ライフサイエンスコーパス: RVM

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

14 mic sumatriptan or alphaCGRP(8-37) abolished RVM lidocaine-induced CPP in IM-treated rats.

15 In adults, RVM lesions decreased behavioural mechanical sensory ref

16 Among RVM neurons, we found that serotonergic (5-hydroxytrypta

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

19 The PAG, LC, and RVM were anatomically discriminated using a probabilisti

20 rphine is thought to act in both the PAG and RVM by pre-synaptic inhibition of inhibitory GABAergic t

21 d cannabinoids, improgan acts in the PAG and RVM to activate descending analgesic systems.

22 transfer attenuates the increase in PVR and RVM, pulmonary vascular remodeling, and pressor response

23 etween the ventral Vi/Vc transition zone and RVM.

24 erve injury induces death of antinociceptive RVM neurons that can be reduced or abolished by TUDCA.

25 Whether the GABAergic neurons at RVM express nicotinic cholinergic receptors (nAChRs) is

26 g, suggesting reciprocal connections between RVM and Vi/Vc.

27 ined including the LASSO, HyperLasso, BhGLM, RVM and the single-QTL mapping method based on logistic

28 ork, relevance vector machine, and Ada-boost RVM are the better performers.

29 Combining techniques using both RVM and SSMoG significantly improved on MLC analysis of

30 the rostroventral medulla of the brainstem (RVM) exclusively facilitates spinal pain transmission bu

31 lleted rats; this right shift was blocked by RVM lidocaine.

32 ue-Dawley rats, we demonstrate that discrete RVM neurons express MOR and CCK2; over 80% of these cell

33 activation of the dual GABA/enkephalinergic RVM neurons in adult animals substantially increased or

34 gs suggest that these CCK2-MOR co-expressing RVM neurons facilitate pain and can be directly activate

35 es confirmed activation of pain-facilitating RVM "on" cells and transient suppression of RVM "off" ce

36 The AUROCs for RVM trained on OCT parameters alone, SAP parameters alon

37 The AUROC curves for RVM and SVM were 0.90 and 0.91, respectively, and increa

38 mizing whole-cell patch-clamp recordings for RVM neurons in animals older than PN day 30 and compared

39 imized whole-cell patch-clamp recordings for RVM neurons in animals older than postnatal day 30 and c

40 The areas under the ROC curves (AUROCs) for RVMs trained on optimized feature sets of CSLO parameter

41 e neurotransmitter 5-HT itself released from RVM-spinal neurons contributes to descending pain modula

42 ROC curve results from RVM analyses of CSLO, SAP, and CSLO and SAP combined wer

43 Results from RVM and SVM trained on SLP RNFL thickness measurements a

44 AUROC curve results from RVM and SVM were compared to those for 14 SLP software-g

45 d GABA release in mature but not in immature RVM neurons suggesting the presence of local endocannabi

46 produced DVs in neurokinin-1 immunoreactive RVM neurons.

47 lular mechanisms underlying these changes in RVM modulation of pain behaviours are not known.

48 1beta) after CCI, and they were expressed in RVM astrocytes at 14 d after injury.

49 y depleting functional phenotypes of 5-HT in RVM neurons with regional shRNA interference (RNAi) of t

50 We also identified an increase in RVM functional connectivity with the region that receive

51 BDNF in PAG and TrkB phosphorylation in RVM neurons are upregulated after inflammation.

52 y, our data reveal the central role of PN in RVM descending facilitation during inflammatory and neur

53 a, respectively, were expressed primarily in RVM neurons exhibiting immunoreactivity to the NMDA rece

54 rt because whole-cell patch-clamp studies in RVM to date have been in young (PN day < 18) animals bec

55 phosphorylation of the NMDAR NR2A subunit in RVM via a signal transduction cascade involving IP(3), P

56 right LC; and main effect of temperature in RVM and a task x temperature interaction in right LC.

57 ndance of KOR in axons and axon terminals in RVM indicates a substantial role for presynaptic effects

58 We show that SNI increases RVM NP1 expression and constitutive deletion or silencin

59 vely correlated with FC between individuals' RVM with their sgACC (RVM-sgACC).

