AustralieFrV1, PascalFrancis, Corpus, bibRecord, 000F61

A reassessment of stress-induced "analgesia" in the rat using an unbiased method

Identifieur interne : 000F61 ( PascalFrancis/Corpus ); précédent : 000F60; suivant : 000F62

A reassessment of stress-induced "analgesia" in the rat using an unbiased method

Auteurs : Pascal Carrive ; Maxim Churyukanov ; Daniel Le Bars

Source :

Pain : (Amsterdam) [ 0304-3959 ] ; 2011.

RBID : Pascal:12-0389043

Descripteurs français

Pascal (Inist)
- Stress, Analgésie, Peur, Peau, Vasoconstriction, Chaleur, Douleur, Rat, Animal.

English descriptors

KwdEn :
- Analgesia, Animal, Fear, Heat, Pain, Rat, Skin, Stress, Vasoconstriction.

Abstract

An increased tail-flick latency to noxious heat during or after stress in the rodent is usually interpreted as a stress-induced reduction in pain sensitivity and often described as a form of stress-induced "analgesia." However, this measure is an indirect and flawed measure of the change in nociceptive threshold to noxious heat. A major confound of the latency measure is the initial temperature of the tail, which can drop down to room temperature during stress, the consequence of a marked sympathetically mediated vasoconstriction in the skin of the extremities. We addressed this issue with tail-flick tests during contextual fear using infrared thermography to monitor temperature changes and a CO₂ laser to deliver the heat stimulus. The experiment revealed a 4.2°C increase of the nociceptive threshold, confirming a true antin-ociceptive effect. However, its contribution to the increased withdrawal latency was less than two-thirds (63.2%). Nearly one-third (32.2%) was due to the drop in tail temperature (4.4°C), which also slowed conduction along sensory fibers (2.2%, included in the 32.2%). The remaining 4.6% was due to an increase in decisional/motor latency. This new unbiased method establishes beyond doubt that a conditioned stress response is associated with true antinociception to noxious heat. It also confirms that stress-induced changes in skin temperature can be a major confound in tail-flick tests. The present study shows, for the first time, the exact contribution of these two components of the tail-flick latency for a stress response.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A02	`01`			`@0 PAINDB`
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A08	`01`	`1`	`ENG`	`@1 A reassessment of stress-induced "analgesia" in the rat using an unbiased method`
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A11	`02`	`1`		`@1 CHURYUKANOV (Maxim)`
A11	`03`	`1`		`@1 LE BARS (Daniel)`
A14	`01`			`@1 School of Medical Sciences, University of New South Wales @2 NSW 2052 @3 AUS @Z 1 aut.`
A14	`02`			`@1 Department of Neurology, Moscow Medical Academy @2 Moscow 119021 @3 RUS @Z 2 aut.`
A14	`03`			`@1 Team "Pain", INSERM UMRS 975, CNRS UMR 7225, Faculté de Médecine UPMC, Université Pierre et Marie Curie @2 Paris @3 FRA @Z 3 aut.`
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C01	`01`		`ENG`	@0 An increased tail-flick latency to noxious heat during or after stress in the rodent is usually interpreted as a stress-induced reduction in pain sensitivity and often described as a form of stress-induced "analgesia." However, this measure is an indirect and flawed measure of the change in nociceptive threshold to noxious heat. A major confound of the latency measure is the initial temperature of the tail, which can drop down to room temperature during stress, the consequence of a marked sympathetically mediated vasoconstriction in the skin of the extremities. We addressed this issue with tail-flick tests during contextual fear using infrared thermography to monitor temperature changes and a CO₂ laser to deliver the heat stimulus. The experiment revealed a 4.2°C increase of the nociceptive threshold, confirming a true antin-ociceptive effect. However, its contribution to the increased withdrawal latency was less than two-thirds (63.2%). Nearly one-third (32.2%) was due to the drop in tail temperature (4.4°C), which also slowed conduction along sensory fibers (2.2%, included in the 32.2%). The remaining 4.6% was due to an increase in decisional/motor latency. This new unbiased method establishes beyond doubt that a conditioned stress response is associated with true antinociception to noxious heat. It also confirms that stress-induced changes in skin temperature can be a major confound in tail-flick tests. The present study shows, for the first time, the exact contribution of these two components of the tail-flick latency for a stress response.
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C03	`01`	`X`	`SPA`	`@0 Estrés @5 01`
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C03	`03`	`X`	`SPA`	`@0 Miedo @5 03`
C03	`04`	`X`	`FRE`	`@0 Peau @5 04`
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C03	`04`	`X`	`SPA`	`@0 Piel @5 04`
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C03	`07`	`X`	`SPA`	`@0 Dolor @5 07`
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C03	`08`	`X`	`ENG`	`@0 Rat @5 54`
C03	`08`	`X`	`SPA`	`@0 Rata @5 54`
C03	`09`	`X`	`FRE`	`@0 Animal @5 69`
C03	`09`	`X`	`ENG`	`@0 Animal @5 69`
C03	`09`	`X`	`SPA`	`@0 Animal @5 69`
C07	`01`	`X`	`FRE`	`@0 Vasomotricité @5 20`
C07	`01`	`X`	`ENG`	`@0 Vasomotricity @5 20`
C07	`01`	`X`	`SPA`	`@0 Vasomotricidad @5 20`
C07	`02`	`X`	`FRE`	`@0 Facteur milieu @5 21`
C07	`02`	`X`	`ENG`	`@0 Environmental factor @5 21`
C07	`02`	`X`	`SPA`	`@0 Factor medio @5 21`
C07	`03`	`X`	`FRE`	`@0 Température @5 22`
C07	`03`	`X`	`ENG`	`@0 Temperature @5 22`
C07	`03`	`X`	`SPA`	`@0 Temperatura @5 22`
C07	`04`	`X`	`FRE`	`@0 Rodentia @2 NS`
C07	`04`	`X`	`ENG`	`@0 Rodentia @2 NS`
C07	`04`	`X`	`SPA`	`@0 Rodentia @2 NS`
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C07	`05`	`X`	`SPA`	`@0 Mammalia @2 NS`
C07	`06`	`X`	`FRE`	`@0 Vertebrata @2 NS`
C07	`06`	`X`	`ENG`	`@0 Vertebrata @2 NS`
C07	`06`	`X`	`SPA`	`@0 Vertebrata @2 NS`
N21				`@1 303`
N44	`01`			`@1 OTO`
N82				`@1 OTO`

