Biphasic time-course of capsaicin-induced substance P depletion: failure to correlate with thermal analgesia in the rat

Bittner, M.A.; LaHann, T. R.

doi:10.1016/0006-8993(84)90122-7

Cited by 24 publications

(8 citation statements)

References 15 publications

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“…Thus, the presently observed excitation of LC neurons by capsaicin might contribute to the analgetic actions observed by acute administration of the drug (Bittner & LaHann 1984). Dr M. Haj6s was a recipient of a fellowship from the Swedish Institute.…”

Section: R E S U J > T Smentioning

confidence: 90%

“…One major mode of action by capsaicin is to release or deplete various neuropeptides, particularly substance P (SP) (Gamse et al 1979, Jancso et al 1981, Bittner & LaHann 1984). An alternative primary target for capsaicin to activate the L C could be a SP-mediated excitatory innervation of the nucleus (Guyenet & Aghajanian 1977, Engberg et al 1981.…”

Section: R E S U J > T Smentioning

confidence: 99%

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Capsaicin‐induced excitation of locus coeruleus neurons

Hajós¹,

Jancsó²,

Engberg³

1987

Acta Physiologica Scandinavica

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The noradrenergic pontine nucleus locus coeruleus (LC) seems to be involved in sensory processing. In the present study, the effect of capsaicin, a drug which specifically interferes with chemosensitive primary afferents, on LC firing rate was analysed, utilizing electrophysiological techniques. In control rats, low doses of capsaicin (1-8 micrograms kg-1 i.v.) caused a marked excitation of LC units. The effect was instantaneous in onset but short-lasting and no signs of tachyphylaxis were observed. The excitation was maintained in adult rats treated as neonates with high doses of capsaicin (50 mg kg-1 s.c.) but almost totally prevented by pretreatment of adult rats with high doses of capsaicin (300 mg kg-1 s.c.). According to our histological data, using selective silver impregnation techniques, the LC seems not to receive innervation by sensory primary afferents. It is proposed that the capsaicin-induced excitation of LC neurons is a centrally mediated effect and might, in part, be involved in the analgetic effect induced by the drug.

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Section: R E S U J > T Smentioning

confidence: 90%

Section: R E S U J > T Smentioning

confidence: 99%

Capsaicin‐induced excitation of locus coeruleus neurons

Hajós¹,

Jancsó²,

Engberg³

1987

Acta Physiologica Scandinavica

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“…in the Randall–Selitto test), this approach has been exploited for studying thermonociception only in a very limited manner (see below). Examining the nocifensive behaviour of capsaicin‐pretreated rats with the conventional hot plate and tail‐flick tests led to controversial results (Szolcsányi, 1976; Obál et al ., 1979; Hayes & Tyers, 1980; Gamse, 1982; Bittner & Lahann, 1984), although this agent desensitized to heat a major subgroup of primary afferent neurons, the polymodal nociceptors (Szolcsányi, 1987a,1987b) expressing the capsaicin VR1 receptor, which is also activated by noxious heat (Caterina et al ., 1997; Tominaga et al ., 1998). On the other hand, modifying the paw‐withdrawal test for an approximate measurement of the noxious heat threshold temperature (by immersing the rat hindpaw in a water bath whose temperature was increased in a stepwise manner in 1°C units until paw withdrawal occurred) instead of the reflex latency revealed a clearcut dose‐dependent thermal antinociceptive effect of capsaicin (Szolcsányi, 1985,1987b).…”

Section: Introductionmentioning

confidence: 99%

“…For this latter purpose, RTX seemed to be an ideal candidate since the acute heat‐sensitizing effect of VR1 receptor agonism is well known (Szolcsányi, 1977; Simone et al ., 1987; Gilchrist et al ., 1996; Yeomans et al ., 1996). Furthermore, the long‐term sensory desensitizing effect of RTX on the noxious heat threshold was also examined in order to determine whether the ITHP is suitable to reveal the lasting thermal antinociceptive effect of VR1 receptor agonism for which ambiguous results have been provided previously (Szolcsányi, 1976; Obál et al ., 1979; Hayes & Tyers, 1980; Gamse, 1982; Bittner & Lahann, 1984). I‐RTX's in vivo VR1 receptor antagonistic action (with special reference to its selectivity) and its own effect on the noxious heat threshold (both acutely and in the long term) were also investigated to detect any possible VR1 receptor agonistic action and/or conversion to RTX.…”

Section: Introductionmentioning

confidence: 99%

Effect of resiniferatoxin on the noxious heat threshold temperature in the rat: a novel heat allodynia model sensitive to analgesics

