The effects of sub-chronic administration of hydrocortisone on hormonal and psychological responses to L-tryptophan in normal male volunteers

Abstract

The attenuation in GH response following hydrocortisone pre-treatment could indicate a reduction in 5-HT(1A) receptor function, although it is probable that it is attributable to the action of hydrocortisone at the pituitary level. More precise, non-neuroendocrine models of 5-HT(1A) receptor function are necessary to clarify this.

Corticosteroid-serotonin interactions in depression: a review of the human evidence

“…However, these studies were smaller and did not measure other LNAA levels. One study (Bhagwagar et al 2002a) suggests an effect of administration of hydrocortisone on L-TRP levels both in healthy controls and recovered depressed subjects but our own studies do not (Porter et al 1998(Porter et al , 2002a.…”

“…In Cushing's disease, PRL secretory dynamics are altered but there is no difference in the PRL response to TRH (Caufriez et al 1981). Furthermore, pre-treatment with a chronic schedule of hydrocortisone (see Table 1) had no effect on the PRL response to TRH in healhy volunteers (Porter et al 2002a).…”

“…A similar result was found with the sub-chronic schedule (20 mg b.d. for 1 week) (Porter et al 2002a). Both can be interpreted as an effect at the pituitary level, given the finding of a similar effect of the same pretreatments on GHRH mediated GH release (Watson et al 2000).…”

Effect of sub-chronic hydrocortisone on responses to amphetamine in normal male volunteers

“…Pretreatment medication consisted of either placebo or hydrocortisone (20 mg orally, twice daily) administered in a balanced order, double-blind, cross-over design. This subchronic dose of hydrocortisone is well tolerated and has been shown to increase urinary cortisol into the range seen in depressed patients without altering baseline prolactin (Porter et al 2002).…”

Cortisol Stress Response and in Vivo PET Imaging of Human Brain Serotonin 1A Receptor Binding

“…This relationship is of potential importance in the pathogenesis of mood disorders, because major depressive episodes are associated with trait abnormalities in the serotonin system, including 5-HT 1A receptor upregulation (Parsey et al, 2006a), and with hyperactive HPA axis responses to stress, which are state dependent (Cowen, 2010; Stetler and Miller, 2011). More severe depressive episodes, such as those characterized by psychomotor agitation or psychotic features, have more severely dysregulated HPA axis function as indicated by heavier adrenal glands, higher levels of corticotropin releasing factor (CRF) in brain tissue and cerebrospinal fluid, lower CRF receptor binding in prefrontal cortex postmortem, a blunted cortisol suppression response to dexamethasone, and greater cortisol release both at baseline and in response to social stressors (Lindy et al, 1985; Brown et al, 1986; Nemeroff et al, 1988; Arató et al, 1989; Pfennig et al, 2005; Mann et al, 2006; Melhem et al, 2016). Genetic and epigenetic associations with enhanced HPA axis stress responses have also been observed in major depressive disorder (MDD) and in those reporting early-life stress, which is a risk factor for MDD (McGowan et al, 2009; Coplan et al, 2011; Yin et al, 2016).…”