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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 ects of epileptic seizure on the activity of trigeminovascular Adelta-, C-, wide-dynamic range, and h
5 mplicated in migraine visual aura, activates trigeminovascular afferents and evokes a series of corti
6  nucleus stimulation exhibited both neuronal trigeminovascular and cranial autonomic manifestations.
7  a CGRP-mAb, on the activity of second-order trigeminovascular dorsal horn neurons that receive perip
8 is study identifies massive axonal arbors of trigeminovascular (dura-sensitive) thalamic neurons in m
9 c neurons of rats responding to nocioceptive trigeminovascular inputs and tested the effect of olcege
10  of neuronal and vascular information in the trigeminovascular network represents a key event in the
11 reatment of acute migraine through selective trigeminovascular neuronal inhibition.
12  provide descending modulation of both basal trigeminovascular neuronal tone and Adelta-fiber dural-n
13  intracranial mechanical stimuli) in central trigeminovascular neurons (recorded in the dorsal horn),
14 d in the dorsal horn), but not in peripheral trigeminovascular neurons (recorded in the trigeminal ga
15                                        In 25 trigeminovascular neurons activated by CSD, mean firing
16 ion between axon terminals of the peripheral trigeminovascular neurons and cell bodies of their centr
17  suggest that neither peripheral nor central trigeminovascular neurons are directly inhibited by suma
18 es photic signal from the retina to thalamic trigeminovascular neurons believed to play a critical ro
19 nd sensitization of high-threshold (central) trigeminovascular neurons by cortical spreading depressi
20 gh-threshold (HT) but not wide-dynamic range trigeminovascular neurons by cortical spreading depressi
21 tral (wide dynamic range and high-threshold) trigeminovascular neurons in intact and anesthetized dur
22 rtical spreading depression (CSD)-sensitized trigeminovascular neurons in the spinal trigeminal nucle
23 -we now report that CSD can activate central trigeminovascular neurons in the spinal trigeminal nucle
24 uced activation and sensitization of central trigeminovascular neurons in the spinal trigeminal nucle
25                                        In 27 trigeminovascular neurons not activated by CSD, mean fir
26 that sensitization of peripheral and central trigeminovascular neurons plays an important role in the
27           Most preclinical studies involving trigeminovascular neurons sample neurons that are respon
28 capable of activating peripheral and central trigeminovascular neurons that underlie the headache of
29 old (HT) neurons, but not wide-dynamic range trigeminovascular neurons, and that the inhibitory effec
30  a manifestation of sensitization of central trigeminovascular neurons, we examined whether triptan t
31 d directly on peripheral rather than central trigeminovascular neurons.
32 d activation and sensitization of HT and WDR trigeminovascular neurons.
33 e dynamic range (WDR) central dura-sensitive trigeminovascular neurons.
34                             In this model of trigeminovascular nociception, adenosine A1 receptor act
35 ead to studies of their effects on models of trigeminovascular nociception.
36 caudal medulla and the spinal cord following trigeminovascular nociceptive activation by electrical s
37              Activation and sensitization of trigeminovascular nociceptive pathways is believed to co
38  modulation of dural and/or cutaneous facial trigeminovascular nociceptive responses, from the brains
39 ically analgesic, are known to inhibit dural trigeminovascular nociceptive responses.
40 GABAA receptor that results in inhibition of trigeminovascular nociceptive transmission.
41 role of adenosine A1 receptors in a model of trigeminovascular nociceptive transmission.
42  enhanced transmission of sensory, including trigeminovascular nociceptive, signals from thalamic nuc
43 ain fibers is inflamed and in turn activates trigeminovascular nociceptors that reach the affected pe
44 ned, but appear to involve either peripheral trigeminovascular or brainstem pathways, or both.
45 t the following sequence of events along the trigeminovascular pain pathway of this patient.
46 that the activation of all components of the trigeminovascular pathway (i.e., peripheral and central
47 tions that manifest at various levels of the trigeminovascular pathway and lead to the recruitment of
48  unique qualities point to activation of the trigeminovascular pathway as a prerequisite for explaini
49               Evidence for modulation of the trigeminovascular pathway by light and identification of
50  nociceptors--the first-order neurons of the trigeminovascular pathway thought to underlie migraine h
51 itization of primary afferent neurons in the trigeminovascular pathway, but the underlying mechanisms
52 SD that lead up to delayed activation of the trigeminovascular pathway.
53 -related areas in the CNS and the peripheral trigeminovascular pathway.
54 from the activation and sensitization of the trigeminovascular pathway.
55                              We propose that trigeminovascular projections from the medullary dorsal
56 nisms underlying the modulation of medullary trigeminovascular (Sp5C) neurons have not been fully ide
57 itive NMDA receptor antagonist MK-801, and a trigeminovascular-specific stimulus.
58 d volume increases, inflammation and related trigeminovascular system activation.
59 l spreading depression and activation of the trigeminovascular system and its constituent neuropeptid
60 ignalling, shedding light on its role in the trigeminovascular system and migraine pathogenesis.
61 leased centrally following activation of the trigeminovascular system and that each may be involved i
62 pheral and central nervous systems, with the trigeminovascular system and the cerebral cortex among t
63  (CGRP) is associated with activation of the trigeminovascular system and transmission of nociceptive
64 ood, the activation and sensitization of the trigeminovascular system are believed to play a major ro
65       Bidirectional trafficking by which the trigeminovascular system can activate the same brain are
66 e there ascending pathways through which the trigeminovascular system can induce the wide variety of
67 ucleus caudalis following stimulation of the trigeminovascular system in anaesthetised guinea-pigs.
68 ys, 40 years after the initial proposal, the trigeminovascular system is widely accepted as having a
69 ifferential peptidergic innervation from the trigeminovascular system to cranial vessels and may be i
70 o recognize the implicit contribution of the trigeminovascular system to their pathophysiology.
71 vation of the central noradrenergic systems, trigeminovascular system, and hypothalamic pituitary adr
72          We also discuss the role of SD, the trigeminovascular system, and the impact of pharmacologi
73 ctivation of the different components of the trigeminovascular system, and the second is that the act
74                            CSD activates the trigeminovascular system, evoking a meningeal inflammato
75  cortical spreading depression activated the trigeminovascular system, which is followed by a series
76                  This system is known as the trigeminovascular system.
77 sion is likely to be involved in nociceptive trigeminovascular transmission within the trigeminocervi