Format Inist (serveur)

NO :	PASCAL 12-0389043 INIST
ET :	A reassessment of stress-induced "analgesia" in the rat using an unbiased method
AU :	CARRIVE (Pascal); CHURYUKANOV (Maxim); LE BARS (Daniel)
AF :	School of Medical Sciences, University of New South Wales/NSW 2052/Australie (1 aut.); Department of Neurology, Moscow Medical Academy/Moscow 119021/Russie (2 aut.); Team "Pain", INSERM UMRS 975, CNRS UMR 7225, Faculté de Médecine UPMC, Université Pierre et Marie Curie/Paris/France (3 aut.)
DT :	Publication en série; Papier de recherche; Niveau analytique
SO :	Pain : (Amsterdam); ISSN 0304-3959; Coden PAINDB; Pays-Bas; Da. 2011; Vol. 152; No. 3; Pp. 676-686; Bibl. 62 ref.
LA :	Anglais
EA :	An increased tail-flick latency to noxious heat during or after stress in the rodent is usually interpreted as a stress-induced reduction in pain sensitivity and often described as a form of stress-induced "analgesia." However, this measure is an indirect and flawed measure of the change in nociceptive threshold to noxious heat. A major confound of the latency measure is the initial temperature of the tail, which can drop down to room temperature during stress, the consequence of a marked sympathetically mediated vasoconstriction in the skin of the extremities. We addressed this issue with tail-flick tests during contextual fear using infrared thermography to monitor temperature changes and a CO₂ laser to deliver the heat stimulus. The experiment revealed a 4.2°C increase of the nociceptive threshold, confirming a true antin-ociceptive effect. However, its contribution to the increased withdrawal latency was less than two-thirds (63.2%). Nearly one-third (32.2%) was due to the drop in tail temperature (4.4°C), which also slowed conduction along sensory fibers (2.2%, included in the 32.2%). The remaining 4.6% was due to an increase in decisional/motor latency. This new unbiased method establishes beyond doubt that a conditioned stress response is associated with true antinociception to noxious heat. It also confirms that stress-induced changes in skin temperature can be a major confound in tail-flick tests. The present study shows, for the first time, the exact contribution of these two components of the tail-flick latency for a stress response.
CC :	002A25F
FD :	Stress; Analgésie; Peur; Peau; Vasoconstriction; Chaleur; Douleur; Rat; Animal
FG :	Vasomotricité; Facteur milieu; Température; Rodentia; Mammalia; Vertebrata
ED :	Stress; Analgesia; Fear; Skin; Vasoconstriction; Heat; Pain; Rat; Animal
EG :	Vasomotricity; Environmental factor; Temperature; Rodentia; Mammalia; Vertebrata
SD :	Estrés; Analgesia; Miedo; Piel; Vasoconstricción; Calor; Dolor; Rata; Animal
LO :	INIST-17241.354000193693550310
ID :	12-0389043

