Forced swim-induced musculoskeletal hyperalgesia is mediated by CRF2 receptors but not by TRPV1 receptors

Abdelhamid, Ramy E.; Kovács, Katalin; Pasley, Jeffrey D.; Nunez, Myra G.; Larson, Alice A.

doi:10.1016/j.neuropharm.2013.04.016

Cited by 33 publications

(32 citation statements)

References 66 publications

(100 reference statements)

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“…Mice usually have only a transient increase in plasma corticosterone immediately following a cold swim [23], however, UCP2-deficient mice maintained an elevated concentration of corticosterone for 24 h after the conditioning swim. This suggests that corticosterone, released in response to the stress, is normally inhibited by increasing concentrations of UCP2, perhaps in a feedback inhibitory fashion.…”

Section: Discussionmentioning

confidence: 99%

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After a cold conditioning swim, UCP2-deficient mice are more able to defend against the cold than wild type mice

Abdelhamid

Kovács

Nunez

et al. 2014

Physiology & Behavior

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Uncoupling protein 2 (UCP2) is widely distributed throughout the body including the brain, adipose tissue and skeletal muscles. In contrast to UCP1, UCP2 does not influence resting body temperature and UCP2-deficient (-/-) mice have normal thermoregulatory responses to a single exposure to cold ambient temperatures. Instead, UCP2-deficient mice are more anxious, exhibit anhedonia and have higher circulating corticosterone than wild type mice. To test the possible role of UCP2 in depressive behavior we exposed UCP2-deficient and wild type mice to a cold (26°C) forced swim and simultaneously measured rectal temperatures during and after the swim. The time that UCP2-deficient mice spent immobile did not differ from wild type mice and all mice floated more on day 2. However, UCP2-deficient mice were more able to defend against the decrease in body temperature during a second daily swim at 26°C than wild type mice (area under the curve for wild type mice: 247.0 ± 6.4; for UCP2-deficient mice: 284.4 ± 3.8, P<0.0001, Student's t test). The improved thermoregulation of wild type mice during a second swim at 26°C correlated with their greater immobility whereas defense against the warmth during a swim at 41°C correlated better with greater immobility of UCP2-deficient mice. Together these data indicate that while the lack of UCP2 has no acute effect on body temperature, UCP2 may inhibit rapid improvements in defense against cold, in contrast to UCP1, whose main function is to promote thermogenesis.

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Section: Discussionmentioning

confidence: 99%

“…Rectal temperatures were routinely taken in a room with an ambient temperature of 25°C. The animal was placed under a clean towel to create a barrier on three sides, and its colonic temperature was measured using a rectal thermometer (ETI Microtherma 2K Thermometer connected to a RET-3 rectal probe), as previously described [23-25]. …”

Section: Methodsmentioning

confidence: 99%

After a cold conditioning swim, UCP2-deficient mice are more able to defend against the cold than wild type mice

Abdelhamid

Kovács

Nunez

et al. 2014

Physiology & Behavior

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“…This depth was sufficient that mice could not touch their feet or tail to the bottom. Grip force was evaluated after a 15-min swim, previously found to induce an optimal stress-induced hyperalgesia [2], and at various time-intervals thereafter to establish the time-course of the resulting hyperalgesia. Forced swims were repeated daily and the grip force values after each swim were routinely compared to other control groups or, where indicated, to their baseline measurements.…”

Section: Methodsmentioning

confidence: 99%

“…To test this, we examined decreases in grip force as a measure of musculoskeletal hyperalgesia in mice [19], after a forced swim, a stress frequently used to induce hyperalgesia in rodents [2; 13; 19; 37; 44; 49]. Acute stress typically causes antinociception or has no effect on thermal and tactile mechanical nociception; hyperalgesia develops only after chronic stress.…”

Section: Introductionmentioning

confidence: 99%

Modulation of musculoskeletal hyperalgesia by brown adipose tissue activity in mice

