Acute Stress Desensitizes Hypothalamic CRH Neurons to Norepinephrine and Physiological Stress
| Autor: | Xin Fu, Marc O Fisher, Grant L. Weiss, Carly R. Stevens, Laura M. Harrison, John C. Begley, Chun Chen, Zhiying Jiang, Jeffrey G. Tasker |
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| Rok vydání: | 2020 |
| Předmět: |
endocrine system
0303 health sciences medicine.medical_specialty Chemistry 03 medical and health sciences Corticotropin-releasing hormone Norepinephrine 0302 clinical medicine Endocrinology medicine.anatomical_structure Desensitization (telecommunications) Hypothalamus Internal medicine Negative feedback medicine Excitatory postsynaptic potential Nucleus hormones hormone substitutes and hormone antagonists 030217 neurology & neurosurgery Glucocorticoid 030304 developmental biology medicine.drug |
| Popis: | Noradrenergic afferents to corticotropin releasing hormone (CRH) neurons of the hypothalamic paraventricular nucleus (PVN) provide a major excitatory drive to the hypothalamic-pituitary-adrenal (HPA) axis via α1 adrenoreceptor activation. The ascending noradrenergic afferents are recruited preferentially by physiological, rather than psychological, stress modalities.Glucocorticoids secreted in response to HPA activation feed back onto the hypothalamus to negatively regulate the HPA axis, providing a critical autoregulatory constraint that prevents glucocorticoid overexposure. Whether differential negative feedback mechanisms target stress modality-specific HPA activation is not known. Here, we reveal a desensitization of the α1 adrenoreceptor activation of the HPA axis following acute stress that is mediated by rapid glucocorticoid regulation of adrenoreceptor trafficking. Prior stress desensitized the HPA axis to subsequent physiological, but not psychological, stress. Our findings demonstrate rapid glucocorticoid suppression of adrenoreceptor signaling in CRH neurons that is specific to physiological stress activation, and reveal, therefore, a rapid, modality-selective glucocorticoid feedback mechanism. |
| Databáze: | OpenAIRE |
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