Heat loss reaction to capsaicin through a peripheral site of action

Donnerer, Josef; Lembeck, Fred

doi:10.1111/j.1476-5381.1983.tb10009.x

Cited by 41 publications

(20 citation statements)

References 21 publications

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“…found by Donnerer and Lembeck (1983). However, this was not the case with the hyperthermic response to AMG0347, which, when administered intravenously in rats, showed a tendency to increase deep T b at a dose of 6 g/kg and had a significant effect at 10 g/kg (the minimally effective intravenous dose).…”

Section: Trpv1 In Body Temperature Regulationmentioning

confidence: 57%

“…Several authors suggest that a contribution of a peripheral action of TRPV1 agonists to the hypothermic response cannot be excluded (Dib, 1983;Donnerer and Lembeck, 1983;Osaka et al, 1998). However, an action in a single thermoeffector tissue (e.g., skin vasculature) cannot explain the involvement of multiple effectors (Fig.…”

Section: B Thermoregulatory Effects Of Transient Receptormentioning

confidence: 99%

“…To explain the recruitment of multiple thermoeffectors, an involvement of DRG neurons in the thermal afferent pathways has been proposed (Dib, 1983;Donnerer and Lembeck, 1983;Obá l et al, 1987;Szallasi and Blumberg, 1990;Benham et al, 2003;Tominaga and Caterina, 2004;Yamashita et al, 2008). Even though the prominent association of TRPV1 channels with polymodal nociceptors (rather than with neurons sensitive to innocuous warming) weakens this proposition, some populations or TRPV1-expressing visceral DRG neurons modulate the activity of autonomic effectors (see section IV.E.5).…”

Section: Site Of Desensitization: the Preoptic Hypothalamus?mentioning

confidence: 99%

“…Long before this channel received its current name, TRPV1, it was suspected to play the roles of both a peripheral thermosensor (Dib, 1983;Donnerer and Lembeck, 1983;Obá l et al, 1987) and a central thermosensor (Szolcsá nyi et al, 1971;Hori and Shinohara, 1979;Dib, 1982) for autonomic and behavioral thermoregulation (i.e., to detect those thermal signals that are used in the control of autonomic and behavioral thermoeffectors). More recently, interest in the thermoregulatory role of TRPV1 has surged because of a serious problem with the development of TRPV1 antagonists, widely regarded as nextgeneration pain therapeutics.…”

mentioning

confidence: 99%

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The Transient Receptor Potential Vanilloid-1 Channel in Thermoregulation: A Thermosensor It Is Not

et al. 2009

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Section: Trpv1 In Body Temperature Regulationmentioning

confidence: 57%

Section: B Thermoregulatory Effects Of Transient Receptormentioning

confidence: 99%

Section: Site Of Desensitization: the Preoptic Hypothalamus?mentioning

confidence: 99%

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confidence: 99%

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The Transient Receptor Potential Vanilloid-1 Channel in Thermoregulation: A Thermosensor It Is Not

et al. 2009

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“…Capsaicin was administered to neonatal rats (2nd day of life) in a dose of 50mgkg-1, subcutaneously, under ether anaesthesia as described by Donnerer & Lembeck (1983) to destroy capsaicin sensitive afferent nerve fibres (Jancs6 et al, 1977 [-40 paw skin and in several visceral organs of the rat (data not shown). This effect of diphenhydramine and ranitidine resembles the histamine blocking effect of a similar dose of mepyramine and cimetidine .…”

Section: Drug Pretreatmentsmentioning

confidence: 99%

Substance P in sensory nerve fibres contributes to the development of oedema in the rat hind paw after thermal injury

