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1 stions closely related to clinically treated visceral pain.
2 d interpretation of brain-imaging studies of visceral pain.
3 erve as a viable target for the treatment of visceral pain.
4 iding a suitable target for the treatment of visceral pain.
5 lamus and the DC play major roles in chronic visceral pain.
6 onal hyperexcitability in a model of chronic visceral pain.
7 , and may be a potential target for treating visceral pain.
8 odels of acute pain, postoperative pain, and visceral pain.
9 or mediator of acute, acute inflammatory, or visceral pain.
10 tinal motility and modulation of somatic and visceral pain.
11 ropod cells is a major step in understanding visceral pain.
12 ood may be vulnerability factors for chronic visceral pain.
13 el diseases (IBD) for its ability to promote visceral pain.
14 ial therapeutic targets for the treatment of visceral pain.
15 able probiotics have the potential to modify visceral pain.
16 t-cell-dependent mechanism induced increased visceral pain.
17 r (OBD) underlie the most prevalent forms of visceral pain.
18 del of cystitis, a well-established model of visceral pain.
19 ive GUCY2C neuropod-cell signaling underlies visceral pain.
20 eption in psychiatric conditions and chronic visceral pain.
21 hat determines hemispheric lateralization of visceral pain.
22 era may be insufficient in targeting chronic visceral pain.
23 mechanisms by which the ECS links stress and visceral pain.
24 r non-pain negative affect do not respond to visceral pain.
25 ut motility, and increases the perception of visceral pain.
26 eptive effects in assays of inflammatory and visceral pain.
27 revented chronic stress-induced increases in visceral pain.
28 the involvement of TLR4 in the modulation of visceral pain.
29 (including opioid-induced constipation), and visceral pain.
30 hysiologic response, and brain processing of visceral pain.
31 reducing amygdala engagement during expected visceral pain.
32 ly to contribute to the emergence of chronic visceral pain.
33  of negative affect on central processing of visceral pain.
34  sumatriptan was investigated in 2 models of visceral pain.
35 bs of the functional responses associated to visceral pain.
36 ify the receptor involved in facilitation of visceral pain.
37 redict efficacy of medications developed for visceral pain.
38 e sensation and pattern of referral of their visceral pain.
39 A receptor signalling could be used to treat visceral pain.
40 represents an important component of chronic visceral pain(1).
41 g butyrate enemas to induce non-inflammatory visceral pain, acute morphine administration produced do
42 ion during the expectation and experience of visceral pain, along with unpleasantness ratings in a co
43 ception, motility, and central processing of visceral pain; although further research is required in
44 ized As safe) bacterium in the management of visceral pain and anxious profile of IBS patients.
45 ut involvement of this signalling pathway in visceral pain and attendant sex differences has not been
46 ypes, correlates with perceived intensity of visceral pain and discomfort, and shows specificity to p
47 rious acute stimuli such as ischemic insult, visceral pain and electroconvulsive shock.
48 fferents during mesenteric ischaemia induces visceral pain and evokes excitatory cardiovascular respo
49 le of neurokinin (NK) B and NK3 receptors in visceral pain and gastrointestinal disorders has not bee
50 ite stable activation of networks processing visceral pain and its anticipation.
51           Genetic mechanisms associated with visceral pain and motor functions in health and function
52 y motor cortex) for the treatment of chronic visceral pain and new parameters of stimulation, such as
53                  The TLR4 deficiency reduced visceral pain and prevented the development of chronic p
54 fferents during mesenteric ischaemia induces visceral pain and reflexly excites the cardiovascular sy
55 network involved in aversive conditioning of visceral pain and, thus, anticipation.
56 a mouse p-phenylquinone (PPQ) model of acute visceral pain, and a rat spinal nerve ligation (SNL) mod
57  complex CNS disorders including depression, visceral pain, and cocaine addiction.
58 res underlying chronic musculoskeletal pain, visceral pain, and headaches.
59                               ExPANs mediate visceral pain, and myenteric neurons mediate colon motil
60  to NTS2, may be potentially useful to treat visceral pain, and psychosis without concomitant side ef
61 hase included areas commonly associated with visceral pain (anterior cingulate cortex, insula, and pr
62 tal and hippocampal circuitry engaged during visceral pain anticipation as well as on pain experience
63 on sensory neurons and their contribution to visceral pain are unknown.
64 d fear and anxiety (the affective aspects of visceral pain) are the domain of nodose afferents.
