersensitised auto/post receptors
-need time to desensitise in response to drugs

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11
Q

Breedlove (2007)

A

HPA feedback loop as a stress regulator

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12
Q

Pariante+ Miller (2001)

A
higher stress-CRH-ACTH-cortisol
floods/ desensitises GR 
decreases feedback loop
increases cortisol
damages brain
MDD
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13
Q

Seyle (50s)

A

MDD associated with increased life stress

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14
Q

Auer (2005)

A

increased cortisol- neurodegeneration/ changes in receptors

reduced TL+ PFC density

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15
Q

Krystal (2013)

A

ket produces rapid AD effects, but not via monoamine pathways

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16
Q

Sramek (2002)

A

buspirone (anxiolytic) works by reducing 5-HT but has AD effects

17
Q

Fava+ Kendler (2000)

A

not all patients respond well to their Rx

18
Q

Wilner (2000s)

A

future for dopamine- its role in pleasure pathway and link to MDD cardinal symptoms

19
Q

Shorter+ Tyrer (2003)

A

should A+D be separated diagnostically?