Monoamine theory of Depression Flashcards
Fava+ Kendler (2000)
reserpine
leaky vesicles
reduce neuronal store of 5-HT and NA
indicated involvement of these in depression
Vetulani+ Nalepa (2000)
higher levels of MPHG+ 5-HIAA in blood/ urine
Maas (1975)
increased/ normal levels of NA
Asberg (1976)
increased/ normal levels of 5-HT
Spillman (2001)
blocking NA/5-HT receptors induces depression in remitted patients
Vetulani+ Nalepa (2000)
1st gen (MAOI/TCAs) work my increasing monoamine levels
Van Praag (1997)
amitryptilline (5-HT) good for normal NA
desipramine (NA) good for low NA
therefore 2 biological mechanisms/ subtypes
Pringle (2013)
2nd gen (SSRIs/ NSRIs) work SNRIs= most effective
Caspi (2003)
short 5-HTT gene increases risk of MDD
Schloss+ Henn (2004)
symptoms of depression
explain therapeutic delay
-normally hypersensitised auto/post receptors
-need time to desensitise in response to drugs
Breedlove (2007)
HPA feedback loop as a stress regulator
Pariante+ Miller (2001)
higher stress-CRH-ACTH-cortisol floods/ desensitises GR decreases feedback loop increases cortisol damages brain MDD
Seyle (50s)
MDD associated with increased life stress
Auer (2005)
increased cortisol- neurodegeneration/ changes in receptors
reduced TL+ PFC density
Krystal (2013)
ket produces rapid AD effects, but not via monoamine pathways