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1 n (garlic), and allyl isothiocyanate (AITC) (mustard oil).
2 e to ligands of TRPV1 (capsaicin) and TRPA1 (mustard oil).
3 sory neurons sensitive to the TRPA1 agonist, mustard oil.
4 hey are exposed to noxious compounds such as mustard oil.
5 lgesia to punctate stimuli on treatment with mustard oil.
6 ungent chemicals, such as cinnamaldehyde and mustard oil.
7 esponses of sensory neurons to capsaicin and mustard oil.
8 n the range of 48.5 to 54.2% was observed in mustard oil..
9 on of capsaicin (1 microm; 8 of 9 LF cells), mustard oil (100 microm; 10 of 12 LF cells), and low pH
11 rents were sensitized by capsaicin (3 of 9), mustard oil (2 of 7), or low pH (1 of 6) application.
13 ted capsaicin (a specific TRPV1 agonist) and mustard oil (a specific TRPA1 agonist) behavioral respon
14 ow that TRPA1 is desensitized by homologous (mustard oil; a TRPA1 agonist) and heterologous (capsaici
17 in lamina II neurons that also responded to mustard oil (allyl isothiocyanate), indicating a presyna
18 rring electrophilic plant compounds, such as mustard oil and cinnamaldehyde, are TRPA1 agonists, it i
19 show that derivatives of two such compounds, mustard oil and cinnamaldehyde, covalently bind mouse TR
21 his channel is the sole target through which mustard oil and garlic activate primary afferent nocicep
22 eralgesia produced by topical application of mustard oil and measuring the nociceptive tail-flick ref
23 fants receiving topical cord applications of mustard oil and other potentially unclean substances, re
24 is study, the erucic acid content in several mustard oils and prepared mustard samples from Germany a
25 d molecular target for the pungent action of mustard oils and support an emerging role for TRP channe
26 ere we show that AITC (allyl isothiocyanate; mustard oil) and menthol represent two distinct types of
27 pounds that cause a burning sensation (e.g., mustard oil) and, indirectly, by components of the infla
29 in cinnamon oil, wintergreen oil, clove oil, mustard oil, and ginger all activate TRPA1 (ANKTM1).
30 of trigeminal neurons that express TRPA1, a mustard oil- and cinnamaldehyde-sensitive channel, and t
31 tagonist proglumide (10 micrograms) prior to mustard oil application completely blocked both the less
34 al and/or thermal hyperalgesia after topical mustard oil application, carrageenan inflammation, or ne
36 spinalised, pentobarbitone-sedated animals, mustard oil applied to any site on the ipsilateral hind
37 reflexes of an acute noxious stimulus (20 % mustard oil) applied to a number of locations around the
38 ted cells that respond to capsaicin (but not mustard oil) as well as large-diameter myelinated neuron
40 that reduces plant predation, the so-called "mustard oil bomb," in which vacuole breakage in cells ha
41 cosinolate-myrosinase system, the so-called "mustard-oil bomb." Tissue damage caused by insect feedin
42 uR1, markedly reduced the activity evoked by mustard oil, but not that elicited by brushing of the re
43 by the TRPA1 agonists allyl-isothiocyanate (mustard oil), carvacrol, and polyunsaturated fatty acids
44 osensor, we establish that capsaicin, unlike mustard oil, consistently activates phospholipase C in s
46 lowing stimulation of peripheral nerves with mustard oil, demonstrating that NMB contributes to neuro
48 ibition of the tail-flick reflex produced by mustard oil following spinal or supraspinal administrati
49 ist L-365260 i.t. dose-dependently inhibited mustard oil hyperalgesia (ID50 = 364 ng) at doses approx
50 R48692 (3.5 micrograms) into the RVM blocked mustard oil hyperalgesia and inhibited the tail-flick re
52 s in outward rectification of single channel mustard oil (I(MO)) current-voltage relationships (I-V)
53 zation of TRPV1 after TRPA1 stimulation with mustard oil in a calcium and cAMP/protein kinase A (PKA)
55 n is regulated by TRPV1, and it appears that mustard oil-induced TRPA1 internalization is prevented b
58 gest that secondary hyperalgesia produced by mustard oil is mediated largely by a central, centrifuga
59 al desensitization of TRPA1 by capsaicin and mustard oil is not influenced by activation of protein p
61 so exhibited by ART-OE mice to capsaicin and mustard oil, measured using a two-choice drinking test.
62 supratentorial dura mater were activated by mustard oil (MO) and the responses of second-order neuro
64 g behavior following masseteric injection of mustard oil (MO) was quantified in lightly anesthetized
65 ects of ACEA on the TRPA1-selective agonist, mustard oil (MO), for calcitonin gene-related peptide (C
66 cular injection of an inflammatory irritant, mustard oil (MO), induces significant edema formation in
68 ion, NGF evoked a time-dependent increase of mustard oil (MO)-evoked TRPA1 activation in trigeminal g
70 Saturating activation by cinnamaldehyde or mustard oil occluded potentiation but did not interfere
74 e, the pungent principle of wasabi and other mustard oils, produces pain by activating TRPA1, an exci
77 are innervated by menthol-, capsaicin-, and mustard oil-responsive sensory neurons and are required
80 racolonic application of either capsaicin or mustard oil, stimuli known to evoke sustained nociceptor
81 fibre brush stimulus and a noxious C fibre (mustard oil) stimulus were extracellularly recorded and
82 e display behavioral deficits in response to mustard oil, to cold ( approximately 0 degrees C), and t
83 uced Fos expression in the spinal cord after mustard oil treatment but significantly increased the re
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