Anandamide deficiency and heightened neuropathic pain in aged mice

Damaging of peripheral nerves may result in chronic neuropathic pain for which the likelihood is increased in the elderly. We assessed in mice if age-dependent alterations of endocannabinoids contributed to the heightened vulnerability to neuropathic pain at old age. We assessed nociception, endocan...

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Veröffentlicht in:Neuropharmacology 2013-08, Vol.71, p.204-215
Hauptverfasser: Bishay, Philipp, Häussler, Annett, Lim, Hee-Young, Oertel, Bruno, Galve-Roperh, Ismael, Ferreirós, Nerea, Tegeder, Irmgard
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container_issue
container_start_page 204
container_title Neuropharmacology
container_volume 71
creator Bishay, Philipp
Häussler, Annett
Lim, Hee-Young
Oertel, Bruno
Galve-Roperh, Ismael
Ferreirós, Nerea
Tegeder, Irmgard
description Damaging of peripheral nerves may result in chronic neuropathic pain for which the likelihood is increased in the elderly. We assessed in mice if age-dependent alterations of endocannabinoids contributed to the heightened vulnerability to neuropathic pain at old age. We assessed nociception, endocannabinoids and the therapeutic efficacy of R-flurbiprofen in young and aged mice in the spared nerve injury model of neuropathic pain. R-flurbiprofen was used because it is able to reduce neuropathic pain in young mice in part by increasing anandamide. Aged mice developed stronger nociceptive hypersensitivity after sciatic nerve injury than young mice. This was associated with low anandamide levels in the dorsal root ganglia, spinal cord, thalamus and cortex, which further decreased after nerve injury. In aged mice, R-flurbiprofen had only weak antinociceptive efficacy and it failed to restore normal anandamide levels after nerve injury. In terms of the mechanisms, we found that fatty acid amide hydrolase (FAAH) which degrades anandamide, was upregulated after nerve injury at both ages, so that this upregulation likely did not account for the age-dependent differences. However, enzymes contributing to oxidative metabolism of anandamide, namely cyclooxygenase-1 and Cyp2D6, were increased in the brain of aged mice, possibly enhancing the oxidative breakdown of anandamide. This may overwhelm the capacity of R-flurbiprofen to restore anandamide homeostasis and may contribute to the heightened risk for neuropathic pain at old age. •Old mice developed stronger pain after nerve injury than young mice.•Old mice had lower anandamide levels in the peripheral and central nervous system.•R-flurbiprofen failed to restore pathologically reduced anandamide in old mice.•R-flurbiprofen also failed to inhibit neuropathic pain in old mice.•Anandamide deficiency in old mice may be due to an increase of oxidative metabolism.
doi_str_mv 10.1016/j.neuropharm.2013.03.021
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We assessed in mice if age-dependent alterations of endocannabinoids contributed to the heightened vulnerability to neuropathic pain at old age. We assessed nociception, endocannabinoids and the therapeutic efficacy of R-flurbiprofen in young and aged mice in the spared nerve injury model of neuropathic pain. R-flurbiprofen was used because it is able to reduce neuropathic pain in young mice in part by increasing anandamide. Aged mice developed stronger nociceptive hypersensitivity after sciatic nerve injury than young mice. This was associated with low anandamide levels in the dorsal root ganglia, spinal cord, thalamus and cortex, which further decreased after nerve injury. In aged mice, R-flurbiprofen had only weak antinociceptive efficacy and it failed to restore normal anandamide levels after nerve injury. In terms of the mechanisms, we found that fatty acid amide hydrolase (FAAH) which degrades anandamide, was upregulated after nerve injury at both ages, so that this upregulation likely did not account for the age-dependent differences. However, enzymes contributing to oxidative metabolism of anandamide, namely cyclooxygenase-1 and Cyp2D6, were increased in the brain of aged mice, possibly enhancing the oxidative breakdown of anandamide. 