Collateral reinnervation of sweat glands

Abstract

The collateral reinnervation of mouse sweat glands has been studied by a method that allows serial evaluation of the course of reinnervation in intact animals. The method is based on the finding that the activation of secretion from newly denervated sweat glands by pilocarpine or nerve stimulation is completely absent seven days after nerve section but returns with reinnervation. These characteristics allowed serial detection of footpad sweat glands newly reinnervated by collateral sprouting of the remaining intact saphenous nerve after section of the sciatic nerve. The number of saphenous innervated glands increased five- to sevenfold and the total saphenous sweat territory was greatly expanded across the volar surface of the hind paw. There was less enlargement when the sciatic nerve was allowed to regenerate and participate in reinnervation of sweat glands. None of the reinnervated glands were dually innervated by saphenous and sciatic nerves, as is the case in normal glands. When the saphenous nerve was sectioned after saphenous collateral sprouting was complete and after sciatic regeneration had innervated an apparent maximal number of glands, the sciatic nerve reacted by advancing farther into the formerly enlarged saphenous territory and re-reinnervated many of the glands. Collateral sprouting by sudomotor axons is more abundant and more widely dispersed than reported for larger nerve fibers to skeletal muscle and to low-threshold mechanoreceptors. It more closely resembles sprouting of nociceptive axons.

A neuropathic deficit, decreased sweating, is prevented and ameliorated by euglycemia in streptozocin diabetes in rats.

“…This supports previous observations showing that sweat gland of the rat (32), mouse (15,16), and man (33, 34) that have been denervated become unresponsive to cholinergic agonists. When the denervated sweat glands in the rat and in the mouse are reinnervated they recover the response to cholinergic agonists.…”

“…In this study, the pilocarpine-induced silicone mold sweat response (SR)' (15,16) in control and in diabetic rats, in good (GC) and in poor glycemic control (PC), was quantitated in a crossover design. The end point was the number ofsweat droplets per group of foot pads although some attention was also given to size ofthe sweat droplets.…”

Correlation between GAP43 and nerve growth factor receptors in rat sensory neurons

“…The fact that such sprouting is blocked by antiserum to NGF (Diamond et al, 1987) suggests the involvement of NGF and participation of NGF-receptor-bearing neurons: the latter population is shown here also to express the GAP43 gene. By similar conjecture, the outgrowth of uninjured sympathetic neurons in response to partial denervation (Kennedy and Sakuta, 1984;Kessler, 1985) might also depend upon the presence of GAP43 within neurons and some local stimulus from denervated Schwann cells or target cells. On the other hand, uninjured motoneurons are also capable of sprouting (Brown et al.…”

Effects of Topiramate on Mouse Eccrine Sweat Gland Responsiveness to Heat Exposure

“…Consequently, sweat production is essential for heat tolerance, preventing hyperthermia, and influences performance during physical activity [18]. Sweat glands are innervated by sympathetic postganglionic axons, which, in contrast to the ordinary sympathetic innervation, use acetylcholine as the principal neurotransmitter [19][20][21].In the current study, we investigated the effects of topiramate on the responsiveness of mouse eccrine sweat glands to heat exposure and evaluated sudomotor function utilizing silicone imprints, a method that allows accurate quantitation of sweat gland secretion repeatedly over time, and following different types of nerve lesions or treatments [22][23][24][25][26][27]. Additionally, immunolabelling was used to examine the effects of topiramate on choline acetyltransferase (ChAT) in cholinergic sudomotor nerves, tyrosine hydroxylase (TH) in noradrenalinergic nerves, as well as total innervation of sweat glands (protein gene product 9.5, PGP9.5) and sweat gland acinar size.…”

“…In the current study, we investigated the effects of topiramate on the responsiveness of mouse eccrine sweat glands to heat exposure and evaluated sudomotor function utilizing silicone imprints, a method that allows accurate quantitation of sweat gland secretion repeatedly over time, and following different types of nerve lesions or treatments [22][23][24][25][26][27]. Additionally, immunolabelling was used to examine the effects of topiramate on choline acetyltransferase (ChAT) in cholinergic sudomotor nerves, tyrosine hydroxylase (TH) in noradrenalinergic nerves, as well as total innervation of sweat glands (protein gene product 9.5, PGP9.5) and sweat gland acinar size.…”