Abstract
The suprachiasmatic nucleus (SCN) is required for the daily rhythm of plasma glucocorticoids; however, the independent contributions from oscillators within the different subregions of the SCN to the glucocorticoid rhythm remain unclear. Here, we use genetically and neurologically intact, forced desynchronized rats to test the hypothesis that the daily rhythm of the glucocorticoid, corticosterone, is regulated by both light responsive and light-dissociated circadian oscillators in the ventrolateral (vl-) and dorsomedial (dm-) SCN, respectively. We show that when the vlSCN and dmSCN are in maximum phase misalignment, the peak of the plasma corticosterone rhythm is shifted and the amplitude reduced; whereas, the peak of the plasma adrenocorticotropic hormone (ACTH) rhythm is also reduced, the phase is dissociated from that of the corticosterone rhythm. These data support previous studies suggesting an ACTH-independent pathway contributes to the corticosterone rhythm. To determine if either SCN subregion independently regulates corticosterone through the sympathetic nervous system, we compared unilateral adrenalectomized, desynchronized rats that had undergone either transection of the thoracic splanchnic nerve or sham transection to the remaining adrenal. Splanchnicectomy reduced and phase advanced the peak of both the corticosterone and ACTH rhythms. These data suggest that both the vlSCN and dmSCN contribute to the corticosterone rhythm by both reducing plasma ACTH and differentially regulating plasma corticosterone through an ACTH- and sympathetic nervous system-independent pathway.
Highlights
Activation of the hypothalamic-pituitary-adrenal (HPA) axis and the ultimate release of glucocorticoids (GCs) under conditions of stress is an adaptive response that is critical for the survival of all vertebrates
The suprachiasmatic nucleus (SCN) has been shown to modulate GC release, in part, by controlling the release of corticotropin-releasing hormone (CRH) from neurons in the paraventricular nucleus (PVN) of the hypothalamus, which in turn induces the release of the GC primary secretagogue, adrenocorticotropic hormone (ACTH), from the anterior pituitary gland
The goal of this experiment was to use the LD22 forced desynchrony model to determine whether the rhythmic activity of the HPA axis is associated with the 22 h rhythm, the ~25 h rhythm or both, and how oscillators in the vl- and dmSCN contribute to the plasma ACTH and corticosterone daily rhythm
Summary
Activation of the hypothalamic-pituitary-adrenal (HPA) axis and the ultimate release of glucocorticoids (GCs) under conditions of stress is an adaptive response that is critical for the survival of all vertebrates. In addition to its homeostatic response to stress, the HPA axis exhibits a characteristic daily rhythm, with peak GC secretion occurring prior to the onset of activity (i.e. morning for humans, and evening for nocturnal animals, like rats). This coinciding GC rise with the onset of activity aids in preparing the organism for the increased energetic demands of wake relative to sleep. Initial studies in rats showed that the SCN was responsible for inhibiting HPA activity at the nadir of the rhythm through vasopressinergic input to neurons in the dorsal medial nucleus of the hypothalamus (DMH), which in turn project to parvocellular regions of the PVN [3,4,5]. Further studies have suggested that the evening rise in HPA activity may be the result of stimulatory influences from the SCN via the release of vasoactive intestinal peptide (VIP) and possibly other transmitters [6]
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