ライフサイエンスコーパス: supraspinal

1 of previous studies suggest that spinal and supraspinal 5-HT(1A) receptors are involved in multiple

2 The influence of supraspinal 5-HT(1A) receptors on reflex bladder activit

3 cts were prevented by blockade of spinal and supraspinal A3AR, lost in A3AR knock-out mice, and indep

4 istinguish between a peripheral/spinal and a supraspinal action, we administered acetaminophen and AM

5 Thirteen cases with supraspinal active demyelinating NMO lesions were analyz

6 onal magnetic resonance imaging to study the supraspinal activity during the withdrawal period of the

7 esonance imaging was used to examine whether supraspinal activity might contribute to the maintenance

8 produced by mustard oil following spinal or supraspinal administration of receptor antagonists sugge

9 Supraspinal administration of the NOS inhibitor NOArg lo

10 In this experiment, we examined whether supraspinal afferent input by means of descending spinal

11 The removal of supraspinal afferents resulted in extremely local effect

12 lained by an indirect action of estradiol on supraspinal afferents.

13 onidine antinociception (40 microg, i.c.v.), supraspinal alpha(2) receptors seem to mediate the antin

14 These results suggest that spinal (but not supraspinal) alpha(2) adrenergic receptors play a signif

15 refore exclusively of spinal origin, whereas supraspinal alpha2-GABAARs had neither synergistic nor a

16 sible synergistic or antagonistic actions of supraspinal alpha2-GABAARs on spinal antihyperalgesia ha

17 ntrally administered morphine, implying that supraspinal analgesia resulted from a combination of cen

18 ine-induced analgesia in tests of spinal and supraspinal analgesia.

19 three DOR-1 exons all block both spinal and supraspinal analgesic actions of the delta2 ligand [D-Al

20 and neurochemical pathways in exerting their supraspinal analgesic effects.

21 analgesia, but peptide delta agonists retain supraspinal analgesic potency that is only partially ant

22 al and neurochemical circuitry mediating the supraspinal analgesic responses induced by morphine and

23 The information about supraspinal and initial spinal pRS axon trajectories sho

24 ith Schwann cell grafts promotes significant supraspinal and proprioceptive axon sparing and myelinat

25 spinal cord tissue support the remodeling of supraspinal and segmental pathways that may underlie rec

26 interneurons represent the main targets for supraspinal and sensory afferent signals adjusting gait.

27 We also evaluated the role of supraspinal and sensory inputs in modulating the occurre

28 SPNs are subject to control from both supraspinal and spinal inputs that exert effects through

29 is model, low frequency SCS likely activates supraspinal and spinal mechanisms to produce analgesia,

30 Although supraspinal and spinal morphine-6 beta-glucuronide (M6G)

31 iceptive interaction of morphine activity at supraspinal and spinal sites has been clearly establishe

32 licative antinociceptive interaction between supraspinal and spinal sites to acute noxious stimuli an

33 natural products display centrally mediated (supraspinal and spinal) antinociceptive (analgesic) acti

34 GS proteins as negative regulators of opioid supraspinal antinociception and also reveal a potential

35 tion and hotplate test, mainly reflective of supraspinal antinociception were evaluated.

36 sia in others, yet producing both spinal and supraspinal antinociceptive actions in other studies.

37 dial medulla (RVM) is a crucial site for the supraspinal antinociceptive actions of opioids.

38 The loss of spinal/supraspinal antinociceptive synergy and lack of antiallo

39 Supraspinal antisense mapping suggested that this effect

40 intrasegmental and intersegmental as well as supraspinal, are exclusively glycinergic.

41 es the set-related activity found in various supraspinal areas, indicating that movement preparation

42 udies have addressed a novel contribution of supraspinal astrocytes and associated cytokines as well

43 ze the origins, anatomical organization, and supraspinal axon trajectories of these pathways via retr

44 There was no evidence for growth of supraspinal axons across lesions made at PD33.

45 In the present study, we asked whether supraspinal axons grow through a complete transection of

46 We conclude that supraspinal axons grow through the lesion after transect

47 opossum is transected early in development, supraspinal axons grow through the lesion.