60 Intra-RVM injection of microglial and astrocytic inhibitors at

61 Intra-RVM sequestration of BDNF and knockdown of TrkB by RNA i

62 In addition, intra-RVM CC12 pretreatment nearly completely blocked the effe

63 ore, in control shRNA-treated animals, intra-RVM microinjection of brain-derived neurotrophic factor

64 Descending inhibition induced by intra-RVM electrical stimulation, but not microinjection of th

65 uced anti-hyperalgesia were blocked by intra-RVM mu, but not kappa, receptor antagonists.

66 fects of FeTMPyP(5+) were abrogated by intra-RVM naloxone, implicating potential interplay between PN

67 etion of the descending 5-HT system by intra-RVM Tph-2 shRNA interference.

68 Finally, intra-RVM administration of recombinant TNF-alpha or IL-1beta

69 Furthermore, intra-RVM microinjections of the PN decomposition catalyst Fe(

70 When extended to chronic pain, intra-RVM FeTMPyP(5+) produced naloxone-sensitive reversal of

71 machine (SDP-SVM), relevance vector machine (RVM) and Ada-boost relevance vector machine are compared

72 tor machine (SVM), Relevance vector machine (RVM) and the Cubist and Adaptive network-based fuzzy inf

73 ents analyzed with relevance vector machine (RVM) classifiers.

74 ogReg, BLogReg and Relevance Vector Machine (RVM) gene selection algorithms are evaluated over the we

75 on increases in PVR, right ventricular mass (RVM), and pulmonary vascular remodeling that occur in ch

76 ence of local endocannabinoid tone in mature RVM.

77 stral portion of the ventral medial medulla (RVM) is a crucial site for the supraspinal antinocicepti

78 s raphe magnus of the rostroventral medulla (RVM).

79 nd "off" cells of the rostroventral medulla (RVM).

80 inly derived from the rostroventral medulla (RVM).

81 oinjected in the rostroventromedial medulla (RVM) of rats with inflammatory injury induced by injecti

82 Neurons in the rostroventromedial medulla (RVM) project to spinal loci where the neurons inhibit or

83 Rostral ventral medulla (RVM) contains significant numbers of local GABAergic neu

84 were given into the rostral-ventral medulla (RVM), intrathecally (i.th.) or simultaneously into both

85 fused into the rostral ventromedial medulla (RVM) 10 min before a 30-min EA treatment at acupoint Hua

86 mug) into the rostral ventromedial medulla (RVM) also reversed the allodynia, showing this brain are

87 arising in the rostral ventromedial medulla (RVM) and (2) the presence of such pain manifests behavio

88 s, such as the rostral ventromedial medulla (RVM) and locus coeruleus (LC).

89 ty between the rostral ventromedial medulla (RVM) and other brainstem pain-modulatory regions, includ

90 ising from the rostral ventromedial medulla (RVM) and upregulation of spinal dynorphin.

91 Neurons of the rostral ventromedial medulla (RVM) are thought to critically contribute to this proces

92 ivation of the rostral ventromedial medulla (RVM) attenuates hyperalgesia and central sensitization i

93 ections to the rostral ventromedial medulla (RVM) constitute an essential neural circuit for opioid-b

94 the brainstem rostral ventromedial medulla (RVM) contribute to injury-evoked hypersensitivity.

95 neurons in the rostral ventromedial medulla (RVM) directly modulates spinal nociceptive transmission

96 ulation of the rostral ventromedial medulla (RVM) facilitates pain behaviours in neonates but inhibit

97 (PPTg) to the rostral ventromedial medulla (RVM) have been implicated in nociceptive modulation.

98 ences from the rostral ventromedial medulla (RVM) in neuropathic pain, but the underlying mechanisms

99 ystem from the rostral ventromedial medulla (RVM) in the brainstem and the 5-HT(3) receptor subtype i

100 sticity in the rostral ventromedial medulla (RVM) in the initiation and maintenance of experimental n

101 ocesses in the rostral ventromedial medulla (RVM) interfered with its expression.

102 The rostral ventromedial medulla (RVM) is a relay in the descending pain modulatory system

103 The rostral ventromedial medulla (RVM) is an important mediator of the supraspinal compone

104 that PN in the rostral ventromedial medulla (RVM) is essential for descending nociceptive modulation

105 The rostral ventromedial medulla (RVM) is part of a descending pain modulatory system that

106 ntially affect rostral ventromedial medulla (RVM) neuronal activity and nocifensive behaviors.

