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1 RVM and SSMoG Bayesian MLCs trained on OCT and SAP data
2 RVM and SSMoG MLCs were trained and tested on OCT-determ
3 RVM and SVM learning classifiers were trained and tested
4 RVM dermorphin or saporin did not alter SNL-induced expe
5 RVM dermorphin, saporin, or dermorphin-saporin did not c
6 RVM dermorphin-saporin injection prevented the maintenan
7 RVM dermorphin-saporin, but not dermorphin or saporin, s
8 RVM lidocaine blocked SNL-induced tactile and thermal hy
9 RVM lidocaine produced CPP, increased NAc c-Fos, and dop
10 RVM lidocaine, or bilateral lesions of the dorsolateral
11 RVM may be preferable to SVM, because it provides a Baye
12 RVM microinjection of dermorphin-saporin, but not of der
13 RVM neurons were studied 7-14 d after spinal nerve ligat
17 ed dorsal horn and RVM neurons to uncover an RVM-spinal cord-primary afferent circuit controlling pai
18 ng of genetically identified dorsal horn and RVM neurons to uncover an RVM-spinal cord-primary affere
20 rphine is thought to act in both the PAG and RVM by pre-synaptic inhibition of inhibitory GABAergic t
22 ircuit which includes the amygdala, PAG, and RVM is responsible for the expression of several forms o
23 transfer attenuates the increase in PVR and RVM, pulmonary vascular remodeling, and pressor response
25 erve injury induces death of antinociceptive RVM neurons that can be reduced or abolished by TUDCA.
28 ined including the LASSO, HyperLasso, BhGLM, RVM and the single-QTL mapping method based on logistic
31 the rostroventral medulla of the brainstem (RVM) exclusively facilitates spinal pain transmission bu
34 ue-Dawley rats, we demonstrate that discrete RVM neurons express MOR and CCK2; over 80% of these cell
35 activation of the dual GABA/enkephalinergic RVM neurons in adult animals substantially increased or
36 gs suggest that these CCK2-MOR co-expressing RVM neurons facilitate pain and can be directly activate
37 es confirmed activation of pain-facilitating RVM "on" cells and transient suppression of RVM "off" ce
40 mizing whole-cell patch-clamp recordings for RVM neurons in animals older than PN day 30 and compared
41 imized whole-cell patch-clamp recordings for RVM neurons in animals older than postnatal day 30 and c
42 The areas under the ROC curves (AUROCs) for RVMs trained on optimized feature sets of CSLO parameter
43 e neurotransmitter 5-HT itself released from RVM-spinal neurons contributes to descending pain modula
47 d GABA release in mature but not in immature RVM neurons suggesting the presence of local endocannabi
51 y depleting functional phenotypes of 5-HT in RVM neurons with regional shRNA interference (RNAi) of t
54 y, our data reveal the central role of PN in RVM descending facilitation during inflammatory and neur
55 a, respectively, were expressed primarily in RVM neurons exhibiting immunoreactivity to the NMDA rece
56 rt because whole-cell patch-clamp studies in RVM to date have been in young (PN day < 18) animals bec
57 phosphorylation of the NMDAR NR2A subunit in RVM via a signal transduction cascade involving IP(3), P
58 right LC; and main effect of temperature in RVM and a task x temperature interaction in right LC.