48 es to promote the regeneration of descending supraspinal axons represents an ideal strategy for rebui

49 ration of cut axons contributes to growth of supraspinal axons through the lesion after transection o

50 The supraspinal BDNF-TrkB signaling represents a previously

51 Here, we show that supraspinal BDNF-tyrosine kinase receptor B (TrkB) signa

52 receptor-mediated G-protein activity within supraspinal brain areas involved in pain processing and

53 blocks access of nociceptive information to supraspinal brain areas, these data suggest that noxious

54 eptor-mediated G-protein activity within the supraspinal brain regions involved in pain processing of

55 als show marked differences from controls in supraspinal, but not in spinal, responses to painful sti

56 vely activated by designer drugs displayed a supraspinal, but not spinal, antinociceptive effect.

57 changes during persistent pain as well as to supraspinal centers that modulate pain transmission in t

58 differential descending synaptic input from supraspinal centres is not a required component of the d

59 e relatively independent lines of input from supraspinal centres whereas substantial divergence of de

60 on whether spinal networks are connected to supraspinal centres.

61 test whether C(2) hemisection had induced a supraspinal change in respiratory motor drive, we record

62 y in rats with unilateral SCI, segmental and supraspinal changes could be induced in contralateral re

63 y identifying the contribution of individual supraspinal circuit elements to locomotion kinematics, w

64 ncter (EUS) that is controlled by spinal and supraspinal circuitry.

65 ask and/or promotes plasticity of spinal and supraspinal circuitry.

66 espread surrounding inhibition may depend on supraspinal circuitry.

67 ssessing the functional status of spinal and supraspinal circuits.

68 One can conclude that supraspinal commands (caused by MLR stimulation) select

69 ganized synergies activated by spinal and/or supraspinal commands to generate motor outputs by analyz

70 t the CNS, including neurons involved in the supraspinal component of opioid analgesia.

71 edulla (RVM) is an important mediator of the supraspinal component of opioid antinociception.

72 the effect of varying the degree of residual supraspinal connections on chronic detrusor-EUS coordina

73 resent study was to investigate the possible supraspinal contribution of ABT-594 by assessing its abi

74 ral sensitization (CS) that is maintained by supraspinal contributions from the descending pain modul

75 itory, and Ib-inhibitory pathways) and their supraspinal control (via biasing activity, presynaptic i

76 afferent input in the absence of descending supraspinal control is feasible in isolated rodent spina

77 These modules are combined with a supraspinal control layer that adjusts the desired foot

78 Hence, we describe a supraspinal control mechanism for the development and re

79 order to gain a greater understanding of the supraspinal control of balance and walking.

80 structures thought to be key elements in the supraspinal control of locomotion, muscle tone, waking,

81 hs after implantation, the patient recovered supraspinal control of some leg movements, but only duri

82 mediate spontaneous functional recovery and supraspinal control of stepping, even when there has bee

83 To restore supraspinal control of sympathetic preganglionic neurons

84 er PNT with and without SCI, suggesting that supraspinal control significantly affects continence dur

85 ee fine foot motor skills, to a reduction in supraspinal control.

86 by spinal cord injury or other disorders of supraspinal control.

87 ed motor output in the absence of descending supraspinal control.

88 s) in rodent spinal cords lacking descending supraspinal control.

89 motor function in the absence of descending supraspinal control.

90 Using paired supraspinal DA neuron and motoneuron recordings, we furt

91 Targeted laser ablation of supraspinal DA neurons reduces motor episode frequency w

92 However, the types of information encoded by supraspinal DAergic neurons and their relationship to mo

93 lly relevant activity patterns, we show that supraspinal DAergic neurons generate two forms of output

94 cuit flexibility is temporally controlled by supraspinal DAergic pathways and provide important insig

95 ptive information can also directly activate supraspinal descending modulatory systems, suggesting th

96 e delta receptors responsible for spinal and supraspinal DPDPE analgesia can be discriminated at the

97 late sympathetic discharge in the absence of supraspinal drive.

98 have declined, suggesting an involvement of supraspinal dysfunction.

99 il-flick (spinal involvement) and hot-plate (supraspinal effect) tests, respectively; the compound ra

100 firing of motor neurones and that excessive supraspinal excitation could also play a role.

101 e, bulbospinal neurons that provide the main supraspinal excitatory input to sympathetic vasomotor pr

102 ces and additional mechanism(s) that require supraspinal facilitation to maintain such pain.