107 njected in the rostral ventromedial medulla (RVM) of rats 4 hr, 4 d, and 2 weeks after the induction

108 neurons of the rostral ventromedial medulla (RVM) of the rat.

109 y (PAG) or the rostral ventromedial medulla (RVM) or by functional inactivation of neurons in these r

110 Neurons in the rostral ventromedial medulla (RVM) play critical and complex roles in pain modulation.

111 neurons in the rostral ventromedial medulla (RVM) provide the major descending serotonergic projectio

112 input from the rostral ventromedial medulla (RVM) provides positive and negative modulation of spinal

113 ve role in the rostral ventromedial medulla (RVM) under conditions of peripheral inflammatory injury,

114 neurons in the rostral ventromedial medulla (RVM), a brainstem region involved in modulation of nocic

115 ition zone and rostral ventromedial medulla (RVM), a key structure in descending pain modulation.

116 l nerve in the rostral ventromedial medulla (RVM), a major component of brainstem descending pain mod

117 se BDNF in the rostral ventromedial medulla (RVM), a relay between the PAG and spinal cord.

118 tan within the rostral ventromedial medulla (RVM), a site of descending modulation of visceral pain,

119 changes in the rostral ventromedial medulla (RVM), a supraspinal site involved in the processing of p

120 ected into the rostral ventromedial medulla (RVM), but not following co-injections into the periaqued

121 neurons in the rostral ventromedial medulla (RVM), known to modify nociception in the spinal cord dor

122 ted within the rostral ventromedial medulla (RVM), nucleus accumbens (NAc), or rostral anterior cingu

123 caine into the rostral ventromedial medulla (RVM), or dorsolateral funiculus (DLF) lesion, abolishes

124 applied to the rostral ventromedial medulla (RVM).

125 ences from the rostral ventromedial medulla (RVM).

126 cells," in the rostral ventromedial medulla (RVM).

127 l PAG, and the rostral ventromedial medulla (RVM).

128 al gray to the rostral ventromedial medulla (RVM).

129 pposed both serotonergic and nonserotonergic RVM neuronal profiles.

130 r) axons to serotonergic and nonserotonergic RVM neurons in rats, including neurons projecting to the

131 Only 0.9+/-0.1% of RVM neurons retrogradely labeled with Fluoro-Gold from t

132 We found that 43% of RVM projection neurons expressed MOR1 mRNA and 83% of RV

133 ction neurons expressed MOR1 mRNA and 83% of RVM projection neurons expressed DOR1 mRNA.

134 ibitory inputs that modulate the activity of RVM neurons in such a manner as to enhance the effects o

135 The PV-ir cells of RVM and caudal pons were found medial to the facial nucl

136 in the number of DVs in distal dendrites of RVM neurons that were immunoreactive for the neurokinin-

137 ral funiculus lesion (DLF) or destruction of RVM neurons expressing mu-opioid receptors with dermorph

138 was determined by (1) testing the effects of RVM administration of 5HT1(B/D) antagonists on systemic

139 The results demonstrated an involvement of RVM mu, but not kappa, receptors in EA-produced anti-hyp

140 Lesion of RVM cells expressing mu-opioid receptors with dermorphin

141 Thus, loss of RVM mu receptor-expressing cells both prevents and rever

142 We propose that the loss of RVM neurons shifts the balance of descending control fro

143 The loss of RVM neurons was also associated with a bilateral increas

144 The majority of RVM-derived descending inputs were dual GABAergic and en

145 serotonergic neurons comprise a minority of RVM neurons (23% of the total RVM neurons), they appear

146 s receiving SNL, we found that the number of RVM neurons decreased by 23% in the side ipsilateral to

147 sess changes in Sub P release, the number of RVM neurons that exhibited NK1R internalization was exam

148 This possibility and the phenotype of RVM cells that might underlie experimental neuropathic p

149 and morphologically distinct populations of RVM neurons appear to modulate nociception by direct and

150 mechanisms by which distinct populations of RVM neurons facilitate or diminish pain remain elusive.

