BACKGROUND: Numerous interactions between the brainstem locus coeruleus system and the HPA axis have been shown in experimental animals. This relationship is less well characterized in humans and little is known about the influence of psychiatric disorders, which disturb one of these systems, on this relationship. METHODS: Untreated subjects with pure MDD (n = 13), MDD with comorbid anxiety disorders (n = 17), and pure anxiety disorders (n = 15) were recruited by advertising. Age and sex matched control subjects were recruited for each subject with a psychiatric diagnosis (n = 45). All subjects underwent a social stressor, the Trier Social Stress Test (TSST), and blood was collected for ACTH assay. These same subjects also underwent a clonidine challenge study for assessment of growth hormone release as a marker of tonic noradrenergic activation. RESULTS: Examining log transformed area under the curve response for each hormone, a significant negative relationship (simple regression) was observed between systems in normal subjects. This relationship was preserved in anxiety subjects. However, both pure depressed and comorbid depressed and anxiety subjects demonstrated disruption of this relationship. CONCLUSIONS: Under normal circumstances, noradrenergic systems can influence the magnitude of the HPA axis response to stress. However, in subjects with major depression, HPA axis activation appears autonomous of noradrenergic influence.
BACKGROUND: Numerous interactions between the brainstem locus coeruleus system and the HPA axis have been shown in experimental animals. This relationship is less well characterized in humans and little is known about the influence of psychiatric disorders, which disturb one of these systems, on this relationship. METHODS: Untreated subjects with pure MDD (n = 13), MDD with comorbid anxiety disorders (n = 17), and pure anxiety disorders (n = 15) were recruited by advertising. Age and sex matched control subjects were recruited for each subject with a psychiatric diagnosis (n = 45). All subjects underwent a social stressor, the Trier Social Stress Test (TSST), and blood was collected for ACTH assay. These same subjects also underwent a clonidine challenge study for assessment of growth hormone release as a marker of tonic noradrenergic activation. RESULTS: Examining log transformed area under the curve response for each hormone, a significant negative relationship (simple regression) was observed between systems in normal subjects. This relationship was preserved in anxiety subjects. However, both pure depressed and comorbid depressed and anxiety subjects demonstrated disruption of this relationship. CONCLUSIONS: Under normal circumstances, noradrenergic systems can influence the magnitude of the HPA axis response to stress. However, in subjects with major depression, HPA axis activation appears autonomous of noradrenergic influence.
Authors: Jessica M Richards; Brooke A Stipelman; Marina A Bornovalova; Stacey B Daughters; Rajita Sinha; C W Lejuez Journal: Biol Psychol Date: 2011-07-07 Impact factor: 3.251
Authors: Jonathan Evans; Ke Xu; Jon Heron; Mary-Anne Enoch; Ricardo Araya; Glyn Lewis; Nic Timpson; Simon Davies; David Nutt; David Goldman Journal: Am J Med Genet B Neuropsychiatr Genet Date: 2009-03-05 Impact factor: 3.568
Authors: Anna Valenzano; Fiorenzo Moscatelli; Antonietta Messina; Vincenzo Monda; Raffaele Orsitto; Giovanna Zezza; Giovanni Fiorentino; Monica Salerno; Antonio I Triggiani; Andrea Viggiano; Maria P Mollica; Marco Carotenuto; Marcellino Monda; Giuseppe Cibelli; Giovanni Messina Journal: Front Physiol Date: 2018-05-07 Impact factor: 4.566