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development</subject><subject>Peripheral Nerves - metabolism</subject><subject>Polyunsaturated Alkamides - metabolism</subject><subject>R-flurbiprofen</subject><subject>Spinal Cord - drug effects</subject><subject>Spinal Cord - growth &amp; development</subject><subject>Spinal Cord - metabolism</subject><subject>Stereoisomerism</subject><issn>0028-3908</issn><issn>1873-7064</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2013</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUlPwzAQhS0EomX5CyhHLinjJY59BMQmIXGBs-XYk9ZVkxQ7ReLf41KWI0hPtmR_M280j5CCwowClRfLWY-bOKwXNnYzBpTPIIvRPTKlquZlDVLskykAUyXXoCbkKKUlAAhF1SGZMF7pugI5JVeXve297YLHwmMbXMDevRf5rVhgmC9G7NEXOzc7LoIr1jb0RZad548uODwhB61dJTz9uo_Jy-3N8_V9-fh093B9-Vg6IWAsG2nzAE1DtWRMK8brPIWqlZa1FMI7TlG3UiiOSG2bDwWe66aibdOqJsPH5HzXdx2H1w2m0XQhOVytbI_DJhlaMeC5ndL_QCnjTGgm_0Z5VeWtUcEzqnaoi0NKEVuzjqGz8d1QMNtczNL85mK2uRjIYjSXnn25bJoO_U_hdxAZuNoBmDf4FjCa9BkF-hDRjcYP4W-XD-ieob0</recordid><startdate>201308</startdate><enddate>201308</enddate><creator>Bishay, Philipp</creator><creator>Häussler, Annett</creator><creator>Lim, Hee-Young</creator><creator>Oertel, Bruno</creator><creator>Galve-Roperh, Ismael</creator><creator>Ferreirós, Nerea</creator><creator>Tegeder, Irmgard</creator><general>Elsevier Ltd</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7TK</scope></search><sort><creationdate>201308</creationdate><title>Anandamide deficiency and heightened neuropathic pain in aged mice</title><author>Bishay, Philipp ; 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In terms of the mechanisms, we found that fatty acid amide hydrolase (FAAH) which degrades anandamide, was upregulated after nerve injury at both ages, so that this upregulation likely did not account for the age-dependent differences. However, enzymes contributing to oxidative metabolism of anandamide, namely cyclooxygenase-1 and Cyp2D6, were increased in the brain of aged mice, possibly enhancing the oxidative breakdown of anandamide. 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subjects 2-Arachidonoylglycerol
Age
Aging
Amidohydrolases - biosynthesis
Amidohydrolases - metabolism
Anandamide
Animals
Arachidonic Acids - deficiency
Arachidonic Acids - metabolism
Behavior, Animal - drug effects
Brain - drug effects
Brain - growth & development
Brain - metabolism
Cannabinoid receptor
Cyclooxygenase
Cyclooxygenase 1 - biosynthesis
Cyclooxygenase 1 - metabolism
Cyclooxygenase Inhibitors - blood
Cyclooxygenase Inhibitors - pharmacokinetics
Cyclooxygenase Inhibitors - therapeutic use
Cytochrome P-450 CYP2D6 - biosynthesis
Cytochrome P-450 CYP2D6 - metabolism
Disease Models, Animal
Endocannabinoids
Endocannabinoids - deficiency
Endocannabinoids - metabolism
Enzyme Induction
Fatty acid amide hydrolase
Flurbiprofen - blood
Flurbiprofen - pharmacokinetics
Flurbiprofen - therapeutic use
Inhibitory control
Male
Membrane Proteins - biosynthesis
Membrane Proteins - metabolism
Mice
Mice, Inbred C57BL
Nerve Tissue Proteins - biosynthesis
Nerve Tissue Proteins - metabolism
Neuralgia - blood
Neuralgia - drug therapy
Neuralgia - etiology
Neuralgia - metabolism
Nociception
Pain
Peripheral Nerves - drug effects
Peripheral Nerves - growth & development
Peripheral Nerves - metabolism
Polyunsaturated Alkamides - metabolism
R-flurbiprofen
Spinal Cord - drug effects
Spinal Cord - growth & development
Spinal Cord - metabolism
Stereoisomerism
title Anandamide deficiency and heightened neuropathic pain in aged mice
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