151 Differences in these properties of RVM neurons may contribute to the developmental changes

152 Selective rescue of RVM NP1 expression restores behavioral hypersensitivity

153 knock-out mice, demonstrating a key role of RVM NP1 in the pathogenesis of neuropathic pain.

154 ic pain requires the activity of a subset of RVM neurons that are distinguished by co-expression of m

155 RVM "on" cells and transient suppression of RVM "off" cells after IM.

156 The recently-demonstrated suppression of RVM ON-cell activity by improgan may account for the pre

157 the effects of both BLa and MEa morphine on RVM cell activity, and interfered with the behavioral an

158 AUROC curves for optimized RVM and SVM were significantly larger than those for all

159 ed on whether they had greater thal-BA 3a or RVM-sgACC FC respectively, pronociceptive subjects showe

160 nt inflammatory pain, significantly more PAG-RVM cells were activated in males in comparison with fem

161 , with females having significantly more PAG-RVM output neurons in comparison with males.

162 al dimorphism in the organization of the PAG-RVM circuit and its activation by persistent inflammator

163 ion and the functional activation of the PAG-RVM circuit are sexually dimorphic and may provide the a

164 rphine to suppress the activation of the PAG-RVM circuit was also examined.

165 es in the anatomical organization of the PAG-RVM pathway, and its activation during persistent inflam

166 dicate that the descending ventrolateral PAG/RVM system integrates a behavioral response of which ant

167 f MOR1 and DOR1 mRNAs in spinally projecting RVM neurons including serotonergic (5HT) cells by using

168 In addition, spinally projecting RVM neurons were significantly larger than RVM neurons t

169 k synaptic activation of spinally-projecting RVM neurons.

170 e in pulmonary arterial pressure (PAP), PVR, RVM, and pulmonary vascular remodeling in response to ch

171 opamine release in IM-treated rats receiving RVM lidocaine.

172 DLP were used to determine whether the same RVM neurons project to both of these regions.

173 In our sample, RVM analyses of baseline CSLO and SAP measurements could

174 VM and that spinally projecting serotonergic RVM neurons express mu-opioid receptors (MOR).

175 C between individuals' RVM with their sgACC (RVM-sgACC).

176 fore induction of pancreatitis with a single RVM microinjection of dermorphin-saporin to eliminate ce

177 PAG activated by attentional load; specific RVM regions showing pronociceptive and antinociceptive p

178 cross-validation was used to train and test RVM and SVM classifiers on unique subsets of the full 16

179 cross-validation was used to train and test RVMs using the CSLO and SAP features.

180 g RVM neurons were significantly larger than RVM neurons that project to the DLP.

181 Unexpectedly, we found that RVM GABAergic neurons facilitate mechanical pain by inhi

182 The RVM-based ensemble model that combines AdaBoost and redu

183 work of supratentorial brain regions and the RVM whose activity was linearly related to pain intensit

184 nection between SP neurons in the LH and the RVM, the cholinergic agonist carbachol (125 nmol) was mi

185 ally (i.th.) or simultaneously into both the RVM and i.th. (1:1 fixed ratio).

186 whether the antinociception mediated by the RVM is associated with locomotor changes as has been rep

187 n LH-induced antinociception mediated by the RVM, we conducted an anatomical experiment using retrogr

188 These data suggest a prominent role for the RVM in mediating the sensitization of spinal neurons and

189 drive such descending facilitation from the RVM during continuous opioid administration.

190 tivation of descending facilitation from the RVM for the expression of cranial and extracranial cutan

191 s indicate that the descending 5-HT from the RVM is an important contributor to pain facilitation dur

192 uggest that descending facilitation from the RVM plays a critical role in the maintenance, but not th

193 anges in descending control of pain from the RVM to the spinal cord.

194 ivation of bulbospinal facilitation from the RVM, (2) increased pain decreases spinal opioid antinoci

195 de B labeled neurons were not evident in the RVM 4 days after microinjection of Sub P, although such

196 physiologically characterized neurons in the RVM after spinal nerve ligation, a model of neuropathic

197 CCK in the RVM also acutely displaced the spinal morphine antinocic

198 e RVM, and blockade of CCK2 receptors in the RVM also blocked the rightward displacement of the spina

199 tly prolonged downregulation of Tph-2 in the RVM and 5-HT in spinal dorsal horn.

