| NeurosCIeNCe | artiCLe
paravertebral ganglia with postganglionic sympathetic cholinergic sudomotor axons30
. The effective duration of impaired sweat secretion
with botulinum toxin is much longer compared with that of impaired muscle contraction, suggesting different mechanisms in these tissues. Botulinum toxin is capable of inhibiting sweat secretion by reducing the responsiveness of the sweat gland to ACh, while not altering ACh-mediated cutaneous vasodilatation31
.
GABA The inhibiting role of GABA among the other neurotransmitters in the brain has resulted in it being sidelined when considering the skin. GABA is involved in the processes of healing and anti-inflammation, and it accentuates the proliferation of fibroblasts. It also actively contributes to immunity by working with monocytes, neutrophils, and skin lymphocytes (32). Collagen is more prolific and the orientation of better fibres and fibroblasts is facilitated in their maturation. Growth factors increase (epidermal (eGF), platelet-dervied (PdGF), and fibroblast (FGF)), which demonstrate that the regulatory action of GABA is similar to that of its activity concerning the brain. The action of GABA, or its antagonists, when applied
topically, is remarkable; after breaking the skin’s layer it accelerates its regeneration. It also has a preventive role against epidermic hyperplasia. The GABA receptor is stimulated by certain steroids (such as progesterone) and benzodiazepines. The presence of benzodiazepine receptors in keratinocytes has also been noted, and GABA features in their differentiation33
. With regard to the brain, GABA is an inhibitor and this
same function is also found in the skin. The chloride channel decreases the Ca++ (calcium) effect, contributing to homeostasis and the repair process. Pruritus may also be associated with the GABA . For example, the GABA ligand and its GABAA
system34
receptor may play a role in the pathogenesis of psoriasis, as well as for pruritus in this skin condition. The GABA release depends on the ph — an acid milieu will increase GABA. The skin ph seems to contribute to the balance of neurotransmitters.
Noradrenaline Noradrenaline increases the synthesis of melanin in melanocytes, which is a mechanism introduced by the uVBs that stimulate it. Keratinocytes have the enzyme equipment necessary for the conversion of tyrosine into adrenaline and melanin as a result. healing processes are improved by blocking the catecholamines (with propranolol)35
, and this can be used therapeutically.
Plasma noradrenaline can increase progressively with whole-body heat stress, and this is implicated in many external treatments for cellulite36
. The vasoconstriction
induced by noradrenaline can be counteracted by the vascular endothelial growth factor (VeGF), for the prevention and treatment of skin ischemia37 Lundberg et al38
. describe the following vasoconstrictor potencies of sympathetic neurotransmitters: Collagen types
Collagen I Skin, tendon, vascular, ligature, organs, bone
Collagen II Cartilage
Collagen III Reticulate (main component of reticular fibres), commonly found alongside type I
Collagen IV Forms bases of cell basement membrane
Collagen V Cell surfaces, hair and placenta
Collagen types I–III make up 80–90% of collagen in the body
prime-journal.com | July 2011 ❚ 57 L – TRYPTOPHAN Genes (IFNG, TNF-alpha) KYNURENINE (tryptophan 2,3-dioxygenase (TDO) and indoleamine 2,3-dioxygenase (IDO))
Figure 4 Life stresses disturb and modify tryptophan levels
■ Neuropeptide Y (NPY) produces a slow-acting, potent, and persistent increase in vascular contractile state ■ Noradrenaline-induced vasoconstriction develops and dissipates more quickly Adenosine
■ triphosphate
vasoconstriction has a rapid onset, but short duration. It has been postulated33
that the duration of the effects
for each transmitter relies on the unique mode of deactivation/removal. For example, the vascular effects of noradrenaline are removed quickly via noradrenaline reuptake, or rapid degradation by CoMT; whereas the prolonged duration of NPY-induced vasoconstriction is mediated by slower enzymatic degradation of ‘free’ NPY39
.
Serotonin serotonin and dopamine are often referred to as the ‘biogenic amines’. It must be remembered that if tryptophan is really the precursor of serotonin and melatonin, cortisol (and alcohol) becomes a natural hormone in order to block the action of serotonin. If the level of cortisol rises in the skin, the natural pathway providing serotonin from tryptophan is diverted, and produces kynurenine, suppressing serotonin advantages for skin rejuvenation. A vitamin B6 deficiency can enhance the kynurenine production. serotonin prevents immunosuppression, which can be a source of skin cancers40
. uVBs create a barrier to IDO IDO
Life stresses (cortisol, prolactin)
Serotonin NAS Melatonin
(ATP)-induced
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