Changes in cholinergic responses of sweat glands during denervation and reinnervation

Vilches, J; Rodríguez, Francisco; Verdú, Enrique; Valero, Antoni; Navarro, Xavier

doi:10.1016/s0165-1838(98)00152-0

Cited by 8 publications

(7 citation statements)

References 48 publications

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“…In PNL mice, sweat was determined to be less on the injured side compared to healthy control subjects. This is in line with patients suffering from peripheral nerve lesions who sweat less over the cutaneous distribution of the damaged nerve (Phelps & Walker, 1977) and fits with the results on sweat output after experimental nerve lesions in the mouse (Navarro & Kennedy, 1989;Vilches, Rodriguez, Verdu, Valero, & Navarro, 1998). Beyond the expected result of neuropathic mice sweating less on the injured side, our results on PNL animals proof side-specific sweating differences for an outbred mouse strain on CD1 background.…”

Section: Discussionsupporting

confidence: 90%

Sweating disorders in mice with and without nerve lesions

Guhl

Birklein

Hirsch

2019

European Journal of Pain

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Background Hypersensitivity and altered sweating are often present in neuropathy patients. Nerve lesions are known to produce sudomotor dysfunctions but also patients suffering from complex regional pain syndrome, CRPS1—a condition without a nerve lesion—present with sweating disorders. Methods Using proton nuclear magnetic resonance of sweat water, we quantified sweat output of mice suffering from a nerve lesion or a bone fracture without nerve lesion and correlated their sweating with behavioural paw hypersensitivity accessed in von Frey testings, water applications and weight‐bearing measured with an incapacitance metre. Results Lesioned animals sweat less and are hypersensitive compared to healthy controls, as expected. Fractured animals on the injured side sweat less acutely after the injury but more in the chronic phase. They are hypersensitive acutely as well as chronically after the fracture. These findings resemble human bone trauma patients in the acute phase and CRPS patients in the chronic phase. Conclusions Sweating disorders are present both in neuropathic animals and in those with a bone fracture without nerve lesions, and autonomic dysfunctions might be considered as an important component in the aetiology of neuropathies. Significance Sweat output changes in mice after bone trauma, potentially indicative of posttraumatic processes leading to CRPS in humans.

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Section: Discussionsupporting

confidence: 90%

Sweating disorders in mice with and without nerve lesions

Guhl

Birklein

Hirsch

2019

European Journal of Pain

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“…For example, 5 days following sciatic nerve crush in mice, sweat glands in the plantar surface of the hindpaws became unresponsive to cholinergic stimulation with pilocarpine (26). Furthemore, Yaggie et al (27) reported that the pilocarpineinduced sweat rate of the forearm of healthy subjects was 0.76 mg⅐cm Ϫ2 ⅐min Ϫ1 but was only 0.11 mg ⅐cm Ϫ2 ⅐min Ϫ1 in subjects with tetraplegia.…”

Section: Discussionmentioning

confidence: 99%

Is active sweating during heat acclimation required for improvements in peripheral sweat gland function?

Buono

Numan

Claros

et al. 2009

American Journal of Physiology-Regulatory, Integrative and Comp

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We investigated whether the eccrine sweat glands must actively produce sweat during heat acclimation if they are to adapt and increase their capacity to sweat. Eight volunteers received intradermal injections of BOTOX, to prevent neural stimulation and sweat production of the sweat glands during heat acclimation, and saline injections as a control in the contralateral forearm. Subjects performed 90 min of moderate-intensity exercise in the heat (35 degrees C, 40% relative humidity) on 10 consecutive days. Heat acclimation decreased end-exercise heart rate (156 +/- 22 vs. 138 +/- 17 beats/min; P = 0.0001) and rectal temperature (38.2 +/- 0.3 vs. 37.9 +/- 0.3 degrees C; P = 0.0003) and increased whole body sweat rate (0.70 +/- 0.29 vs. 1.06 +/- 0.50 l/h; P = 0.030). During heat acclimation, there was no measurable sweating in the BOTOX-treated forearm, but the control forearm sweat rate during exercise increased 40% over the 10 days (P = 0.040). Peripheral sweat gland function was assessed using pilocarpine iontophoresis before and after heat acclimation. Before heat acclimation, the pilocarpine-induced sweat rate of the control and BOTOX-injected forearms did not differ (0.65 +/- 0.20 vs. 0.66 +/- 0.22 mg x cm(-2) x min(-1)). However, following heat acclimation, the pilocarpine-induced sweat rate in the control arm increased 18% to 0.77 +/- 0.21 mg x cm(-2) x min(-1) (P = 0.021) but decreased 52% to 0.32 +/- 0.18 mg x cm(-2) x min(-1) (P < 0.001) in the BOTOX-treated arm. Using complete chemodenervation of the sweat glands, coupled with direct cholinergic stimulation via pilocarpine iontophoresis, we demonstrated that sweat glands must be active during heat acclimation if they are to adapt and increase their capacity to sweat.

