Measurement of body temperature in neonatal mice

Goodrich, Cecilie A.

doi:10.1152/jappl.1977.43.6.1102

Cited by 22 publications

(11 citation statements)

References 3 publications

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“…Body weight, temperature and urine ketones were monitored to determine potential side effects of GH administration. Temperature was determined on the thorax using a contact thermocouple connected to a temperature readout device according to previous procedures [17]. Levels of ketones in the urine were determined by applying a small droplet of urine to the testing end of a Ketodiastix (Bayer) and verifying ketone concentration according to the color coded scale provided by the manufacturer.…”

Section: Methodsmentioning

confidence: 99%

Growth hormone regulates the sensitization of developing peripheral nociceptors during cutaneous inflammation

Liu

Green

Ford

et al. 2016

Pain

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Cutaneous inflammation alters the function of primary afferents and gene expression in the affected dorsal root ganglia (DRGs). However specific mechanisms of injury-induced peripheral afferent sensitization and behavioral hypersensitivity during development are not fully understood. Recent studies in children suggest a potential role for growth hormone (GH) in pain modulation. GH modulates homeostasis and tissue repair after injury, but how GH effects nociception in neonates is not known. To determine if GH played a role in modulating sensory neuron function and hyper-responsiveness during skin inflammation in young mice, we examined behavioral hypersensitivity and the response properties of cutaneous afferents using an ex vivo hairy skin-saphenous nerve-dorsal root ganglion (DRG)-spinal cord preparation. Results show that inflammation of the hairy hindpaw skin initiated at either postnatal day 7 (P7) or P14 reduced GH levels specifically in the affected skin. Furthermore, pretreatment of inflamed mice with exogenous GH reversed mechanical and thermal hypersensitivity in addition to altering nociceptor function. These effects may be mediated via an upregulation of insulin-like growth factor 1 receptor (IGFr1) as GH modulated the transcriptional output of IGFr1 in DRG neurons in vitro and in vivo. Afferent-selective knockdown of IGFr1 during inflammation also prevented the observed injury-induced alterations in cutaneous afferents and behavioral hypersensitivity similar to that following GH pretreatment. These results suggest that GH can block inflammation-induced nociceptor sensitization during postnatal development leading to reduced pain-like behaviors, possibly by suppressing the upregulation of IGFr1 within DRGs.

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Section: Methodsmentioning

confidence: 99%

Growth hormone regulates the sensitization of developing peripheral nociceptors during cutaneous inflammation

Liu

Green

Ford

et al. 2016

Pain

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show abstract

“…Formation of urate crystals, at this early age, may be explained by several parameters. First, urine has a more acidic pH in newborn than in adult mice (see Results); second, there is a transient increase (3-to 4-fold) in uricosuria during the first 2 weeks of life in the mouse (25); third, suckling newborn mice may not compensate for polyuria-induced dehydration by increasing milk intake (26), hence limiting the possibility to dilute urine; fourth, newborn mice are highly susceptible to hypothermia (27) favoring crystal formation. The early formation of urate crystals and similar progressive kidney morphological alterations have also been observed in hyperuricemic, hyperuricosuric uricase knockout mice, despite native renal Glut9 expression (28).…”

Section: Discussionmentioning

confidence: 99%

Glut9 is a major regulator of urate homeostasis and its genetic inactivation induces hyperuricosuria and urate nephropathy

Preitner¹,

Bonny²,

Laverrière

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

225

184

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Elevated plasma urate levels are associated with metabolic, cardiovascular, and renal diseases. Urate may also form crystals, which can be deposited in joints causing gout and in kidney tubules inducing nephrolithiasis. In mice, plasma urate levels are controlled by hepatic breakdown, as well as, by incompletely understood renal processes of reabsorption and secretion. Here, we investigated the role of the recently identified urate transporter, Glut9, in the physiological control of urate homeostasis using mice with systemic or liver-specific inactivation of the Glut9 gene. We show that Glut9 is expressed in the basolateral membrane of hepatocytes and in both apical and basolateral membranes of the distal nephron. Mice with systemic knockout of Glut9 display moderate hyperuricemia, massive hyperuricosuria, and an early-onset nephropathy, characterized by obstructive lithiasis, tubulointerstitial inflammation, and progressive inflammatory fibrosis of the cortex, as well as, mild renal insufficiency. In contrast, liver-specific inactivation of the Glut9 gene in adult mice leads to severe hyperuricemia and hyperuricosuria, in the absence of urate nephropathy or any structural abnormality of the kidney. Together, our data show that Glut9 plays a major role in urate homeostasis by its dual role in urate handling in the kidney and uptake in the liver.gout ͉ knockout ͉ nephrolithiasis ͉ uric acid

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“…Temperature was determined on the thorax using a contact thermocouple connected to a temperature readout device according to previous procedures [17]. Levels of ketones in the urine were determined by applying a small droplet of urine to the testing end of a Ketodiastix (Bayer) and verifying ketone concentration according to the color coded scale provided by the manufacturer.…”

Section: Growth Hormone Treatments and Side Effects Analysismentioning

confidence: 99%

Growth hormone regulates the sensitization of developing peripheral nociceptors during cutaneous inflammation: Erratum.

2017

PAIN

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Cutaneous inflammation alters the function of primary afferents and gene expression in the affected dorsal root ganglia (DRGs). However specific mechanisms of injury-induced peripheral afferent sensitization and behavioral hypersensitivity during development are not fully understood. Recent studies in children suggest a potential role for growth hormone (GH) in pain modulation. GH modulates homeostasis and tissue repair after injury, but how GH effects nociception in neonates is not known. To determine if GH played a role in modulating sensory neuron function and hyper-responsiveness during skin inflammation in young mice, we examined behavioral hypersensitivity and the response properties of cutaneous afferents using an ex vivo hairy skinsaphenous nerve-dorsal root ganglion (DRG)-spinal cord preparation. Results show that inflammation of the hairy hindpaw skin initiated at either postnatal day 7 (P7) or P14 reduced GH levels specifically in the affected skin. Furthermore, pretreatment of inflamed mice with exogenous GH reversed mechanical and thermal hypersensitivity in addition to altering nociceptor function. These effects may be mediated via an upregulation of insulin-like growth factor 1 receptor (IGFr1) as GH modulated the transcriptional output of IGFr1 in DRG neurons in vitro and in vivo. Afferent-selective knockdown of IGFr1 during inflammation also prevented the observed injury-induced alterations in cutaneous afferents and behavioral hypersensitivity similar to that following GH pretreatment. These results suggest that GH can block inflammation-induced nociceptor sensitization during postnatal development leading to reduced pain-like behaviors, possibly by suppressing the upregulation of IGFr1 within DRGs.

show abstract

Measurement of body temperature in neonatal mice

Cited by 22 publications

References 3 publications

Growth hormone regulates the sensitization of developing peripheral nociceptors during cutaneous inflammation

Growth hormone regulates the sensitization of developing peripheral nociceptors during cutaneous inflammation

Glut9 is a major regulator of urate homeostasis and its genetic inactivation induces hyperuricosuria and urate nephropathy

Growth hormone regulates the sensitization of developing peripheral nociceptors during cutaneous inflammation: Erratum.

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