Almási

Pethő

Bölcskei

et al. 2003

British J Pharmacology

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1 An increasing-temperature hot plate (ITHP) was introduced to measure the noxious heat threshold (45.370.31C) of unrestrained rats, which was reproducible upon repeated determinations at intervals of 5 or 30 min or 1 day. 2 Morphine, diclofenac and paracetamol caused an elevation of the noxious heat threshold following i.p. pretreatment, the minimum effective doses being 3, 10 and 200 mg kg À1 , respectively. 3 Unilateral intraplantar injection of the VR1 receptor agonist resiniferatoxin (RTX, 0.048 nmol) induced a profound drop of heat threshold to the innocuous range with a maximal effect (8 -101C drop) 5 min after RTX administration. This heat allodynia was inhibited by pretreatment with morphine, diclofenac and paracetamol, the minimum effective doses being 1, 1 and 100 mg kg À1 i.p., respectively. 4 The long-term sensory desensitizing effect of RTX was examined by bilateral intraplantar injection (0.048 nmol per paw) which produced, after an initial threshold drop, an elevation (up to 2.970.51C) of heat threshold lasting for 5 days. 5 The VR1 receptor antagonist iodo-resiniferatoxin (I-RTX, 0.05 nmol intraplantarly) inhibited by 51% the heat threshold-lowering effect of intraplantar RTX but not a,b-methylene-ATP (0.3 mmol per paw). I-RTX (0.1 or 1 nmol per paw) failed to alter the heat threshold either acutely (5 -60 min) or on the long-term (5 days). The heat threshold of VR1 receptor knockout mice was not different from that of wild-type animals (45.670.5 vs 45.270.41C). 6 In conclusion, the RTX-induced drop of heat threshold measured by the ITHP is a novel heat allodynia model exhibiting a high sensitivity to analgesics. British Journal of Pharmacology (2003) 139, 49 -58. doi:10.1038/sj.bjp.0705234 Keywords: Increasing-temperature hot plate; noxious heat threshold temperature; resiniferatoxin; heat allodynia; morphine; diclofenac; paracetamol; sensory desensitization; iodo-resiniferatoxin; a,b-methylene-ATP Abbreviations: I-RTX, iodo-resiniferatoxin; ITHP, increasing-temperature hot plate; a,b-meATP, a,b-methylene adenosine 5 0 -triphosphate; PPADS, pyridoxalphosphate-6-azophenyl-2 0 ,4 0 -disulphonic acid; RTX, resiniferatoxin; VR1, vanilloid receptor type 1

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“…As shown in Figure 4, 20 days after CAPS treatment the level of SP and CGRP in CAPS-treated animals is comparable to the level of controls. This observation suggests that chemical peripheral sensory denervation with CAPS only transiently aect the local level of these neuropeptide (Bittner & Lahann, 1984;Maggi et al, 1987). Our data, showing that the increase of NGF synthesis in CAPS/CCK-8-treated mice correlates with the recovery of sensory responses and with the overexpression of SP and CGRP in the paw skin, support previous evidence indicating that sensory neurones are dependent on NGF for their survival, particularly during loss of nerve endings and/or severe neuronal de®cits (Verge et al, 1995).…”

Section: Discussionmentioning

confidence: 86%

Cholecystokinin‐8 Enhances Nerve Growth Factor Synthesis And Promotes Recovery Of Capsaicin‐Induced Sensory Deficit

Manni

Lundeberg

Tirassa

et al. 2000

J Peripheral Nervous Sys

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1 Alterations of nerve growth factor (NGF) expression have been demonstrated during peripheral nerve disease and the impaired expression or synthesis and transportation of NGF has been correlated with the pathogenesis of several peripheral neuropathies. Since exogenous NGF administration seems to cause undesired side-eects, therapeutical strategies based on the regulation of endogenous synthesis of NGF could prove useful in the clinical treatment of these disorders.2 The aim of the present study was to analyse the eects of exogenous peripheral administration of the neuropeptide cholecystokinin-8 (CCK-8) on endogenous NGF synthesis, NGF mRNA and distribution of peripheral neuropeptides which are known to be regulated by this neurotrophin.3 To address these questions we studied the eects of capsaicin (CAPS) before and after the administration of CCK-8 on NGF levels, NGF mRNA expression and localization, and the concentration of substance P (SP) and calcitonin gene-related peptide (CGRP) in peripheral tissue. 4 These studies demonstrate that administration of the CCK-8 induces an increase of NGF protein and mRNA in peripheral tissue. NGF level in paw skin of CAPS/CCK-8-treated mice is 3 fold higher than in controls (1241+110 pg gr 71 of tissue wet weight versus 414+110 pg gr 71 of controls) and nearly 6 fold higher than in CAPS-treated mice (1241+110 pg gr 71 versus 248+27 pg gr 71 ). The increase of NGF is correlated with the recovery of impaired nocifensive behaviour and with an overexpression of SP and CGRP. 5 The evidence that CCK-8 promotes the recovery of sensory de®cits suggests a potential clinical use for this neuropeptide in peripheral neuropathies.

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Biphasic time-course of capsaicin-induced substance P depletion: failure to correlate with thermal analgesia in the rat

Cited by 24 publications

References 15 publications

Capsaicin‐induced excitation of locus coeruleus neurons

Capsaicin‐induced excitation of locus coeruleus neurons

Effect of resiniferatoxin on the noxious heat threshold temperature in the rat: a novel heat allodynia model sensitive to analgesics

Cholecystokinin‐8 Enhances Nerve Growth Factor Synthesis And Promotes Recovery Of Capsaicin‐Induced Sensory Deficit

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