200 and [Leu(5)]enkephalin were increased in the RVM and in other brainstem nuclei in CFA-treated rats.

201 yr-D-Trp-Arg-Thr-Pen-Thr-NH(2) (CTAP) in the RVM antagonized both the marginal enhancement of the pot

202 monstrate that both on- and off-cells in the RVM are sensitized to innocuous and noxious mechanical s

203 entify CCK2-MOR co-expressing neurons in the RVM as potential therapeutic targets for neuropathic pai

204 Enhanced, endogenous CCK activity in the RVM during sustained morphine exposure may diminish spin

205 he endogenous opioid enkephalin (ENK) in the RVM during thermal hyperalgesia, suggesting potential in

206 -703,606 (5 microg) was microinjected in the RVM following LH stimulation with carbachol and abolishe

207 ce that CB2 receptor function emerges in the RVM in persistent inflammation and that selective CB2 re

208 indicating that CB2 receptor function in the RVM is increased during persistent inflammation.

209 hat phasic or evoked release of Sub P in the RVM is increased in response to noxious peripheral stimu

210 suggest that the distribution of KORs in the RVM may be influenced by reproductive hormone levels.

211 ABA release was significantly reduced in the RVM of CFA-treated rats compared with naive rats.

212 oinjection of NTB alone, but not CTAP in the RVM of CFA-treated rats, enhanced the hyperalgesia prese

213 onist AM630 increased mIPSC frequency in the RVM of CFA-treated rats, indicating that CB2 receptors a

214 ceptor (Tacr1) mRNA was not increased in the RVM of CFA-treated rats.

215 appa opioid receptor immunoreactivity in the RVM of male and female rats.

216 ammatory injury increased the release in the RVM of opioid peptides with preferential affinity for th

217 of mRNA encoding either MOR1 or DOR1 in the RVM of rats.

218 is not known whether the same neurons in the RVM produce both direct and indirect modulation of nocic

219 Microinjection of 5-200 pmol Sub P in the RVM produced a concentration-dependent increase in the n

220 In opioid-naive rats, CCK in the RVM produced acute tactile and thermal hypersensitivity

221 eceptors (MOR1 and DOR1 respectively) in the RVM produces the antinociception mediated by spinally pr

222 est that activation of CCK2 receptors in the RVM promotes mechanical and thermal hypersensitivity and

223 of endogenous TNF-alpha and IL-1beta in the RVM significantly reduced CCI-induced behavioral hyperse

224 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

225 oride (100 nM) was then microinjected in the RVM to block synaptic activation of spinally-projecting

226 roinjection of lidocaine in the NG or in the RVM to determine the importance of neural activity at th

227 Neuronal hypersensitivity in the RVM was correlated with behavioral hypersensitivity.

228 number of NK1R-immunoreactive neurons in the RVM was increased by 30%, and there was a concomitant in

229 d increase in the basal levels of CCK in the RVM when compared with controls.

230 Agonist-directed cell lesion in the RVM with the cytotoxin, saporin, using either CCK-sapori

231 Of 192 retrogradely labeled cells in the RVM, 51 cells (27%) were immunoreactive for 5HT.

232 ition of GABA on serotonergic neurons in the RVM, and activation of these serotonergic neurons inhibi

233 n a time-dependent manner by L365,260 in the RVM, and blockade of CCK2 receptors in the RVM also bloc

234 inal dorsal horn after microinjection in the RVM, and these events were significantly prevented by fu

235 osal that an upregulation of the NK1R in the RVM, as well as enhanced release of Sub P following noxi

236 onstitutive deletion or silencing NP1 in the RVM, before or after SNI, attenuates allodynia and hyper

237 Endocannabinoids inhibit GABA release in the RVM, but it is not known whether this effect persists in

238 vation of spinally-projecting neurons in the RVM.

239 IL-1R levels and NR1 phosphorylation in the RVM.

240 also examined the origins of EM-2-ir in the RVM.

241 -NH2) (EM-2) have been reported to be in the RVM.

242 crease in extracellular 5-HT observed in the RVM.