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“…Quantitative measurement methods were developed to be able to detect small differences in the rate of sweat secretion as discussed further below. Experiments were carried out using maximal agonist stimulation of sweat secretion based on reports that cholinergic agents such as pilocarpine elicit the strongest sweat response in adult rodents (Sato, 1977; Sato et al 1994; Vilches et al 1998). The rationale for inducing maximal sweat secretion was to allow detection of subtle differences in wild‐type vs. AQP5 null mice, since the effects of reduced epithelial water permeability are predicted to be seen best at high rates of active, isosmolar fluid transport.…”

Section: Discussionmentioning

confidence: 99%

“…The functional significance of this finding was investigated by comparing sweat secretion and sweat gland morphology in wild‐type mice and transgenic mice lacking AQP5. These studies required the development of novel approaches to measuring sweat secretion in mice, after having found that reported approaches involving individual gland isolation (Sato & Sato, 1978), sweat evaporation (Van Gasselt & Vierhout, 1963; Sato et al 1994), iodine/starch treatment (Tafari et al 1997; Shamsuddin & Togawa, 2000), and impression moulds (Kennedy et al 1984; Vilches et al 1998) were not sufficiently quantitative and/or reproducible for detection of potentially small differences in the knockout mice (see Discussion). Our method for measuring total paw sweat secretion involved proton nuclear magnetic resonance (NMR) of sweat water, and our method for measuring sweat secretion in individual glands involved real‐time imaging of sweat droplet accumulation under oil.…”

mentioning

confidence: 99%

Localization of aquaporin‐5 in sweat glands and functional analysis using knockout mice

Song

Sonawane

Verkman

2002

The Journal of Physiology

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Sweat secretion involves the transport of salt and water into the lumen of the secretory coil of the sweat gland. By analogy to salivary and submucosal glands, where fluid secretion is aquaporin‐5 (AQP5) dependent, we postulated that aquaporin water channels might facilitate sweat secretion. Immunolocalization with specific antibodies revealed strong expression of AQP5 at the luminal membrane of secretory epithelial cells in sweat glands in mouse paw skin. Novel quantitative methods were developed to compare sweat secretion in wild‐type mice and mice lacking AQP5. Total hindpaw sweat secretion was measured by proton nuclear magnetic resonance of sweat‐derived 1H2O in 2H2O solvent, and sweat secretion from individual glands was measured by real‐time video imaging of sweat droplet formation under oil. Sweat secretion rates after pilocarpine stimulation did not differ in wild‐type mice (0.21 ± 0.03 nl min−1 gland−1) vs. mice lacking AQP5 (0.19 ± 0.04 nl min−1 gland−1). The lack of effect of AQP5 on sweat secretion rate was confirmed by microcapillary collections of sweat from defined regions of mouse paws. Also, as by direct counting of droplets, the number of functional sweat glands was not affected by AQP5 deletion. Sweat gland morphology was similar in wild‐type and AQP5 null mice. From sweat coil geometry and gland secretion rate, the rate of fluid secretion was estimated to be 130 nl min−1 cm−2 of secretory epithelium, substantially lower than that of > 500 nl min−1 cm−2 in kidney proximal tubules and salivary glands, where active fluid absorption or secretion is aquaporin dependent. These results indicate the expression of AQP5 in sweat gland secretory epithelium, but provide direct evidence against its physiological involvement in sweat fluid secretion in mice.

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Changes in cholinergic responses of sweat glands during denervation and reinnervation

Cited by 8 publications

References 48 publications

Sweating disorders in mice with and without nerve lesions

Sweating disorders in mice with and without nerve lesions

Is active sweating during heat acclimation required for improvements in peripheral sweat gland function?

Localization of aquaporin‐5 in sweat glands and functional analysis using knockout mice

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