59 ndance of KOR in axons and axon terminals in RVM indicates a substantial role for presynaptic effects
65 ore, in control shRNA-treated animals, intra-RVM microinjection of brain-derived neurotrophic factor
68 fects of FeTMPyP(5+) were abrogated by intra-RVM naloxone, implicating potential interplay between PN
73 machine (SDP-SVM), relevance vector machine (RVM) and Ada-boost relevance vector machine are compared
75 ogReg, BLogReg and Relevance Vector Machine (RVM) gene selection algorithms are evaluated over the we
76 on increases in PVR, right ventricular mass (RVM), and pulmonary vascular remodeling that occur in ch
78 stral portion of the ventral medial medulla (RVM) is a crucial site for the supraspinal antinocicepti
82 oinjected in the rostroventromedial medulla (RVM) of rats with inflammatory injury induced by injecti
83 Neurons in the rostroventromedial medulla (RVM) project to spinal loci where the neurons inhibit or
85 were given into the rostral-ventral medulla (RVM), intrathecally (i.th.) or simultaneously into both
86 fused into the rostral ventromedial medulla (RVM) 10 min before a 30-min EA treatment at acupoint Hua
87 mug) into the rostral ventromedial medulla (RVM) also reversed the allodynia, showing this brain are
88 arising in the rostral ventromedial medulla (RVM) and (2) the presence of such pain manifests behavio
90 ty between the rostral ventromedial medulla (RVM) and other brainstem pain-modulatory regions, includ
92 Neurons of the rostral ventromedial medulla (RVM) are thought to critically contribute to this proces
93 ivation of the rostral ventromedial medulla (RVM) attenuates hyperalgesia and central sensitization i
94 ections to the rostral ventromedial medulla (RVM) constitute an essential neural circuit for opioid-b
96 neurons in the rostral ventromedial medulla (RVM) directly modulates spinal nociceptive transmission
97 ulation of the rostral ventromedial medulla (RVM) facilitates pain behaviours in neonates but inhibit
99 ences from the rostral ventromedial medulla (RVM) in neuropathic pain, but the underlying mechanisms
100 ystem from the rostral ventromedial medulla (RVM) in the brainstem and the 5-HT(3) receptor subtype i
101 sticity in the rostral ventromedial medulla (RVM) in the initiation and maintenance of experimental n
105 that PN in the rostral ventromedial medulla (RVM) is essential for descending nociceptive modulation
108 njected in the rostral ventromedial medulla (RVM) of rats 4 hr, 4 d, and 2 weeks after the induction
110 y (PAG) or the rostral ventromedial medulla (RVM) or by functional inactivation of neurons in these r
111 Neurons in the rostral ventromedial medulla (RVM) play critical and complex roles in pain modulation.
112 ivation of the rostral ventromedial medulla (RVM) prevents the analgesia but not the motor deficits p
113 neurons in the rostral ventromedial medulla (RVM) provide the major descending serotonergic projectio
114 input from the rostral ventromedial medulla (RVM) provides positive and negative modulation of spinal
115 ventricles or rostral ventromedial medulla (RVM) such that male rats exhibit significantly greater a
116 ve role in the rostral ventromedial medulla (RVM) under conditions of peripheral inflammatory injury,
117 neurons in the rostral ventromedial medulla (RVM), a brainstem region involved in modulation of nocic
118 ition zone and rostral ventromedial medulla (RVM), a key structure in descending pain modulation.
119 l nerve in the rostral ventromedial medulla (RVM), a major component of brainstem descending pain mod
121 tan within the rostral ventromedial medulla (RVM), a site of descending modulation of visceral pain,
122 changes in the rostral ventromedial medulla (RVM), a supraspinal site involved in the processing of p
123 ected into the rostral ventromedial medulla (RVM), but not following co-injections into the periaqued
124 neurons in the rostral ventromedial medulla (RVM), known to modify nociception in the spinal cord dor
125 ted within the rostral ventromedial medulla (RVM), nucleus accumbens (NAc), or rostral anterior cingu
126 caine into the rostral ventromedial medulla (RVM), or dorsolateral funiculus (DLF) lesion, abolishes
132 r) axons to serotonergic and nonserotonergic RVM neurons in rats, including neurons projecting to the
136 ibitory inputs that modulate the activity of RVM neurons in such a manner as to enhance the effects o
138 in the number of DVs in distal dendrites of RVM neurons that were immunoreactive for the neurokinin-
139 ral funiculus lesion (DLF) or destruction of RVM neurons expressing mu-opioid receptors with dermorph
140 was determined by (1) testing the effects of RVM administration of 5HT1(B/D) antagonists on systemic
141 The results demonstrated an involvement of RVM mu, but not kappa, receptors in EA-produced anti-hyp
147 serotonergic neurons comprise a minority of RVM neurons (23% of the total RVM neurons), they appear
148 s receiving SNL, we found that the number of RVM neurons decreased by 23% in the side ipsilateral to
149 sess changes in Sub P release, the number of RVM neurons that exhibited NK1R internalization was exam
151 and morphologically distinct populations of RVM neurons appear to modulate nociception by direct and
152 mechanisms by which distinct populations of RVM neurons facilitate or diminish pain remain elusive.