Links to Exploration step

Pascal:12-0389043

Le document en format XML

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<front><div type="abstract" xml:lang="en">An increased tail-flick latency to noxious heat during or after stress in the rodent is usually interpreted as a stress-induced reduction in pain sensitivity and often described as a form of stress-induced "analgesia." However, this measure is an indirect and flawed measure of the change in nociceptive threshold to noxious heat. A major confound of the latency measure is the initial temperature of the tail, which can drop down to room temperature during stress, the consequence of a marked sympathetically mediated vasoconstriction in the skin of the extremities. We addressed this issue with tail-flick tests during contextual fear using infrared thermography to monitor temperature changes and a CO<sub>2</sub>
 laser to deliver the heat stimulus. The experiment revealed a 4.2°C increase of the nociceptive threshold, confirming a true antin-ociceptive effect. However, its contribution to the increased withdrawal latency was less than two-thirds (63.2%). Nearly one-third (32.2%) was due to the drop in tail temperature (4.4°C), which also slowed conduction along sensory fibers (2.2%, included in the 32.2%). The remaining 4.6% was due to an increase in decisional/motor latency. This new unbiased method establishes beyond doubt that a conditioned stress response is associated with true antinociception to noxious heat. It also confirms that stress-induced changes in skin temperature can be a major confound in tail-flick tests. The present study shows, for the first time, the exact contribution of these two components of the tail-flick latency for a stress response.</div>
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 laser to deliver the heat stimulus. The experiment revealed a 4.2°C increase of the nociceptive threshold, confirming a true antin-ociceptive effect. However, its contribution to the increased withdrawal latency was less than two-thirds (63.2%). Nearly one-third (32.2%) was due to the drop in tail temperature (4.4°C), which also slowed conduction along sensory fibers (2.2%, included in the 32.2%). The remaining 4.6% was due to an increase in decisional/motor latency. This new unbiased method establishes beyond doubt that a conditioned stress response is associated with true antinociception to noxious heat. It also confirms that stress-induced changes in skin temperature can be a major confound in tail-flick tests. The present study shows, for the first time, the exact contribution of these two components of the tail-flick latency for a stress response.</s0>
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<fC07 i1="01" i2="X" l="ENG"><s0>Vasomotricity</s0>
<s5>20</s5>
</fC07>
<fC07 i1="01" i2="X" l="SPA"><s0>Vasomotricidad</s0>
<s5>20</s5>
</fC07>
<fC07 i1="02" i2="X" l="FRE"><s0>Facteur milieu</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="ENG"><s0>Environmental factor</s0>
<s5>21</s5>
</fC07>
<fC07 i1="02" i2="X" l="SPA"><s0>Factor medio</s0>
<s5>21</s5>
</fC07>
<fC07 i1="03" i2="X" l="FRE"><s0>Température</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="ENG"><s0>Temperature</s0>
<s5>22</s5>
</fC07>
<fC07 i1="03" i2="X" l="SPA"><s0>Temperatura</s0>
<s5>22</s5>
</fC07>