65                      These results show that visceral pain arising from the proximal colon activates
66                                              Visceral pain associated with irritable bowel syndrome a
67 1 antagonist SB-366791 markedly reduced both visceral pain behavior and referred somatic hyperalgesia
68                                              Visceral pain behaviors were assessed as degree of hunch
69 one-methiodide did not induce an increase in visceral pain behaviors.
70 te to our understanding of the processing of visceral pain, but also have clinical implications for t
71 mote gastrointestinal motility and attenuate visceral pain, but concerns about adverse reactions have
72 hanced interoceptive sensitivity and chronic visceral pain, but their putative interaction remains un
73 ad mood on the expectation and experience of visceral pain by combining experimental endotoxemia with
74 is, we found that enteric glia contribute to visceral pain by secreting factors that sensitized senso
75 tential site of action for the modulation of visceral pain by triptans.
76                                     Although visceral pain can be generally provoked by mechanical di
77 teric glial-neuron signaling might alleviate visceral pain caused by inflammatory disorders.
78 tate of "latent sensitization" to subsequent visceral pain characterized by extended duration of hype
79 nt of strategies that may improve therapy of visceral pain conditions using already available medicat
80 al conditions may provide new treatments for visceral pain conditions.
81 ld induce a state of latent sensitization to visceral pain conditions.
82 treatment toward these mechanisms of chronic visceral pain derived from clinical trials.
83                                      Chronic visceral pain disorders, such as interstitial cystitis/b
84                                              Visceral pain disorders, such as irritable bowel syndrom
85 that central sensitisation may contribute to visceral pain disorders.
86 2Y-dependent mechanisms in the generation of visceral pain during gastrointestinal disease.
87    We have shown that actual and anticipated visceral pain elicit similar cortical responses.
88 n of the MCC and related areas involved with visceral pain encoding are associated with poor clinical
89               Developments in the scientific visceral pain field are encouraging.
90  a new range of applications for them in the visceral pain field.
91                                              Visceral pain following infection or inflammation is a m
92  and spinal plasticity in the maintenance of visceral pain from pancreatitis.
93 could be useful to treat transient and acute visceral pain from the uterine cervix.
94 owever, their efficacy in treatment of acute visceral pain has not been explored.
95                                 Migraine and visceral pain have also been associated with voltage-gat
96 fer in the central nervous system, underlies visceral pain hypersensitivity and non-cardiac chest pai
97                                The prolonged visceral pain hypersensitivity in patients with non-card
98  via the EP-1 receptor, contributes to human visceral pain hypersensitivity.
99                                 Detection of visceral pain in chronic pancreatitis predicts pain reli
100 signalling via p38 MAPK for the treatment of visceral pain in gastrointestinal disease.
101 y of these drug targets for the treatment of visceral pain in gastrointestinal disease.
102  are able to counteract inflammation-induced visceral pain in mice.
103 associated with the onset or exacerbation of visceral pain in patients with irritable bowel syndrome
104 sed by sensory neurons, mediates somatic and visceral pain in response to direct activation or noxiou
105 rategies are considered for the treatment of visceral pain in such conditions as renal colic, interst
106 c mechanisms regulate chronic stress-induced visceral pain in the peripheral nervous systems of rats.
107 gic mechanosensory transduction can initiate visceral pain in urinary bladder, ureter, gut and uterus
108  determine if ACC neuron activation enhances visceral pain in viscerally hypersensitive rats and to i
109 tment reduces excitability and G-CSF-induced visceral pain in vivo.
110 ainst P2X3 may have therapeutic potential in visceral pain indications.
111      This condition likely reflects enhanced visceral "pain" intensity as a consequence of persistent
112  translation of efficacy in animal models of visceral pain into the clinic.
113                            The perception of visceral pain is a complex process involving the spinal
114                                              Visceral pain is a leading cause of morbidity in gastroi
115                                              Visceral pain is a prevalent clinical problem and one of
116                                              Visceral pain is among the most prevalent and bothersome
117 , for >20% of the global population, chronic visceral pain is an unpleasant and often excruciating re
118                         Accordingly, chronic visceral pain is debilitating, reduces the quality of li
119 tely, the diagnosis and treatment of chronic visceral pain is difficult, in part because our understa
120                                      Chronic visceral pain is one of the most common reasons for pati
121           An important step in understanding visceral pain is the development of comprehensive phenot
122  in mice and humans but its significance for visceral pain is unknown.
123       Gastrointestinal (GI) pain - a form of visceral pain - is common in some disorders, such as irr
124  a lot of effort into the development of new visceral pain models.
