Changes in mouse sudomotor function and sweat gland innervation with ageing

Vilches, J; Ceballos, Dolores; Verdú, Enrique; Navarro, Xavier

doi:10.1016/s1566-0702(01)00359-9

Cited by 23 publications

(16 citation statements)

References 58 publications

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“…In addition, extra‐mammary odor substrates are laid down locally through the females' increased self‐licking of the nipple‐lines (in mice: Harvey & Mann, ) and by the pups' themselves through their searching and sucking activities. Thus, physiological and behavioral changes of LF and neonate pups may have the effect of locally increasing the emission and mingling of a variety of substrates bearing semiochemical significance by themselves, including amniotic fluid, nipple skin gland secretions, colostrum/milk, maternal and infantile saliva, infant's saliva‐milk coagulate, mother's and infant's facial glands' secretion (i.e., lachrymal glands: Shahan, Denaro, Gilmartin, Shi, & Derman, ; Meibomian glands: Nien et al, ), infant pedal glands (e.g., Vilches, Ceballos, Verdu, & Naval, ; Nejsum, Praetorius, & Nielsen, ; Stevens & Landis, ), maternal and infants' secretions from ano‐genital glands, and traces of urinary/fecal excretions. Several of these substrates were directly assayed here.…”

Section: Discussionmentioning

confidence: 99%

How does a newly born mouse get to the nipple? odor substrates eliciting first nipple grasping and sucking responses

Aïn

Belin

Schaal

et al. 2012

Developmental Psychobiology

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It is a mammalian female strategy to emit odor cues and signals that direct their inexperienced newborns to the nipple, and optimize their initial sucking success and, hence, viability. Here, natural odorous substrates that contribute to nipple grasping were investigated in mice, a species that has not been much scrutinized on this topic. The response of pups toward the nipples of lactating females (LF) versus nonlactating females (NLF) were first assessed right after watched birth, before and after the first suckling experience, and at 1 day old, after more extended suckling experience. It appeared that only nipples of LF induced grasping at these early ages, leading to take NLF as the baseline setting to present various odor substrates sampled from LF, viz. amniotic fluid, murine milk, LF saliva, pup saliva, LF urine, and an odorless control stimulus (water). Results indicate that: (1) only amniotic fluid and fresh milk induced nipple grasping before the first suckling experience; (2) LF saliva started inducing grasping after the first suckling experience; (3) pup saliva released grasping after 24-36 hr of suckling experience; finally (4) neither LF urine, nor water induced any nipple grasping. In conclusion, the activity of amniotic fluid and murine milk on neonatal pup behavior before any postnatal suckling experience suggests that either prenatal learning and/or predisposed olfactory mechanisms do operate, while the behavioral activation due to maternal and infantile salivas clearly depends on postnatal exposure.

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Section: Discussionmentioning

confidence: 99%

How does a newly born mouse get to the nipple? odor substrates eliciting first nipple grasping and sucking responses

Aïn

Belin

Schaal

et al. 2012

Developmental Psychobiology

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“…Taken together, these observations suggest that, in NSE-AT 1A mice, in basal conditions, vasopressin levels are not altered by increased AT 1A -receptor level and that additional mechanisms may participate in the elimination of water. Among them, sweating, salivation, and lacrimation have been reported in mice and are believed to be modulated by the RAS (18,46,47).…”

Section: Discussionmentioning

confidence: 99%

Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT₁) receptors

Lazartigues

Sinnayah²,

Augoyard³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

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(AT 1A) to blood pressure and volume homeostasis, we generated a transgenic mouse model [neuron-specific enolase (NSE)-AT 1A] with brain-restricted overexpression of AT1A receptors. These mice are normotensive at baseline but have dramatically enhanced pressor and bradycardic responses to intracerebroventricular ANG II or activation of endogenous ANG II production. Here our goal was to examine the water and sodium intake in this model under basal conditions and in response to increased ANG II levels. Baseline water and NaCl (0.3 M) intakes were significantly elevated in NSE-AT 1A compared with nontransgenic littermates, and bolus intracerebroventricular injections of ANG II (200 ng in 200 nl) caused further enhanced water intake in NSE-AT 1A. Activation of endogenous ANG II production by sodium depletion (10 days low-sodium diet followed by furosemide, 1 mg sc) enhanced NaCl intake in NSE-AT 1A mice compared with wild types. Fos immunohistochemistry, used to assess neuronal activation, demonstrated sodium depletion-enhanced activity in the anteroventral third ventricle region of the brain in NSE-AT 1A mice compared with control animals. The results show that brain-selective overexpression of AT 1A receptors results in enhanced salt appetite and altered water intake. This model provides a new tool for studying the mechanisms of brain AT 1A -dependent water and salt consumption. thirst; sodium appetite; transgenic mice; circumventricular organs; volume homeostasis; anteroventral third ventricle THERE IS SUBSTANTIAL EVIDENCE that activation of the reninangiotensin system (RAS) is involved in water and sodium intake. Thirst and sodium depletion are monitored by osmoreceptors and/or sodium receptors located at the periphery and in the brain (5). Although several candidates have been identified (6,27,28,49), the nature and mechanism of action of these receptors remain unclear. However, it is well known that systemically and brain-generated angiotensin II (ANG II) can act directly or indirectly on ANG II receptor type 1 (AT 1 ) receptors located in the lamina terminalis to produce water and salt intake (20,36). While the role and independence of centrally vs. peripherally generated ANG II in these responses still remain unclear, the pivotal involvement of central AT 1 receptors was established by studies where intracerebroventricular (ICV) administration of RAS antagonists reduced sodium appetite of sodium-depleted intact rats (41) and adrenalectomized rats (42). Furthermore, the exaggerated salt appetite observed in spontaneously hypertensive rats was reduced by central treatment with angiotensin-converting enzyme inhibitors, suggesting a role for the brain RAS in the exaggerated salt appetite in this model of hypertension (14).In rodents, water deprivation upregulates the AT 1 receptor in various areas of the brain, including the subfornical organ (SFO) and the anterior pituitary (43), as well as in the periphery (19). In addition, water and sodium intake can be abolished by pretreatment with selective antagonists ...

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“…Image analysis and immunohistochemistry quantification utilized three high-quality images (1280 × 1024 pixels) of three sections from each sample visualized by confocal microscopy and analysed with IPP Image software in the laser scanning confocal microscope to quantify parameters of paw innervation, such as sweat gland area within the secretory coil and nerve length per sweat gland. The background subtraction protocol has been previously described [31]. …”

Section: Methodsmentioning

confidence: 99%

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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Changes in mouse sudomotor function and sweat gland innervation with ageing

Cited by 23 publications

References 58 publications

How does a newly born mouse get to the nipple? odor substrates eliciting first nipple grasping and sucking responses

How does a newly born mouse get to the nipple? odor substrates eliciting first nipple grasping and sucking responses

Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT₁) receptors

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

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Changes in mouse sudomotor function and sweat gland innervation with ageing

Cited by 23 publications

References 58 publications

How does a newly born mouse get to the nipple? odor substrates eliciting first nipple grasping and sucking responses

How does a newly born mouse get to the nipple? odor substrates eliciting first nipple grasping and sucking responses

Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT1) receptors

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

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Enhanced water and salt intake in transgenic mice with brain-restricted overexpression of angiotensin (AT₁) receptors