<fC07 i1="04" i2="X" l="FRE"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="ENG"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="04" i2="X" l="SPA"><s0>Rodentia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="FRE"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="ENG"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="05" i2="X" l="SPA"><s0>Mammalia</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="FRE"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="ENG"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fC07 i1="06" i2="X" l="SPA"><s0>Vertebrata</s0>
<s2>NS</s2>
</fC07>
<fN21><s1>303</s1>
</fN21>
<fN44 i1="01"><s1>OTO</s1>
</fN44>
<fN82><s1>OTO</s1>
</fN82>
</pA>
</standard>
<server><NO>PASCAL 12-0389043 INIST</NO>
<ET>A reassessment of stress-induced "analgesia" in the rat using an unbiased method</ET>
<AU>CARRIVE (Pascal); CHURYUKANOV (Maxim); LE BARS (Daniel)</AU>
<AF>School of Medical Sciences, University of New South Wales/NSW 2052/Australie (1 aut.); Department of Neurology, Moscow Medical Academy/Moscow 119021/Russie (2 aut.); Team "Pain", INSERM UMRS 975, CNRS UMR 7225, Faculté de Médecine UPMC, Université Pierre et Marie Curie/Paris/France (3 aut.)</AF>
<DT>Publication en série; Papier de recherche; Niveau analytique</DT>
<SO>Pain : (Amsterdam); ISSN 0304-3959; Coden PAINDB; Pays-Bas; Da. 2011; Vol. 152; No. 3; Pp. 676-686; Bibl. 62 ref.</SO>
<LA>Anglais</LA>
<EA>An increased tail-flick latency to noxious heat during or after stress in the rodent is usually interpreted as a stress-induced reduction in pain sensitivity and often described as a form of stress-induced "analgesia." However, this measure is an indirect and flawed measure of the change in nociceptive threshold to noxious heat. A major confound of the latency measure is the initial temperature of the tail, which can drop down to room temperature during stress, the consequence of a marked sympathetically mediated vasoconstriction in the skin of the extremities. We addressed this issue with tail-flick tests during contextual fear using infrared thermography to monitor temperature changes and a CO<sub>2</sub>
 laser to deliver the heat stimulus. The experiment revealed a 4.2°C increase of the nociceptive threshold, confirming a true antin-ociceptive effect. However, its contribution to the increased withdrawal latency was less than two-thirds (63.2%). Nearly one-third (32.2%) was due to the drop in tail temperature (4.4°C), which also slowed conduction along sensory fibers (2.2%, included in the 32.2%). The remaining 4.6% was due to an increase in decisional/motor latency. This new unbiased method establishes beyond doubt that a conditioned stress response is associated with true antinociception to noxious heat. It also confirms that stress-induced changes in skin temperature can be a major confound in tail-flick tests. The present study shows, for the first time, the exact contribution of these two components of the tail-flick latency for a stress response.</EA>
<CC>002A25F</CC>
<FD>Stress; Analgésie; Peur; Peau; Vasoconstriction; Chaleur; Douleur; Rat; Animal</FD>
<FG>Vasomotricité; Facteur milieu; Température; Rodentia; Mammalia; Vertebrata</FG>
<ED>Stress; Analgesia; Fear; Skin; Vasoconstriction; Heat; Pain; Rat; Animal</ED>
<EG>Vasomotricity; Environmental factor; Temperature; Rodentia; Mammalia; Vertebrata</EG>
<SD>Estrés; Analgesia; Miedo; Piel; Vasoconstricción; Calor; Dolor; Rata; Animal</SD>
<LO>INIST-17241.354000193693550310</LO>
<ID>12-0389043</ID>
</server>
</inist>
</record>

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A reassessment of stress-induced "analgesia" in the rat using an unbiased method

A reassessment of stress-induced "analgesia" in the rat using an unbiased method

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