103 limb muscle afferents on the development of supraspinal fatigue and the responsiveness of corticospi

104 III/IV locomotor muscle afferents facilitate supraspinal fatigue in remote muscle not involved in the

105 Our data suggest that TIP39 released from supraspinal fibers potentiates aspects of nociception wi

106 S, which could be explained by impairment of supraspinal GABA-ergic neurones, leading to an impaired

107 hether SPS is associated with dysfunction in supraspinal GABA-ergic neurones, we assessed the excitab

108 f GABAergic interneurons may be the cause of supraspinal GABAergic disinhibition.

109 tion of neuropathic pain with an emphasis on supraspinal glial-neuronal relationships.

110 ing the spinal CPG can originate from either supraspinal glutamatergic inputs or from within the spin

111 nistration of morphine at spinal (i.th.) and supraspinal (i.c.v.) sites to the same rat produces anti

112 rogenic component of physiological tremor is supraspinal in origin and ranges from 6 to 40 Hz.

113 rs at the spinal level and is independent of supraspinal influence.

114 2)) spinalization was performed to eliminate supraspinal influence.

115 er two conditions: (1) when neurons received supraspinal influences and (2) when these influences wer

116 uropathic state as independent of descending supraspinal influences and additional mechanism(s) that

117 consistent with the proposition that loss of supraspinal influences plays a significant role in deter

118 We aimed to identify the supraspinal influences that underlie these clinical mani

119 wever, reveals a significant contribution of supraspinal influences to development and maintenance of

120 nal wide dynamic range neurons and producing supraspinal inhibition of spinal nociception through act

121 Here, we addressed the origin of the supraspinal inhibition.

122 results highlight that the interplay between supraspinal input and spinal afferents is relevant for t

123 The observed motor enhancement depended on supraspinal input because it was not present in spinaliz

124 First, the loss of supraspinal input results in a marked change in the func

125 ntegration of segmental, intersegmental, and supraspinal input to propriospinal and motor neurons ove

126 onal growth of CNS pathways and specifically supraspinal input to propriospinal neurons.

127 , the transplant-mediated reestablishment of supraspinal input to spinal circuitry is the mechanism u

128 cating that estrogens do not act by means of supraspinal input to support SNB motoneuron development.

129 plex motor tasks following the disruption of supraspinal input, and evidence for plasticity suggests

130 hese findings suggest that in the absence of supraspinal input, the lumbar spinal circuitry is capabl

131 r in subjects with partial and no detectable supraspinal input.

132 severity, suggesting a role for sensory and supraspinal inputs in stabilizing rhythmic output activi

133 limited bouton numbers suggested that these supraspinal inputs might not be major regulators of the

134 rons receive intraganglion, intraspinal, and supraspinal inputs, the latter of which are mainly deriv

135 spinal locomotor circuits as well as remnant supraspinal inputs.

136 vity of which is modulated by peripheral and supraspinal inputs.

137 A subset of supraspinal lesions from AQP4-IgG-seropositive NMO patie

138 opioid receptor agonist administered at the supraspinal level was abolished in Lmx1bf/f/p mice compa

139 s to be shown whether this is at a spinal or supraspinal level.

140 te axonal regeneration, including those from supraspinal level.

141 the interactions at peripheral, spinal, and supraspinal levels as well as between them, to more full

142 terations within pain pathways at spinal and supraspinal levels associated with inflammation and glia

143 ng these modalities only occurs at spinal or supraspinal levels of processing.

144 e on nociceptive processing at spinal versus supraspinal levels of the neuraxis.

145 FB-containing neurons were still present at supraspinal levels, but they appeared to be fewer in num

146 oth systems are active at the spinal and the supraspinal levels.

147 s spinal LTP affects sensory transmission at supraspinal levels.

148 s at both peripheral and central (spinal and supraspinal) levels of the nervous system Through studie

149 mechanisms, acting alone or in synergy with supraspinal loci, may contribute to pharmacodynamic expl

150 ons forces us to rethink the organization of supraspinal locomotor control, to include a sustained fe

151 of thoracolumbar spinal neurons to CRD by a supraspinal loop and that increasing thoracolumbar proce

152 The neural circuit for lordosis involves a supraspinal loop, which is controlled by an estrogen- an

153 ssing of the same colonic stimulus through a supraspinal loop: homovisceral descending modulation.

154 lpha 1 and Gx/z alpha antisense probes block supraspinal M6G analgesia, whereas Gi alpha 1, Gi alpha

155 zoylhydrazone produces its analgesia through supraspinal mechanisms and is blocked by Gi alpha 1, Gi

156 e existence of multiple, cognitively driven, supraspinal mechanisms for pain modulation.

