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1 orsal horn important for the relay of pelvic visceral afferents.
2 nd directly activated by solitary tract (ST) visceral afferents.
3 n by a mechanism dependent on mast cells and visceral afferents.
4  means of the activation of mechanosensitive visceral afferents.
5 tract, the target of nodose ganglion-derived visceral afferents.
6  targets, resembling those features of known visceral afferents.
7 he presynaptic release of glutamate from the visceral afferents.
8 1), stimulated most (six of seven) abdominal visceral afferents.
9 ar, respiratory, gastrointestinal, and other visceral afferents.
10 thecal nicotine and by stimulation of spinal visceral afferents.
11 tric junctions, characteristic of excitatory visceral afferents.
12 s matched projection patterns of first order visceral afferents.
13                                      Cranial visceral afferents activate central pathways that mediat
14 lutamate antagonist NBQX, but independent of visceral afferent activation.
15   These results demonstrate that somatic and visceral afferent and efferent functional columns are di
16 the antagonist does not increase intake when visceral afferent and efferent pathways have been interr
17  immunohistochemistry for markers of various visceral afferent and efferent systems with c-Fos-based
18 neurons in the NTS are directly activated by visceral afferents and are important for the control of
19 ironment, that has the capacity to stimulate visceral afferents and facilitate neuronal TRPV1 signali
20                             Blockade of both visceral afferents and glutamatergic transmission in the
21 use NTS is a major interface between sensory visceral afferents and the CNS, NTS CA neurons are ideal
22  the relationship between BDNF dependence of visceral afferents and the location and timing of BDNF e
23 he synaptic relationship of these neurons to visceral afferents and their modulation by CCK and opioi
24 for direct actions of MOR ligands on primary visceral afferents and their second-order neuronal targe
25 (e.g., regeneration) manipulations affecting visceral afferents and their target tissues.
26 NTS neurons is generally dominated by single visceral afferents and therefore focused on a single aff
27 n peripheral nociceptive neurons, as well as visceral afferents, and has been shown to act as a thres
28  the Cre-LoxP technology to trace identified visceral afferents, and our data suggest a previously un
29 erential processing of A- and C-type cranial visceral afferents beginning as early as this first cent
30 ibed many of the physiological properties of visceral afferents, but not much is known regarding thei
31 leus (PVN) release oxytocin (OT) to modulate visceral afferent communication with NTS neurons.
32  caudal NTS not only serves as a location of visceral afferent convergence and integration, but may a
33                                   Vestibular-visceral afferents derive from neurons concentrated at c
34 dentify a potential satiety pathway in which visceral afferents directly activate NTS POMC-EGFP neuro
35 ted the effects of inflammatory mediators on visceral afferent discharge and afferent responses to br
36 minal ischaemia contributes to activation of visceral afferents during ischaemia, at least in part, b
37                    Activation of sympathetic visceral afferents during mesenteric ischaemia induces v
38           Activation of abdominal splanchnic visceral afferents during mesenteric ischaemia induces v
39  Activity of ischaemically sensitive cardiac visceral afferents during myocardial ischaemia induces b
40                                      Cranial visceral afferents enter the brain at the solitary tract
41    Although the central terminals of cranial visceral afferents express vanilloid receptor 1 (VR1), l
42                                              Visceral afferents expressing transient receptor potenti
43 uces profuse sprouting of nociceptive pelvic visceral afferent fibers that correlates with increased
44 in the mudpuppy, PACAP is found primarily in visceral afferent fibers, originating from cells in eith
45 atially related to terminal sites of primary visceral afferents from 1) orosensory receptors (e.g., r
46 P2X receptor activation causes excitation of visceral afferents; however, the impact of P2Y receptor
47 TS) receives dense terminations from cranial visceral afferents, including those from the gastrointes
48 DA receptors may explain in part how primary visceral afferents, including vagal afferents, can maint
49           To test how NTS CA neurons process visceral afferent information carried by solitary tract
50                  Such segregation means that visceral afferent information followed separate lines to
51 ies and imply more widespread convergence of visceral afferent information within the insula.
52  amygdala, is considered to rely on embedded visceral afferent information, although few details are
53 ivation of regions involved in processing of visceral afferent information.
