Functional sudomotor responses to cholinergic agonists and antagonists in the mouse

Vilches, J; Navarro, Xavier; Verdú, Enrique

doi:10.1016/0165-1838(95)00033-t

Cited by 28 publications

(16 citation statements)

References 36 publications

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“…While clear cells secrete water and electrolytes, the major components of sweat, dark cells secrete glycoproteins, the most prominent protein constituents in sweat, and have also been suggested to have other functions [18]. In the current study, PGP9.5-, ChAT-and TH-ir nerve fibres were distributed throughout the pad, similar to that previously reported [32,33]. PGP9.5 immunoreactive fibres innervated the secretory coils of the sweat glands, forming a plexus at the boundary between the dermis and epidermis.…”

Section: Immunohistochemistrysupporting

confidence: 75%

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

Jiyu¹,

Huang²,

Deng³

et al. 2007

Basic Clin Pharma Tox

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Young mice (2 weeks old) were given topiramate daily for 1 month, and sudomotor function was evaluated utilizing impression mould techniques to determine the number of sweat glands reactive to heat exposure and sweat output per gland on the plantar surface of mice hind-paws. Immunohistochemical quantitation of protein gene product 9.5, choline acetyltransferase and tyrosine hydroxylase in footpads was determined after topiramate treatment. While a 25% decrease in the number of secreting sweat glands and a 42% decline in sweat output per gland were observed following topiramate treatment, no significant differences were noted in sudomotor innervation, expressed as length of choline acetyltransferase, tyrosine hydroxylase and protein gene product 9.5 immunoreactive nerve profiles in single secretory coils or in sweat gland sizes within the secretory coil area. Long-term topiramate stimulation resulted in a reduction in the number of reactive sweat glands, without changes in sweat gland innervation, suggesting that the diminished responsiveness of the glands to heat exposure induced by topiramate might have resulted from a decrease in the intrinsic regulatory activity of sweat glands, as opposed to the loss of periglandular neurotransmitters or the impairment of the structure of the glands. [12][13][14][15][16][17]. While the effect was reversible, and disappeared with the cessation of the treatment, the mechanism underlying this effect on sweating has not been fully elucidated. The ability of human beings to dissipate heat during exercise and in hot environments depends mainly on the evaporation of sweat secreted by eccrine sweat glands. 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. The aim of this study was to investigate whether topiramate reduced the responsiveness of the glands to heat exposure in mice, and whether the effects on the eccrine sweat glands were related to changes in periglandular neurotransmitters and/or sweat gland structure. Materials and MethodsExperimental design. Animals were housed under standard conditions with water and foo...

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Section: Immunohistochemistrysupporting

confidence: 75%

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

Jiyu¹,

Huang²,

Deng³

et al. 2007

Basic Clin Pharma Tox

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“…M 3 -muscarinic receptors also mediate the effects of acetylcholine on the bladder detrusor and intestinal smooth muscle (causing contraction), vascular smooth muscle (causing nitric oxide synthesis in the endothelium and subsequent vasodilation; for review, see ref. 18), and eccrine sweat glands (27)(28)(29), and are present in iris sphincter muscle (30). In our preliminary study, the autoantibodies seemed to be associated with bladder symptoms and other autonomic features (see Table 1).…”

Section: Discussionmentioning

confidence: 97%

Inhibitory effects of muscarinic receptor autoantibodies on parasympathetic neurotransmission in Sjögren's syndrome

Waterman

Gordon

Rischmueller

2000

Arthritis & Rheumatism

219

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Objective. Sjögren's syndrome (SS) is an autoimmune disorder characterized by dry eyes and mouth (sicca syndrome) and lymphocytic infiltration of the lacrimal and salivary glands. Abnormalities of parasympathetic neurotransmission may contribute to the glandular dysfunction. In this study, we used a functional assay to investigate autoantibody-mediated effects on parasympathetic neurotransmission and smooth muscle contraction.Methods. Serum and purified IgG were obtained from patients with primary and secondary SS and from control subjects. Contraction of isolated bladder strips in response to stimulation of M 3 -muscarinic receptors by a muscarinic receptor agonist, carbachol, or by endogenous acetylcholine released from postganglionic parasympathetic nerves was measured before and after the addition of patient serum or IgG.Results. Sera from 5 of 9 patients with primary SS and from 6 of 6 patients with secondary SS inhibited carbachol-evoked bladder contraction by ϳ50%. Sera from these patients also inhibited the action of neuronally released acetylcholine at M 3 -muscarinic receptors. Sera from 7 of 8 healthy individuals, from patients with rheumatoid arthritis without sicca symptoms, and from patients with systemic lupus erythematosus had no effect. The anti-muscarinic receptor activity was localized in the IgG fraction, since purified IgG from patients with SS also inhibited agonist-and nerve-evoked contractions. In this preliminary study, the autoantibodies seemed to be associated with the presence of bladder symptoms and other autonomic features.Conclusion. Autoantibodies that act as antagonists at M 3 -muscarinic receptors on smooth muscle occur in a subset of patients with primary and secondary SS. Their presence in secondary SS was unexpected and provides new evidence for a common pathogenetic link between primary and secondary SS. These autoantibodies appear to contribute to sicca symptoms and may explain associated features of autonomic dysfunction in some patients.

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“…22,48 In order to abolish emotional or basal sweating, the distal innervation of the paw was blocked by injecting 0.05 mL of 0.75% bupivacaine at the ankle before the injection of pilocarpine. 49 Pain sensibility was tested by light pricking with a needle at five areas, from the most proximal pad to the tip of the second digit on the plantar aspect of the hindpaw, under a dissecting microscope. A subjective score to pinprick (PP) was assigned from no response (0), reduced or inconsistent responses (1), to normal reaction (2) in each area tested.…”

Section: Methodsmentioning

confidence: 99%

Physiological and immunohistochemical characterization of cisplatin-induced neuropathy in mice

et al. 1999

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Functional sudomotor responses to cholinergic agonists and antagonists in the mouse

Cited by 28 publications

References 36 publications

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

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

Inhibitory effects of muscarinic receptor autoantibodies on parasympathetic neurotransmission in Sjögren's syndrome

Physiological and immunohistochemical characterization of cisplatin-induced neuropathy in mice

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