Storyboard

The model articulates the classic monoaminergic hypothesis with more recent mechanisms of neuroplasticity. A functional deficit of monoaminergic neurotransmission (e.g. serotonin, extension of the neurotransmitter kinetics of E4) coexists with sustained hyperactivity of the hypothalamic-pituitary-adrenal axis in response to chronic stress, elevating cortisol levels. Elevated cortisol suppresses the production of the neurotrophic factor BDNF, which in turn is necessary both for hippocampal neurogenesis (extension of the N population dynamics of E14) and to sustain the effective learning rate of synaptic plasticity (extension of the eta parameter of E7). The net result is a reduction in the gain of the reward circuit (anhedonia) and a therapeutic response to antidepressants that follows a characteristic latency curve, consistent with the need to restore plasticity before the clinical effect manifests.

>Model

ID:('ky', 1552)

Description

ID:(0, 1552)