ライフサイエンスコーパス: pronociceptive

1 litatory systems and enhanced expression and pronociceptive actions of spinal dynorphin.

2 ins (PGs) are mediators of inflammation with pronociceptive actions within the PAG under normal condi

3 Medication-induced persistent pronociceptive adaptations might be responsible for lowe

4 in" intensity as a consequence of persistent pronociceptive adaptive changes.

5 Thus, endogenous dynorphin had both pronociceptive and antinociceptive actions after nerve i

6 ive pathways is still controversial, as both pronociceptive and antinociceptive actions have been rep

7 Both pronociceptive and antinociceptive effects of HA are med

8 ipheral pain signaling reflects a balance of pronociceptive and antinociceptive influences; the contr

9 tentional load; specific RVM regions showing pronociceptive and antinociceptive processes (in line wi

10 We show that pronociceptive and inflammatory factors, such as nerve g

11 ge, (2) that upregulated spinal dynorphin is pronociceptive and required for the maintenance of persi

12 peripheral and central 5-HT(3) receptors is pronociceptive and that the contribution of peripheral 5

13 of the delta opioid receptor and the MOR are pronociceptive, and that drugs that spare such heteromer

14 of the rostral ventromedial medulla induces pronociceptive behaviors in rats.

15 The pronociceptive effect of alpha-CTX MII was partially blo

16 The pronociceptive effect of HXA(3) correlated with enhanced

17 ivation of these channels contributes to the pronociceptive effects of ATP.

18 The pronociceptive effects of GAs combined with surgical tis

19 causes generalized hyperalgesia by enhancing pronociceptive effects of immune mediators.

20 of protein kinase Cepsilon (PKCepsilon), the pronociceptive effects of PGE2 in DAMGO-treated rats dem

21 counteract the EP2 and EP4 receptor-mediated pronociceptive effects of PGE2.

22 that such modulation cannot account for the pronociceptive effects of this gasotransmitter.

23 a and hyperalgesia, and at least part of the pronociceptive effects of TNFalpha have been suggested a

24 olecystokinin (CCK) has been identified as a pronociceptive endogenous peptide which also possesses a

25 ciception without activating the concomitant pronociceptive functions that monomeric KOR also subserv

26 ventrolateral periaqueductal gray (vlPAG) is pronociceptive in naive and acutely inflamed animals, bu

27 Here, we tested the hypothesis that pronociceptive individuals have an enhanced TSP response

28 Redirecting the flow of pronociceptive intracellular cAMP toward up-regulation o

29 n-coupled receptor (GPCR), C5aR, is a potent pronociceptive mediator in several models of inflammator

30 The altered response to pronociceptive mediators involved a switch in coupling o

31 , mechanical hyperalgesia induced by diverse pronociceptive mediators involved in inflammatory and ne

32 reverses the hyperalgesia induced by diverse pronociceptive mediators, prostaglandin E2, epinephrine,

33 states via secretion of proinflammatory and pronociceptive mediators, such as tumor necrosis factor

34 nt sensitization characterized by persistent pronociceptive neural adaptations in dural afferents and

35 When subjects were grouped as pronociceptive or antinociceptive based on whether they

36 he possibility that cholecystokinin (CCK), a pronociceptive peptide, may drive such descending facili

37 ia caused by inflammation, nerve injury, and pronociceptive receptor activation.

38 tionally, Pip5k1c haploinsufficiency reduces pronociceptive receptor signaling and TRPV1 sensitizatio

39 (DRG) neurons and if these kinases regulate pronociceptive receptor signaling.

40 levels were elevated coincident with injury/pronociceptive receptor stimulation.

41 vels were elevated in the absence of ongoing pronociceptive receptor stimulation.

42 Numerous pain-producing (pronociceptive) receptors signal via phosphatidylinosito

43 Our data, therefore, supports a pronociceptive role for 5-HT2 receptors, most likely thr

44 nisms by which Substance P (Sub P) assumes a pronociceptive role in the rostral ventromedial medulla

45 5HT3 receptors play a pronociceptive role in the spinal cord and ondansetron h

46 following noxious stimulation, underlie the pronociceptive role of Sub P under conditions of persist

47 ter thal-BA 3a or RVM-sgACC FC respectively, pronociceptive subjects showed greater TSP responses.

48 ing the anti-opioid peptide cholecystokinin, pronociceptive Substance P (SP), Neurokinin B, and a lat

49 e that GPR55 activation at central levels is pronociceptive, suggesting that interfering with GPR55 s

50 ptors eliminated morphine tolerance, OIH and pronociceptive synaptic long-term potentiation without a

51 of KOR and thereby endogenous dynorphin from pronociceptive to antinociceptive.

52 pain-modulatory capabilities are regarded as pronociceptive, whereas individuals with reduced pain pr