The shock of it: sympathetic activation promotes hair greying, and other updates on recent autonomic research
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EDITORIAL
The shock of it: sympathetic activation promotes hair greying, and other updates on recent autonomic research Mitchell G. Miglis1 · Nicholas Larsen1 · Srikanth Muppidi1 Received: 4 November 2020 / Accepted: 5 November 2020 / Published online: 19 November 2020 © Springer-Verlag GmbH Germany, part of Springer Nature 2020
Keywords Stress · Sympathetic · Vagus · Recording · Grey · Hair
The shock of it: sympathetic activation promotes hair greying It is well-known in popular culture that stress causes white hair. Anecdotal evidence dating back to the 1800s suggests this could be indeed the case [1], however the pathophysiological mechanisms have been poorly understood, until now. In the most comprehensive study thus far on hair greying, Zhang and colleagues studied the effect that stress has on tissue regeneration in melanocyte stem cells. The results were recently published in Nature [2]. The investigators used several mouse strains in their study that were balanced based on sex and hair cycle. In the first experiment, mice were exposed to three different types of stress and the number of unpigmented white hair was quantified over time. One of the stressors was nociception, which was achieved by inflicting pain through injectoin of resiniferatoxin, an analogue of capsaicin. The results showed that all three stressors led to increased numbers of unpigmented white hairs over time, with nociception having the strongest effect. All mice subjected to stress had an increase in serum corticosterone and norepinephrine. When mice received the opioid analgesic buprenorphine along with resiniferatoxin, catecholamines did not increase and white hair cells did not develop. To understand how stress effected the melanocyte lineage, resiniferatoxin was injected into mice during the anagen and telogen stage of the cell cycle. This resulted in a selective loss of melanocyte stem cells, however differentiated melanocytes were not affected and continued to produce pigment. When the next round of anagen started, differentiated melanocytes were not produced and unpigmented * Srikanth Muppidi [email protected] 1
Department of Neurology and Neurological Sciences, Stanford University, Palo Alto, CA, USA
hairs emerged. This suggests that melanocyte stem cells are very sensitive to stress, while differentiated melanocytes and melanin synthesis are not directly affected. As a follow-up experiment, the investigators evaluated how stress induces melanocyte stem cell loss. Resiniferatoxin injection into immunodeficient mice did not result in hair greying, suggesting that hair greying is not necessarily immunemediated. To determine whether stress-induced circulating factors have a role in the loss of melanocyte stem cells, the authors depleted glucocorticoid receptors and blocked the β2-adrenergic receptor (Adrb2). Depletion of glucocorticoid receptors resulted in ongoing hair greying in response to stress, while β2-adrenergic receptor (Adrb2) blockade prevented hair greying in response to stress. Furthermore, injection of norepi
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