artiCLe | NeurosCIeNCe | Melanocytes have receptors for hormones (e.g.
thyroid-stimulating hormones, ACTh, Msh, steroids) and neurotransmitters, and are neuroendocrine cells that communicate with langerhans cells, fibroblasts, mast cells, macrophages, and lymphocytes.
Melatonin Melatonin is the main antioxidant in the human body, the effectiveness of which goes way beyond that of a vitamin for example. It is always present when a significant oxidation process takes place, and of course, it is triggered by uV rays. When applied locally, it serves as protection and also heals burns20
, psoriasis, atopic eczema or disturbed
secretions of melatonin at the level of the brain. In psoriasis, for example, there is a high daytime level of melatonin rather than a high nighttime level. At the skin level there is no circadian rhythm. The production of melatonin takes place in
Acetylcholine Choline in combination with acetyl-CoA produces ACh, activating the parasympathetic nerve (glucose is a necessity to get acetyl-CoA). Muscular plaques are linked to ACh; botulinum toxin in its various forms attests to this. The receptors are the subject of much research 18
,
and botulinum toxin, like atropine, blocks the muscarinic receptors, as well as ACh, and reduces wrinkles as a result. Among the agonists of ACh are nicotine and muscarine.
ACh can be active in its own production Botulinum toxin is capable
of inhibiting sweat secretion by reducing the responsiveness
of the sweat gland to aCh, while not altering aCh‑mediated cutaneous vasodilatation.
the melanocytes, keratinocytes, and fibroblasts. It has a regulatory function of inflammatory cytokines, of angiogenesis, and in healing. Melatonin further protects dNA, reduces No and malondialdehyde, increases glutathione and sod, and has been revealed as a protector against melanoma. Its level of penetration clearly depends on dosage21
, and 0.01% is effective for skin
protection. In small doses it stimulates cellular proliferation, but in high doses it blocks it. A range of medications are enemies for melatonin,
such as beta blockers and calcium channel inhibitors, as well as cortisol, caffeine, and alcohol. Furthermore, an insufficient level of serotonin will result in melatonin deregulation. Melatonin is both hydrosoluble and liposoluble, and
can be induced in both milieu. The capillary level of the skin is rich in melatonin receptors, and topical lotions at 0.1% will facilitate production and hair growth. The skin’s melatonin system: ■ Comprises receptors for serotonin and melatonin ■ Allows the cutaneous synthesis of serotonin and melatonin in keratinocytes, fibroblasts, and melanocytes ■ Provides a local antioxidant action, particularly against uV rays ■ Promotes hair growth and pigmentation, and keeps melanoma under control. The melatoninergic system is permanent and
works against both internal and external stressors. one of the main roles of melatonin is as a reactive
oxygen species (ros) scavenger, particularly following the effects of uV rays or pollution. even inner oxidation, as a result of glycation for example, is counteracted by melatonin. Melatonin is an ubiquitous neurohormone able to be present both inside and outside of cells, and the skin’s natural production should be preserved, to provide a natural anti-ageing process for the skin.
56 ❚ July 2011 |
prime-journal.com nicotine, which stimulates ACh receptors23 .
via dMAe (dimethylaminoethanol). This neurotransmitter increases blood flow both locally and systemically, the property of which is decreased by derivatives of botulinum toxin. The motor innervation of the plaque, and its irrigation, influences cells and their surrounding environment, and on this depends the survival of other cells. healing is accelerated, including for those who are diabetic, by low concentrations of . Inflammation
is correlated to muscarinic ACh receptors (mAChrs); the role of the different mAChr antagonists have been used to treat skin inflammatory disorders24
Microvascular function, controlled in part by ACh, is independent of menstrual cycle variations25
. The
relaxation of arteries, induced by ACh, is reduced in the event of ovariectomy, and ros significantly increase26
. dheA treatment corrected the increased
Molecule of the hormone and neurotransmitter adrenaline
phenylephrine (Phe) contraction and the impaired ACh-induced relaxation observed in ovariectomised (oVX) rats, by an increment in No bioavailability and decrease in ros production26 suggests an important action of dheA, improving endothelial function in oVX rats by
. This
acting as an antioxidant and enhancing No bioavailability. Patients with cholinergic urticaria (Cu) show a number of small, short-lasting hives when their body core temperature increases, usually when sweating following exercise or bathing27
. The precise mechanism(s) of hive formation in Cu are not clearly
defined, other than awareness of the involvement of ACh. Thyroid hormones have also been implicated, such as histamine overexpression. Clinical evidence28
itch,
as it inhibits the release of ACh, as well as some other substances that may be involved in the itch. BoNT/A reduced the itch intensity, blood flow, and neurogenic inflammation in response to the histamine
prick test in human skin, proving the ACh–histamine coupling effect29
.
For sweat glands, the parasympathetic influence on sudomotor function is negligible, while the sympathetic influence is derived from the hypothalamus through preganglionic cholinergic neurons that synapse in the
has revealed the antipruritic effect of
botulinum toxin type A (BoNT/A). BoNT/A is believed to be effective against the sensation of
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