Goudie-DeAngelis¹,

Abdelhamid²,

Nunez³

et al. 2016

Pain

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Cold exposure and a variety of types of mild stress increase pain in patients suffering from painful disorders such as fibromyalgia syndrome. Acutely, stress induces thermogenesis by increasing sympathetic activation of beta-3 (β3) adrenergic receptors in brown adipose tissue. Chronic stress leads to the hypertrophy of brown adipose, a phenomenon termed adaptive thermogenesis. Based on the innervation of skeletal muscle by collaterals of nerves projecting to brown adipose, we theorized an association between brown adipose tissue activity and musculoskeletal hyperalgesia and tested this hypothesis in mice. Exposure to a cold swim or injection of BRL37344 (β3 adrenergic agonist) each enhanced musculoskeletal hyperalgesia, as indicated by morphine-sensitive decreases in grip force responses, whereas SR59230A (β3 adrenergic antagonist) attenuated swim-induced hyperalgesia. Chemical ablation of interscapular brown adipose, using Rose Bengal, attenuated the development of hyperalgesia in response to either swim stress or BRL37344. In addition, elimination of the gene expressing uncoupling protein-1 (UCP1), the enzyme responsible for thermogenesis, prevented musculoskeletal hyperalgesia in response to either a swim or BRL37344, as documented in UCP1-knock out (UCP1-KO) mice compared to wild type controls. Together these data provide a convergence of evidence suggesting that activation of brown adipose contributes to stress-induced musculoskeletal hyperalgesia.

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“…at a dose of 5 mg in 1 ml/kg and astressin 2B was given s.c. at a dose of 200 μg in 5 ml/kg. Antagonist doses were selected on the basis of results from our previous studies [2] and published data [4,11,19]. Astres sin 2B was dissolved in distilled water and given 30 min before administration of CRF or physiological saline [2,19].…”

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confidence: 99%

Effects of Corticotropin-Releasing Factor (CRF) on Somatic Pain Sensitivity in Conscious Rats: Involvement of Types 1 and 2 CRF Receptors

Yarushkina

Bagaeva

Filaretova

2016

Neurosci Behav Physi

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Corticotropin-releasing factor (CRF) is involved in regulating somatic pain sensitivity in stress. Exogenous CRF can induce both weakening [15,31] and enhancement [12,16] of somatic pain sensitivity. Although exogenous CRF has been seen to have double effects on pain sensitivity, the results of most studies have provided evidence of suppression of somatic pain sensitivity (an analgesic effect) in both animals [6,9,21] and humans [18,20].The peripheral action of CRF on somatic pain sensitivity has received the most study. Peripheral administration of CRF, both systemically (intravenous [9], intraperitoneal [1], intracardiac [5]) and locally [23], induces analgesic effects both on the background of infl ammation [23] and without infl ammation [9]. The action of CRF is mediated via CRF receptors of types 1 and 2 ( CRF-1 and CRF-2 receptors) [10]. There are few data on the involvement of CRF receptors in mediating the analgesic effect of CRF when given peripherally, and these have been obtained on the background of infl ammation. Use of selective antagonists of CRF receptors have demonstrated the involvement of both CRF-1 and CRF-2 receptors, located on leukocytes, in mediating the analgesic actions of CRF when given locally at the infl ammation site in somatic tissues [22]. Additionally, data have been obtained showing that CRF-1 receptors can contribute to the development of infl ammation-induced hyperalgesia [8,11].Despite the fact that the action of CRF on somatic pain sensitivity is apparent not only in infl ammation, but also in the absence of infl ammation [9,15], there are no data on the involvement of CRF receptors in mediating the peripheral action of CRF on somatic pain sensitivity in normal conditions (in the absence of infl ammation). Our previous studies [2] demonstrated the involvement of CRF-2 receptors in mediating the analgesic effect evoked by systemic administration of CRF in anesthetized rats. Administration of CRF-1 and CRF-2 receptors in mediating this effect in conscious animals has not previously been studied.Corticotrophin-releasing factor (CRF) is involved in regulating pain sensitivity and can elicit analgesic effects in animals and humans. The aim of the present work was to investigate the involvement of types 1 and 2 CRF receptors (CRF-1 and CRF-2 receptors) in mediating the analgesic action of CRF on somatic pain sensitivity when given systemically to conscious rats. Somatic pain sensitivity was tested in terms of the latent period (LP) of the tailfl ick reaction in response to thermal stimulation (the tail fl ick test). The involvement of CRF-1 and CFR-2 receptors was studied by systemic administration of their specifi c antagonists NBI 27914 and astressin 2B, respectively. Systemic administration of CRF increased the latent period of the pain reaction (it had an analgesic effect).

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Forced swim-induced musculoskeletal hyperalgesia is mediated by CRF2 receptors but not by TRPV1 receptors

Cited by 33 publications

References 66 publications

After a cold conditioning swim, UCP2-deficient mice are more able to defend against the cold than wild type mice

After a cold conditioning swim, UCP2-deficient mice are more able to defend against the cold than wild type mice

Modulation of musculoskeletal hyperalgesia by brown adipose tissue activity in mice

Effects of Corticotropin-Releasing Factor (CRF) on Somatic Pain Sensitivity in Conscious Rats: Involvement of Types 1 and 2 CRF Receptors

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