For more information on the hair-raising study check out the link below.
Study featured in Plos ONE scientific journal.
CRF Receptor Antagonist Astressin-B Reverses and Prevents Alopecia in CRF Over-Expressing MiceMore than half a century ago, Hans Selye, the father of the stress concept in biology, stated that “an intense psychic shock may also exert pronounced effects on the hair, e.g., graying and generalized loss of hair” . Subsequent cumulative experimental and clinical evidence indicates indeed, that chronic stress exerts a profound inhibitory effect on hair growth –. Corticotropin-releasing factor (CRF), adrenocorticotropic hormone (ACTH) and glucocorticoids not only are key components of the endocrine and neuroimmune responses to stress but also they interrupt hair follicle growth cycle in humans and mice , , , . In cultured human scalp hair follicles, CRF up-regulates transcription of pro-opiomelanocortin (POMC) and immunoreactivity of ACTH and α-melanocyte-stimulating hormone (MSH), and increases cortisol secretion . Slominski et al. ,  have also shown that CRF, urocortin 1 and CRF receptor subtypes 1 and 2 (CRF1 and CRF2) are expressed in the normal skin and cycling hair follicles of humans and mice.
Mice that over-express CRF (CRF-OE) have been characterized as a model of chronic stress that captures phenotypes of behavioral, endocrine, immunological, autonomic and visceral alterations beside Cushing's syndrome manifestations –. While a number of mouse mutants generated by targeting specific pathways involving hair follicle cycle resulted in nude mice or models of inflammatory alopecia , , , the CRF-OE mouse has not been examined so far as a model relevant to chronic stress-induced alopecia, despite an initial report that CRF-OE mice develop bilateral symmetric hair loss in adulthood .
Based on existing evidence that chronic stress impairs hair growth and that major components of the CRF system are expressed in the mouse and human skin , , we investigated the ability of CRF receptor antagonists to influence hair loss/re-growth in CRF-OE mice. We assessed whether blocking CRF receptors by short-term peripheral treatment with the long acting peptide CRF1/CRF2 receptors antagonist, astressin-B  would induce hair re-growth and pigmentation in adult alopecic CRF-OE mice and prevent the development of alopecia in young CRF-OE mice. We also investigated the specificity of the CRF antagonist action on hair growth or whether it would also affect elevated plasma corticosterone levels and other Cushing-like phenotypes (such as hypertrophy of the adrenal glands and increased adipose deposits) . Lastly, we tested under similar conditions whether the selective CRF1 receptor non peptide antagonist, NBI 27914 , the selective CRF2 receptor peptide antagonist, astressin2-B  or a commercial drug, minoxidil  exert effects on hair growth and pigmentation.
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