156 ic pain requires the activity of a subset of RVM neurons that are distinguished by co-expression of m
158 The recently-demonstrated suppression of RVM ON-cell activity by improgan may account for the pre
159 the effects of both BLa and MEa morphine on RVM cell activity, and interfered with the behavioral an
161 ed on whether they had greater thal-BA 3a or RVM-sgACC FC respectively, pronociceptive subjects showe
162 nt inflammatory pain, significantly more PAG-RVM cells were activated in males in comparison with fem
164 al dimorphism in the organization of the PAG-RVM circuit and its activation by persistent inflammator
165 ion and the functional activation of the PAG-RVM circuit are sexually dimorphic and may provide the a
167 es in the anatomical organization of the PAG-RVM pathway, and its activation during persistent inflam
168 dicate that the descending ventrolateral PAG/RVM system integrates a behavioral response of which ant
169 f MOR1 and DOR1 mRNAs in spinally projecting RVM neurons including serotonergic (5HT) cells by using
172 e in pulmonary arterial pressure (PAP), PVR, RVM, and pulmonary vascular remodeling in response to ch
178 fore induction of pancreatitis with a single RVM microinjection of dermorphin-saporin to eliminate ce
179 PAG activated by attentional load; specific RVM regions showing pronociceptive and antinociceptive p
180 cross-validation was used to train and test RVM and SVM classifiers on unique subsets of the full 16
185 work of supratentorial brain regions and the RVM whose activity was linearly related to pain intensit
186 nection between SP neurons in the LH and the RVM, the cholinergic agonist carbachol (125 nmol) was mi
188 whether the antinociception mediated by the RVM is associated with locomotor changes as has been rep
189 n LH-induced antinociception mediated by the RVM, we conducted an anatomical experiment using retrogr
190 These data suggest a prominent role for the RVM in mediating the sensitization of spinal neurons and
192 tivation of descending facilitation from the RVM for the expression of cranial and extracranial cutan
193 s indicate that the descending 5-HT from the RVM is an important contributor to pain facilitation dur
194 uggest that descending facilitation from the RVM plays a critical role in the maintenance, but not th
196 ivation of bulbospinal facilitation from the RVM, (2) increased pain decreases spinal opioid antinoci
197 de B labeled neurons were not evident in the RVM 4 days after microinjection of Sub P, although such
198 physiologically characterized neurons in the RVM after spinal nerve ligation, a model of neuropathic
200 e RVM, and blockade of CCK2 receptors in the RVM also blocked the rightward displacement of the spina
202 and [Leu(5)]enkephalin were increased in the RVM and in other brainstem nuclei in CFA-treated rats.
203 yr-D-Trp-Arg-Thr-Pen-Thr-NH(2) (CTAP) in the RVM antagonized both the marginal enhancement of the pot
204 monstrate that both on- and off-cells in the RVM are sensitized to innocuous and noxious mechanical s
205 entify CCK2-MOR co-expressing neurons in the RVM as potential therapeutic targets for neuropathic pai
206 Enhanced, endogenous CCK activity in the RVM during sustained morphine exposure may diminish spin
207 he endogenous opioid enkephalin (ENK) in the RVM during thermal hyperalgesia, suggesting potential in
208 -703,606 (5 microg) was microinjected in the RVM following LH stimulation with carbachol and abolishe
209 ce that CB2 receptor function emerges in the RVM in persistent inflammation and that selective CB2 re
211 hat phasic or evoked release of Sub P in the RVM is increased in response to noxious peripheral stimu
212 suggest that the distribution of KORs in the RVM may be influenced by reproductive hormone levels.