243 extracellular serotonin (5-HT) levels in the RVM.

244 y a 3-fold increase in levels of 5-HT in the RVM.

245 acteristics similar to those reported in the RVM.

246 ons as has been extensively described in the RVM.

247 eptor protein expression and function in the RVM.

248 increases expression of NO. synthase in the RVM.

249 spinal cord and serotonergic neurons in the RVM.

250 noreactivity was localized to neurons in the RVM.

251 3-nitrotyrosine (NT), a PN biomarker, in the RVM.

252 -containing neurons were serotonergic in the RVM.

253 th a retrograde tracer, FluoroGold, into the RVM 7 days before injection of an inflammatory agent, co

254 ne (0.2 or 0.5 microl) was injected into the RVM and locomotion and nociception assessed.

255 duced by microinjection of morphine into the RVM and that spinally projecting serotonergic RVM neuron

256 n of 5HT1(B) or 5HT1(D) antagonists into the RVM did not block the effects of systemic sumatriptan.

257 icroinjection of BDNF (10-100 fmol) into the RVM facilitates nociception, which is dependent on NMDA

258 Phaseolus vulgaris leucoagglutinin, into the RVM resulted in labeling profiles overlapped with the re

259 Sumatriptan administered into the RVM similarly produced dose- and time-related blockade o

260 ia induced by microinjection of CCK into the RVM.

261 of myelinated fibres in this region make the RVM a challenging area for whole-cell patch-clamp record

262 Compared with control rats, lesions of the RVM (n=6) or Vi/Vc (n=6) with ibotenic acid led to the e

263 to activity within a distinct region of the RVM alone.

264 ers to identify the GABAergic neurons of the RVM and caudal pons and performed double labeling to eva

265 Graded electrical microstimulation of the RVM at different postnatal ages revealed a robust shift

266 Inactivation of the RVM by muscimol microinjections completely attenuated an

267 bserved following excitotoxic lesions of the RVM in adult and P21 rats.

268 ime, the changing postnatal influence of the RVM in spinal nociception and highlight the central role

269 ave shown that electrical stimulation of the RVM produces pain facilitation in young animals (postnat

270 his age (P28 to adult), the influence of the RVM shifts to biphasic facilitation and inhibition.

271 were present both within and outside of the RVM.

272 engagement of pain-modulating neurons of the RVM.SIGNIFICANCE STATEMENT The lateral parabrachial comp

273 ction of lidocaine into either the NG or the RVM produced a time-related reversal of pancreatitis-ind

274 stimates of conditional probability than the RVM, which are of great importance in medical applicatio

275 rain periaqueductal gray that project to the RVM are postsynaptic to midbrain or medullary 5HT neuron

276 influences from both the BLa and MEa to the RVM are relayed via the PAG.

277 , suggesting that KOR ligands applied to the RVM may be less potent in proestrus females.

278 munoreactive for SP in the LH project to the RVM.

279 an be directly activated by CCK input to the RVM.

280 solitary tract projected their axons to the RVM.

281 s modulate nociception through a link to the RVM.

282 roperties of the relevant neurons within the RVM are essentially unknown.

283 nstem areas, and 2) P450 activity within the RVM is important for supraspinal morphine antinociceptio

284 nd at pre- and postsynaptic sites within the RVM of both sexes.

285 many spinally projecting neurons within the RVM of female rats.

286 Actions at 5HT1(B) receptors within the RVM offer an additional potential site of action for the

287 f specific populations of neurons within the RVM.

288 predominantly on the midline and within the RVM; neurons that project to the DLP had a wider distrib

289 Furthermore, lesion of these RVM neurons did not affect the initial development of ne

290 ral, PB interfered with nociceptive input to RVM under basal conditions, as well as in acute inflamma

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

293 suggesting the activation of the trigeminal-RVM pathway after inflammation.

294 Combining OCT and SAP measurements using RVM and SSMoG increased diagnostic performance marginall

295 Classification performance using RVM and SSMoG was statistically similar.

296 The Vi/Vc-RVM pathway is activated after orofacial deep tissue inj

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

299 In vitro studies with RVM slices show that BDNF induces tyrosine phosphorylati

300 ization of morphine-P450 interactions within RVM circuits will further enhance the understanding of t