ライフサイエンスコーパス: trigeminovascular

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1 In addition, they inhibit surrogates for trigeminovascular activation, including expression of ca

2 rtant consequences for neuroinflammation and trigeminovascular activation.

3 uated the response of spontaneous and evoked trigeminovascular activity of second order trigemontotha

4 mplicated in migraine visual aura, activates trigeminovascular afferents and evokes a series of corti

5 nucleus stimulation exhibited both neuronal trigeminovascular and cranial autonomic manifestations.

6 a CGRP-mAb, on the activity of second-order trigeminovascular dorsal horn neurons that receive perip

7 is study identifies massive axonal arbors of trigeminovascular (dura-sensitive) thalamic neurons in m

8 c neurons of rats responding to nocioceptive trigeminovascular inputs and tested the effect of olcege

9 of neuronal and vascular information in the trigeminovascular network represents a key event in the

10 reatment of acute migraine through selective trigeminovascular neuronal inhibition.

11 provide descending modulation of both basal trigeminovascular neuronal tone and Adelta-fiber dural-n

12 intracranial mechanical stimuli) in central trigeminovascular neurons (recorded in the dorsal horn),

13 d in the dorsal horn), but not in peripheral trigeminovascular neurons (recorded in the trigeminal ga

14 In 25 trigeminovascular neurons activated by CSD, mean firing

15 ion between axon terminals of the peripheral trigeminovascular neurons and cell bodies of their centr

16 suggest that neither peripheral nor central trigeminovascular neurons are directly inhibited by suma

17 es photic signal from the retina to thalamic trigeminovascular neurons believed to play a critical ro

18 gh-threshold (HT) but not wide-dynamic range trigeminovascular neurons by cortical spreading depressi

19 nd sensitization of high-threshold (central) trigeminovascular neurons by cortical spreading depressi

20 -we now report that CSD can activate central trigeminovascular neurons in the spinal trigeminal nucle

21 rtical spreading depression (CSD)-sensitized trigeminovascular neurons in the spinal trigeminal nucle

22 In 27 trigeminovascular neurons not activated by CSD, mean fir

23 that sensitization of peripheral and central trigeminovascular neurons plays an important role in the

24 capable of activating peripheral and central trigeminovascular neurons that underlie the headache of

25 old (HT) neurons, but not wide-dynamic range trigeminovascular neurons, and that the inhibitory effec

26 a manifestation of sensitization of central trigeminovascular neurons, we examined whether triptan t

27 d directly on peripheral rather than central trigeminovascular neurons.

28 In this model of trigeminovascular nociception, adenosine A1 receptor act

29 ead to studies of their effects on models of trigeminovascular nociception.

30 caudal medulla and the spinal cord following trigeminovascular nociceptive activation by electrical s

31 Activation and sensitization of trigeminovascular nociceptive pathways is believed to co

32 modulation of dural and/or cutaneous facial trigeminovascular nociceptive responses, from the brains

33 ically analgesic, are known to inhibit dural trigeminovascular nociceptive responses.

34 GABAA receptor that results in inhibition of trigeminovascular nociceptive transmission.

35 role of adenosine A1 receptors in a model of trigeminovascular nociceptive transmission.

36 ain fibers is inflamed and in turn activates trigeminovascular nociceptors that reach the affected pe

37 ned, but appear to involve either peripheral trigeminovascular or brainstem pathways, or both.

38 t the following sequence of events along the trigeminovascular pain pathway of this patient.

39 unique qualities point to activation of the trigeminovascular pathway as a prerequisite for explaini

40 Evidence for modulation of the trigeminovascular pathway by light and identification of

41 nociceptors--the first-order neurons of the trigeminovascular pathway thought to underlie migraine h

42 SD that lead up to delayed activation of the trigeminovascular pathway.

43 We propose that trigeminovascular projections from the medullary dorsal

44 nisms underlying the modulation of medullary trigeminovascular (Sp5C) neurons have not been fully ide

45 itive NMDA receptor antagonist MK-801, and a trigeminovascular-specific stimulus.

46 l spreading depression and activation of the trigeminovascular system and its constituent neuropeptid

47 leased centrally following activation of the trigeminovascular system and that each may be involved i

48 pheral and central nervous systems, with the trigeminovascular system and the cerebral cortex among t

49 (CGRP) is associated with activation of the trigeminovascular system and transmission of nociceptive

50 Bidirectional trafficking by which the trigeminovascular system can activate the same brain are

51 e there ascending pathways through which the trigeminovascular system can induce the wide variety of

52 ucleus caudalis following stimulation of the trigeminovascular system in anaesthetised guinea-pigs.

53 ifferential peptidergic innervation from the trigeminovascular system to cranial vessels and may be i

54 o recognize the implicit contribution of the trigeminovascular system to their pathophysiology.

55 vation of the central noradrenergic systems, trigeminovascular system, and hypothalamic pituitary adr

56 cortical spreading depression activated the trigeminovascular system, which is followed by a series

57 This system is known as the trigeminovascular system.

58 sion is likely to be involved in nociceptive trigeminovascular transmission within the trigeminocervi

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