Abstract
BackgroundPredatory stress as a psychological stressor can elicit the activation of the hypothalamic–pituitary–adrenal (HPA) axis, which is involved in the dialogue of the neuroimmunoendocrine network. The brain has been proven to regulate the activity of the HPA axis by way of lateralization. In the present study, we probed the pivotal elements of the HPA circuitry including CRH, GR and a multifunctional cytokine in behavior-lateralized mice to determine their changes when the animals were subjected to predator exposure.MethodsBehavior-lateralized mice were classified into left-pawed and right-pawed mice through a paw-preference test. Thereafter, mice in the acute stress group received a single 60-min cat exposure, and mice in the chronic group received daily 60-min cat exposure for 14 consecutive days. The plasma CS and TNF-α were determined by ELISA, the hypothalamic CRH mRNA and hippocampal GR mRNA were detected by real-time PCR, and the hippocampal GR protein was detected by western blot analysis.ResultsThe results revealed that the levels of plasma CS were significantly elevated after chronic predatory exposure in both right-pawed and left-pawed mice; the right-pawed mice exhibited a higher plasma CS level than the left-pawed mice. Similarly, the acute or chronic cat exposure could induce the release of plasma TNF-α, and the left-pawed mice tended to show a higher level after the acute stress. Chronic stress significantly upregulated the expression of hypothalamic CRH mRNA in both left-pawed and right-pawed mice. Normally, the left-pawed mice exhibited a higher GR expression in the hippocampus than the right-pawed mice. After the cat exposure, the expression of GR in both left-pawed and right-pawed mice was revealed to be greatly downregulated.ConclusionOur findings indicate that predatory stress can invoke a differential response of stressful elements in behavior-lateralized mice. Some of these responses shaped by behavioral lateralization might be helpful for facilitating adaption to various stimuli.
Highlights
Predatory stress as a psychological stressor can elicit the activation of the hypothalamic–pituitary– adrenal (HPA) axis, which is involved in the dialogue of the neuroimmunoendocrine network
The analysis demonstrated a significant effect of predatory stress [F(2,42) = 197.13; P < 0.001] but no effects of behavioral lateralization [F(1,42) = 3.50; P = 0.068] and stress × lateralization interaction [F(2,42) = 0.934; P = 0.401]
One-way analysis of variance (ANOVA) revealed that the tumor necrosis factor-α (TNF-α) levels were significantly elevated in the acute (P < 0.001) and chronic stress groups (P < 0.001) (Fig. 2a), especially in the chronic stress mice
Summary
Predatory stress as a psychological stressor can elicit the activation of the hypothalamic–pituitary– adrenal (HPA) axis, which is involved in the dialogue of the neuroimmunoendocrine network. Resembling most types of stimuli, predatory stress elicits increased activity of the hypothalamic–pituitary–adrenal (HPA) axis, which is involved in the dialogue of neuroimmunoendocrine networks. The activity of the HPA axis is modulated by a series of elements in the central loop such as corticotropin releasing hormone (CRH), adrenocorticotrophic hormone (ACTH) and glucocorticoids [8]. A stressful state might trigger the secretion of CRH from the hypothalamus; in turn, CRH activates the release of ACTH from the pituitary and stimulates the release of glucocorticoids from the adrenal cortex. All stressful elements in the circuitry orchestrate and regulate the basal activity of the HPA axis to maintain homeostasis
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