The impact of treatment on HPA axis activity in unipolar major depression

Examining the role of neuroinflammation in major depression

“…Most recently, it has been proposed that the relationship between MDD and immune processes (see Table 1) may be at least in part attributable to anomalous feedback inhibition from endogenous glucocorticoids, resulting in hyperactivity of the hypothalamic-pituitaryadrenal (HPA) axis, downstream changes in the secretion of adrenocorticotropic hormone releasing factor (ACRF), and vasopressin. Ultimately, this can result in stimulation of the pituitary gland and the facilitation of cortisol secretion from the adrenal cortex (Pariante and Lightman, 2008;McKay and Zakzanis, 2010).…”

“…The role of inflammatory cytokines has also been receiving increasing interest in depression research (see Table 2), with a specific focus on IL-6 and TNF-α; both of which have been shown to be involved in the stimulation of corticotropin-releasing hormone production and subsequently activation of the HPA axis and hypercortisolemia (McKay and Zakzanis, 2010). The resulting hyperactivity of the HPA axis in turn has been shown to trigger symptoms of depression (Udina et al, 2014), as well as changes in appetite, fatigue, difficulties with sleep, anhedonia, and decreased physical activity (Euteneuer et al, 2011).…”

Fetal hormonal programming of sex differences in depression: linking women's mental health with sex differences in the brain across the lifespan

“…Studies demonstrated elevated levels of cortisol in plasma, CSF, and 24-h urine samples, high CSF corticotrophin releasing hormone (CRH) levels, blunted responses to CRH administration, and non-suppression of cortisol secretion on the dexamethasone suppression test in MDD (Carroll et al, 1976, 1981; Jarrett et al, 1983; Nemeroff et al, 1984; Halbreich et al, 1985; Holsboer et al, 1985; Banki et al, 1987; Evans and Nemeroff, 1987; Rubin et al, 1987; Heim et al, 2001; Newport et al, 2003; Raison and Miller, 2003). HPA axis dysregulation was related to age (Nelson et al, 1984a,b; Bremmer et al, 2007), depression subtype (Brouwer et al, 2005), recurrence (Poor et al, 2004), and treatment response, albeit inconsistently (Nemeroff et al, 1991; De Bellis et al, 1993; Veith et al, 1993; McKay and Zakzanis, 2010). One potential confound was whether HPA axis dysregulation reflected clinical state or diagnostic trait.…”

Antidepressant-like Effects of Electroconvulsive Seizures Require Adult Neurogenesis in a Neuroendocrine Model of Depression

“…Successful ECT treatment is associated with normalization of hypothalamic-pituitary-adrenal (HPA) axis abnormalities in this patient population [3, 4]. The hippocampus is a limbic brain region that is particularly sensitive to excitotoxic insults that arise from elevated levels of circulating glucocorticoids, and it plays a key role in the stress response by providing negative feedback inhibition over the HPA axis[5-7].…”