From Stahl's: 'the precipitous decline in circulating and presumably brain levels of allopregnanolone hypothetically trigger the onset of a major depressive episode in vulnerable women. Rapidly restoring neurosteroid levels over a 60-hour period rapidly reverses the depression, and the 60 hour period seems to provide the time necessary for postpartum patients to accommodate their lower levels'. So the idea is the taper of the steroid is a helpful part.
Also, (also Stahl's), there are two GABA-A receptors with comprosied of different sub-units as you mentioned. Benzodiazepines bind to, cleverly named, benzodiazepine-sensitive GABA-A receptors while allopregnalone bind to their cousins- the benzodiazepine-insensitive GABA-A receptor. The former is found post-synaptically and involved with phasic, quick bursts of GABA (i.e. useful information processing) while the latter is found extrasynaptically and involved with tonic (i.e. chronic) 'tone' setting of the neuron. So they seem to have very different functions despite both involving GABA.
Stahl's goes onto say that allopregnanlone 'hypothetically could cause more efficient information processing in over excited brain circuits causing symptoms of depression', but that just seems hand-wavy to me.
From Stahl's: 'the precipitous decline in circulating and presumably brain levels of allopregnanolone hypothetically trigger the onset of a major depressive episode in vulnerable women. Rapidly restoring neurosteroid levels over a 60-hour period rapidly reverses the depression, and the 60 hour period seems to provide the time necessary for postpartum patients to accommodate their lower levels'. So the idea is the taper of the steroid is a helpful part.
Also, (also Stahl's), there are two GABA-A receptors with comprosied of different sub-units as you mentioned. Benzodiazepines bind to, cleverly named, benzodiazepine-sensitive GABA-A receptors while allopregnalone bind to their cousins- the benzodiazepine-insensitive GABA-A receptor. The former is found post-synaptically and involved with phasic, quick bursts of GABA (i.e. useful information processing) while the latter is found extrasynaptically and involved with tonic (i.e. chronic) 'tone' setting of the neuron. So they seem to have very different functions despite both involving GABA.
Stahl's goes onto say that allopregnanlone 'hypothetically could cause more efficient information processing in over excited brain circuits causing symptoms of depression', but that just seems hand-wavy to me.