214 oinjection of NTB alone, but not CTAP in the RVM of CFA-treated rats, enhanced the hyperalgesia prese
215 onist AM630 increased mIPSC frequency in the RVM of CFA-treated rats, indicating that CB2 receptors a
218 ammatory injury increased the release in the RVM of opioid peptides with preferential affinity for th
220 is not known whether the same neurons in the RVM produce both direct and indirect modulation of nocic
221 Microinjection of 5-200 pmol Sub P in the RVM produced a concentration-dependent increase in the n
223 eceptors (MOR1 and DOR1 respectively) in the RVM produces the antinociception mediated by spinally pr
224 est that activation of CCK2 receptors in the RVM promotes mechanical and thermal hypersensitivity and
225 of endogenous TNF-alpha and IL-1beta in the RVM significantly reduced CCI-induced behavioral hyperse
226 e estimated the total number of cells in the RVM to be 1.50 x 10(4) and of these up to 70% were retro
227 oride (100 nM) was then microinjected in the RVM to block synaptic activation of spinally-projecting
228 roinjection of lidocaine in the NG or in the RVM to determine the importance of neural activity at th
230 number of NK1R-immunoreactive neurons in the RVM was increased by 30%, and there was a concomitant in
234 ition of GABA on serotonergic neurons in the RVM, and activation of these serotonergic neurons inhibi
235 n a time-dependent manner by L365,260 in the RVM, and blockade of CCK2 receptors in the RVM also bloc
236 inal dorsal horn after microinjection in the RVM, and these events were significantly prevented by fu
237 osal that an upregulation of the NK1R in the RVM, as well as enhanced release of Sub P following noxi
238 onstitutive deletion or silencing NP1 in the RVM, before or after SNI, attenuates allodynia and hyper
239 Endocannabinoids inhibit GABA release in the RVM, but it is not known whether this effect persists in
255 th a retrograde tracer, FluoroGold, into the RVM 7 days before injection of an inflammatory agent, co
257 duced by microinjection of morphine into the RVM and that spinally projecting serotonergic RVM neuron
258 n of 5HT1(B) or 5HT1(D) antagonists into the RVM did not block the effects of systemic sumatriptan.
259 icroinjection of BDNF (10-100 fmol) into the RVM facilitates nociception, which is dependent on NMDA
260 Phaseolus vulgaris leucoagglutinin, into the RVM resulted in labeling profiles overlapped with the re
263 of myelinated fibres in this region make the RVM a challenging area for whole-cell patch-clamp record
264 Compared with control rats, lesions of the RVM (n=6) or Vi/Vc (n=6) with ibotenic acid led to the e
266 ers to identify the GABAergic neurons of the RVM and caudal pons and performed double labeling to eva
267 Graded electrical microstimulation of the RVM at different postnatal ages revealed a robust shift
270 ime, the changing postnatal influence of the RVM in spinal nociception and highlight the central role
271 ave shown that electrical stimulation of the RVM produces pain facilitation in young animals (postnat
272 his age (P28 to adult), the influence of the RVM shifts to biphasic facilitation and inhibition.
274 ction of lidocaine into either the NG or the RVM produced a time-related reversal of pancreatitis-ind
275 stimates of conditional probability than the RVM, which are of great importance in medical applicatio
276 rain periaqueductal gray that project to the RVM are postsynaptic to midbrain or medullary 5HT neuron
284 nstem areas, and 2) P450 activity within the RVM is important for supraspinal morphine antinociceptio
287 Actions at 5HT1(B) receptors within the RVM offer an additional potential site of action for the
289 predominantly on the midline and within the RVM; neurons that project to the DLP had a wider distrib
291 ats, indicating antinociceptive "tolerance." RVM lidocaine or bilateral DLF lesion did not alter the
292 a minority of RVM neurons (23% of the total RVM neurons), they appear to be selectively apposed by E
294 Combining OCT and SAP measurements using RVM and SSMoG increased diagnostic performance marginall
297 matriptan action and (2) determining whether RVM application of sumatriptan reproduced the actions of
298 igation (SNL) injury in rats pretreated with RVM dermorphin-saporin failed to elicit the expected inc
300 ization of morphine-P450 interactions within RVM circuits will further enhance the understanding of t
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