125 he formalin, complete Freund's adjuvant, and visceral pain models.
126 lockade of referred hypersensitivity in both visceral pain models.
127 esses either inflammatory or noninflammatory visceral pain, most likely through peripheral 5HT1(B)/(D
128  overlap of gastroduodenal symptoms, such as visceral pain or hypersensitivity, is often observed in
129                                              Visceral pain originates from visceral organs in respons
130 en made towards improving the translation of visceral pain, particularly with regard to the activatio
131 ng evidence in support of the existence of a visceral pain pathway that ascends in the dorsal column
132 ative behavioural models evoking somatic and visceral pain pathways, we identify the requirement for
133 equent development of neuroplasticity within visceral pain pathways.
134 enal and rectal barostat studies to evaluate visceral pain perception measured with a visual analog s
135 rain-imaging studies to date have confounded visceral pain perception with anticipation.
136                       In mice, it attenuates visceral pain perception, indicating an antinociceptive
137 s suggest sex differences in somatic but not visceral pain perception, motility, and central processi
138  can prevent the establishment of persistent visceral pain postcolitis.
139       Here we examine the role of NaV 1.7 in visceral pain processing and the development of referred
140                            Current models of visceral pain processing derived from metabolic brain im
141 entral nervous system (CNS) abnormalities in visceral pain processing in IBS.
142 c noxious heat pain, but is not required for visceral pain processing, and advocate that pharmacologi
143 ng aetiology, physiology and pharmacology of visceral pain proves the clinical importance of this pai
144 have shown a significant tonic modulation of visceral pain, raising the question of whether endogenou
145                                As a model of visceral pain, rectal distensions were implemented, whic
146  of these models addresses specific types of visceral pain, related to the urogenital tract (n=3), to
147  displayed spontaneous, morphine-reversible, visceral pain-related behaviors such as hunching and voc
148 tage pancreatic cancer displayed significant visceral pain-related behaviors, whereas systemic admini
149 ficantly, OEA administration in mice induced visceral pain-related behaviours that were inhibited by
150          The effective management of chronic visceral pain remains of critical importance for the qua
151 uroticism, of which little is known about in visceral pain research.
152 ed that this caused a robust increase in the visceral pain response.
153 f/f/p) mutant mice showed normal thermal and visceral pain responses but were less sensitive to mecha
154 e in the modulation of ACC sensitization and visceral pain responses in VH rats.
155 C) neurons has a critical role in modulating visceral pain responses in viscerally hypersensitive (VH
156 C plays a critical role in the modulation of visceral pain responses in viscerally hypersensitive rat
157 LR4 specific antagonist, TAK-242, attenuated visceral pain sensation in animals with functional TLR4
158 d histone acetylation of genes that regulate visceral pain sensation in the peripheral nervous system
159 However, the central contribution of TLR4 in visceral pain sensation remains elusive.
160 he gut microbiota is required for the normal visceral pain sensation.
161 tic (noxious heat pain threshold) but not in visceral pain signalling.
162 ce or correct microbial dysbiosis may impact visceral pain.SIGNIFICANCE STATEMENT Commercially availa
163 sfunction in both early episodic and chronic visceral pain states points to an urgent need to elucida
164      In all sessions, an identical series of visceral pain stimuli was accomplished, signaled by pred
165 ponses to mechanical, thermal, chemical, and visceral pain stimuli, as well as itch.
166 ith either repeated administration of a mild visceral pain stimulus (intraperitoneal injection of ace
167 siology of irritable bowel syndrome (IBS), a visceral pain syndrome occurring more commonly in women.
168 volved in sensory and cognitive appraisal of visceral pain; the right prefrontal cortex seems to be i
169 hosocial impairment, high life stress, a low visceral pain threshold, and activation of the midcingul
170 heral NMDA receptors are important in normal visceral pain transmission, and may provide a novel mech
171 t potent antinociception in a mouse model of visceral pain upon systemic administration.
172 s, and Cat-S activates nociceptors to induce visceral pain via protease-activated receptor-2.
173                                              Visceral pain (VP) is a global problem with complex etio
174                                              Visceral pain was evaluated with colorectal distension.
175                                              Visceral pain was measured in response to colorectal dis
176 la (RVM), a site of descending modulation of visceral pain, was determined by (1) testing the effects
177 eased number and size along with severity of visceral pain, which may be associated with enhanced neu
178 ht be used to promote motility and alleviate visceral pain, while restricting systemic bioavailabilit
179 algesic activity in a mouse model of chronic visceral pain, without inducing unwanted central effects

 
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