Saria¹

1984

British J Pharmacology

114

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1 Immersion of the hind paws of anaesthetized rats in hot water for 5 min induced massive plasma protein leakage as indicated by extravasation of Evans blue dye in the skin. The threshold temperature which caused noticeable plasma extravasation was 45°C, a maximal response was obtained between 55°C and 60°C. 2 Pretreatment of rats 2 days after birth with 50mg kg-capsaicin significantly reduced the Evans blue extravasation induced by hot water at 50°C, 55°C and 60°C, whereas guanethidine pretreatment 24 h before the experiment caused a significantly increased response at 40°C, 45°C and 50°C. 3 When Evans blue was injected between 10 and 120 min after immersion of the paw in hot water, a significant extravasation of the dye was no longer detectable. However, the weight of the paw as well as the weight of the piece of skin taken for Evans blue quantification increased during this period indicating the progressive development of oedema in the skin and underlying tissues. 4 In rats treated with capsaicin as neonates, the increase in paw weight after immersion in water of 50°C for 5 min was significantly delayed during the first hour, but there was no difference after two hours.5 In rats pretreated with D-Argt,D-Pro2,D-Trp7'9, Leull-substance P, a substance P (SP) antagonist, the Evans blue extravasation was significantly reduced. However, the response, which remained in rats treated with capsaicin as neonates was not blocked by the SP-antagonist. 6 It is concluded that activation of peripheral branches of sensory SP neurones contributes to the initial massive protein extravasation and to the subsequent rate of development of oedema following heat injury. Release of histamine did not significantly contribute to this response at the lower temperatures, although the response was reduced by histamine receptor blocking drugs at 55°C and 60°C. Decreasing the sympathetic vasoconstrictor tone by guanethidine resulted in an increased response.

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Importance of endogenous nitric oxide synthase in the rat hypothalamus and amygdala in mediating the response to capsaicin

2000

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Although capsaicin has been shown to activate certain neuronal groups in the hypothalamus and amygdala, the neurotransmitters involved and the exact mechanism of action are not clearly understood at present. The aim of this study was to examine the hypothesis that the effect of capsaicin in the rat hypothalamus and amygdala primarily involves direct activation of the endogenous nitric oxide synthase (NOS) neurons responsible for the synthesis of nitric oxide (NO). Subcutaneous capsaicin injection in male rats, compared with vehicle, caused a significant increase in Fos expression in the paraventricular nucleus (PVN), supraoptic nucleus (SON), and medial and cortical amygdala. The expression of nicotinamide adenine dinucleotide phosphate diaphorase, a histochemical marker for NOS, was also increased in these brain areas in addition to the periventricular and lateral hypothalamic area and central amygdaloid nucleus. Also, capsaicin significantly increased the expression of neuronal NOS messenger RNA and protein in the PVN, SON, and medial amygdala as demonstrated by in situ hybridization and immunohistochemistry, respectively. A higher proportion of the NOS neurons in the PVN, periventricular region, SON and amygdala showed Fos expression in response to capsaicin than vehicle injection. There was little, if any, Fos activation in the NOS-positive neurons in the lateral hypothalamic area. The capsaicin-induced activation of the hypothalamic PVN and SON neurons and the medial amygdaloid nucleus was attenuated in the NOS inhibitor N(omega)-nitro-L-arginine methyl ester (L-NAME) -pretreated animals in comparison with the inactive enantiomer D-NAME. These observations indicate that activation of the endogenous NOS system and production of NO constitute a major pathway through which capsaicin exerts its effect within the hypothalamus and amygdala.

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Heat loss reaction to capsaicin through a peripheral site of action

Abstract: 1The intravenous injection of 15 tLg capsaicin produced an increase in the temperature of tail skin and paw pad and a fall in the colon temperature in conscious rats. These reactions reflect increased heat dissipation.

Cited by 41 publications

References 21 publications

The Transient Receptor Potential Vanilloid-1 Channel in Thermoregulation: A Thermosensor It Is Not

The Transient Receptor Potential Vanilloid-1 Channel in Thermoregulation: A Thermosensor It Is Not

Substance P in sensory nerve fibres contributes to the development of oedema in the rat hind paw after thermal injury

Importance of endogenous nitric oxide synthase in the rat hypothalamus and amygdala in mediating the response to capsaicin

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