Chronic Isoproterenol Treatment of Neonatal Rats

Klingman, Gerda I.; McKay, Genie

doi:10.1002/jps.2600620709

Cited by 3 publications

(3 citation statements)

References 17 publications

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“…hair loss by premature termination of anagen) (30,31). Also excessive chronic treatment with isoproterenol, probably leading to downregulation and desensitization of b-ARs (10,12), causes hair loss and other features of sympathetic denervation in rats (13).…”

Section: Discussionmentioning

confidence: 99%

“…Adrenergic nerve fibers also appear as single nerve fibers in the dermis (5,8) as well as around blood vessels in the subcutis (5,9). Stimulation of b-ARs affects epidermal proliferation and differentiation (10)(11)(12) and several lines of circumstantial evidence support that sympathetic skin nerves are involved in HF growth (13)(14)(15)(16)(17). For example, loss of adrenergic skin innervation has been reported to be associated with the interruption of hair follicle morphogenesis until recovery of innervation (15,16) while experimentally induced adrenergic skin hyperinnervation following denervation was associated with premature HF development and hair growth (14,17).…”

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confidence: 98%

“…In the current study, we therefore investigated whether alterations in adrenergic skin innervation or b-AR stimulation by neurotransmitters may stimulate telogen-anagen transformation of murine HFs in vivo. Using the C57BL/6 mouse model for hair research, the NAdepleting agent guanethidine was administered s.c. to transiently empty noradrenaline stores of cutaneous adrenergic nerve fiber endings (20); the neurotoxin 6-OHDA was applied s.c. to selectively destroy noradrenergic nerve fiber endings (15); and the b-AR agonist isoproterenol was studied to test the effect of b-AR stimulation (13).…”

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Hair growth‐modulation by adrenergic drugs

Peters

Maurer

Botchkarev

et al. 1999

Experimental Dermatology

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Since we have recently shown that the β2‐adrenoreceptor (β2‐AR) expression of selected regions of the hair follicle (HF) epithelium as well as the number of adrenergic nerve fibers in murine skin change in a hair cycle‐dependent manner, this has raised the possibility that adrenergic nerves may exert “trophic” functions during HF cycling. To further explore this concept, we have investigated the effect of neuro‐pharmacological manipulations on hair growth (anagen) induction in quiescent telogen mouse skin in vivo. Here, we demonstrate that subcutaneous injections of the noradrenaline (NA)‐depleting agent guanethidine, or of the neurotoxin 6‐hydroxydopaine, but not of the β2‐AR agonist isoproterenol induce a premature onset of anagen in the lower back skin of C57BL/6 mice. On day 20 after the start of treatment, more than 80% of the guanethidine‐treated mice and ca. 65% of the 6‐hydroxydopamine‐treated (6‐OHDA) mice exhibited premature skin darkening and hair growth at the site of drug application, whereas less than one‐third of all control animals showed macroscopic signs of anagen developent. This was confirmed by histology, demonstrating mature anagen VI HFs only at the immediate site of treatment with guanethidine of 6‐OHDA as opposed to resting telogen HFs in the neighboring untreated skin area. This observation further supports the concept that sympathetic nerves are intimately involved in hair growth control and invites one to explore the neuro‐pharmacological manipulation of piloneural interactions as a novel therapeutic strategy for the management of hair growth disorders.

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Section: Discussionmentioning

confidence: 99%

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confidence: 98%

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confidence: 99%

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Hair growth‐modulation by adrenergic drugs

Peters

Maurer

Botchkarev

et al. 1999

Experimental Dermatology

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