54                                      Cranial visceral afferents innervate second-order nucleus tractu
55 er, the impact of P2Y receptor activation on visceral afferents innervating the gut is unclear.
56 mmation, in the dermatome that overlaps with visceral afferent innervations.
57 tary tract (NST; principal locus integrating visceral afferent input and part of the gastric vagovaga
58 e solitary tract (NST) processes substantial visceral afferent input and sends divergent projections
59 on, consistent with differences in ascending visceral afferent input.
60 cerally hypersensitive rats is restricted to visceral afferent input.
61 he principal site for integration of primary visceral afferent inputs to central autonomic pathways a
62 cted capsaicin, which preferentially excites visceral afferents, is mediated by the hypothalamo-pitui
63        Acute intestinal ischaemia stimulates visceral afferent nerves but the mechanisms responsible
64 80 years elapsed before it became clear that visceral afferent neurons could themselves also be targe
65 ic factor (BDNF) supports survival of 50% of visceral afferent neurons in the nodose/petrosal sensory
66 ignals that alter the chemical properties of visceral afferent neurons.
67 nce of transmitter phenotype of these mature visceral afferent neurons.
68  first time that persistence of a heightened visceral afferent nociceptive input to the ACC induces A
69              Together, we found that cranial visceral afferent pathways are structured distinctly wit
70 activation profiles mean that these parallel visceral afferent pathways encode viscerosensory signals
71  we examined the synaptic characteristics of visceral afferent pathways to the central nucleus of the
72 istent activation in regions associated with visceral afferent processing (ie, thalamus, insula, ante
73                                           TL visceral afferents projecting seem to be more involved i
74    The development of human gastrointestinal visceral afferent recordings has allowed direct comparis
75 ypophagia, as the PBN receives gustatory and visceral afferent relays and descending input from sever
76 tested the hypothesis that duodenal-specific visceral afferent sensitivity exists in patients with SO
77 y described in brainstem areas associated to visceral afferent sensory integration.
78  proposed mechanisms of injury in peripheral visceral afferents (sensory) pathways and the enteric ne
79 hindbrain to produce malaise by potentiating visceral afferent signaling at the central processes of
80 fects of CB1 cannabinoid agonists and TNF on visceral afferent signaling in the rat hindbrain.
81 arly a century has left the issue of whether visceral afferent signals are essential for emotional ex
82 he dorsal vagal complex (DVC) that processes visceral afferent signals from and provides parasympathe
83 d in altered processing and/or modulation of visceral afferent signals.
84 fferences in processing and/or modulation of visceral afferent signals.
85 nent in regions corresponding to the general visceral afferent subdivision; the AP showed no such top
86 system represent a component of an ascending visceral afferent system.
87                    In the brainstem, cranial visceral afferent terminals in caudal solitary tract nuc
88 seizure suppression evoked by stimulation of visceral afferents terminating in NTS.
89             The vagus nerve contains primary visceral afferents that convey sensory information from
90 K stimulates ischaemically sensitive cardiac visceral afferents through a mechanism that is, at least
91 imulation of ischaemically sensitive cardiac visceral afferents through activation of kinin B2 recept
92 also show that exogenous IL-1beta sensitizes visceral afferents to histamine.
93 IL-1beta stimulates or sensitizes splanchnic visceral afferents to ischaemia and to the action of che
94 nucleus selectively relays input from pelvic visceral afferents to the LC.
95 d-order neurons within medial NTS to enhance visceral afferent transmission via presynaptic and posts
96 ultiplicative interaction between the pelvic visceral afferent transmitter vasoactive intestinal poly
97 ctive intestinal polypeptide (VIP), a pelvic visceral afferent transmitter.
98                                      Cranial visceral afferents travel via the solitary tract (ST) to
99                                      Primary visceral afferents were identified as sources of NADPHd-
100 ell degranulation with cromolyn, ablation of visceral afferents with capsaicin, and antagonism of cal
101  PE elicited by graded stimulation of spinal visceral afferents with intraperitoneal capsaicin and by
102  Thus, NTS CA neurons are directly driven by visceral afferents with output being modulated by presyn

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