Neurobiology of skin appendages: Eccrine, apocrine, and apoeccrine sweat glands

Abstract

Eccrine sweat gland innervation is mostly cholinergic: The major neurotransmitter released from the periglandular nerve endings is acetylcholine, whose concentration determines the sweat rate in humans. Eccrine sweat glands express various muscarinic acetylcholine receptor subtypes and eccrine sweat secretion can be blocked effectively by anti-muscarinic substances. Eccrine sweat secretion can be blocked effectively by botulinum toxin (BTX): Botulinum neurotoxins are metalloproteases that cleave SNARE (soluble n-ethylmaleimide sensitive factor attachment protein receptor) proteins, thereby inhibiting the trafficking process of acetylcholine vesicles, their fusion with pre-synaptic membranes and finally the release of acetylcholine. Dermcidin (DCD): Patients suffering from atopic dermatitis have reduced DCD concentrations in eccrine sweat. Therefore, in contrast to healthy patients, sweating does not lead to a reduction of bacteria on the skin. Frey's syndrome: This pathological state of gustatory sweating which affects the area of the cheek can occur after parotid surgery due to disruption of parasympathetic secretomotor fibers. These fibers anastomose with sudomotor sympathetic fibers of the skin, thereby gaining control of sweat gland activity. Apocrine sweat gland innervation is believed to be adrenergic: The apocrine secretion is controlled via epinephrine and norepinephrine but it is still unclear whether activation of apocrine glands takes place via sympathetic innervation or via circulating catecholamines. Cystic fibrosis: Patients suffering from cystic fibrosis show increased sweat chloride levels due to a defect in CFTR, which plays an important role in chloride reabsorption from sweat. © 2009 Springer Berlin Heidelberg.