157 th persistent pain depend on a transition to supraspinal mechanisms involving the serotonin system in

158 analgesia can be mediated by both spinal and supraspinal mechanisms.

159 nterneurons and was not due to activation of supraspinal micturition reflex pathways.

160 nociception is subject to complex spinal and supraspinal modulation, however, the relevant locations

161 450 activity within the RVM is important for supraspinal morphine antinociception.

162 Here, the possible loss of spinal/supraspinal morphine antinociceptive synergy and relatio

163 In turn, host supraspinal motor axons penetrated human iPSC grafts and

164 l motoneurons and suppression of activity in supraspinal motor facilitatory systems.

165 g Gi alpha 2, G(o) alpha, and Gs alpha block supraspinal mu-opioid analgesia, whereas Gi alpha 2 and

166 Supraspinal multiplicative opiate analgesic interactions

167 nduced synaptic facilitation was mediated by supraspinal naloxonazine-insensitive, but CTOP-sensitive

168 Multiple peripheral, segmental, and supraspinal neuronal activities control nociceptive proc

169 s but are under direct excitatory control of supraspinal neurons and, principally inhibitory, control

170 We assumed that supraspinal neurons that contained FB survived axotomy a

171 5 days, sympathetic pre-motor neurons (i.e., supraspinal neurons that project to the IML) were identi

172 ious messages and hyperalgesia by activating supraspinal neurons that project to the spinal cord.

173 that project into the spinal cord, including supraspinal neurons, dorsal root ganglia, and local neur

174 le the inhibitory nNOS-1 system is the major supraspinal nNOS system.

175 In the hot-plate test, a measure of supraspinal nociception, morphine antinociception was in

176 ail flick and hot plate tests for spinal and supraspinal nociceptive responses than wild-type mice.

177 containing neurons were found in each of the supraspinal nuclei labeled by comparable injections in a

178 cumented for axons originating in all of the supraspinal nuclei that innervate the lumbar cord by PD1

179 s in that atlas should instead be called the supraspinal nucleus.

180 ngs revise the conventional understanding of supraspinal opioid analgesia and demonstrate that RM pro

181 g that involvement of GABAergic neurons with supraspinal opioid antinociception may extend to primate

182 receptors have been demonstrated to mediate supraspinal opioid antinociception.

183 Since activation of either supraspinal or spinal alpha(2) adrenergic receptors can

184 e the data confirm that activation of either supraspinal or spinal CB1 receptors leads to significant

185 ed spinal (hindlimb withdrawal reflexes) and supraspinal pain behavior of awake arthritic rats, inclu

186 her include excessive ascending signaling to supraspinal pain centers.

187 al serotonergic system is a key component of supraspinal pain modulatory circuitry mediating opioid a

188 little is known regarding the role of Ih in supraspinal pain pathways.

189 ance our understanding of the involvement of supraspinal pain pathways.

190 the PEAP may be more sensitive to changes in supraspinal pain processing and could contribute to the

191 ate test, a paradigm that primarily assesses supraspinal pain responsiveness.

192 Our results suggest that CART is involved in supraspinal pain transmission.

193 Surprisingly, regeneration from supraspinal pathways and recovery of motor function were

194 to remain intact despite the interruption of supraspinal pathways and the resultant loss of activity.

195 irreversible interruption of long descending supraspinal pathways in mice.

196 h is attributable to lack of regeneration of supraspinal pathways that control the bladder.

197 wal strategy that is modulated by descending supraspinal pathways to adapt the response to the biomec

198 d contusion injury (SCI) in the rat, certain supraspinal pathways, such as the corticospinal tract, a

199 Vagal inhibition required supraspinal pathways.

200 finitive evidence for the existence of these supraspinal presympathetic (PS) neurons with inhibitory

201 Here we tested the hypothesis that supraspinal processes of fatigue would be increased afte

202 e counted in the rhombencephalon (where most supraspinal projecting neurons are located) and spinal c

203 spinal cord and rhombencephalon (where most supraspinal projecting neurons are located).

204 The generation of both propriospinal and supraspinal projection neurons began on embryonic day 13

205 the literature, suggest that the majority of supraspinal projection neurons in the SDH fall into two

206 The neurogenesis of supraspinal projection neurons in the SDH proceeded alon

207 e descending connections, and many (presumed supraspinal projection neurons) did not demonstrate shor

208 in lamina I have characteristic patterns of supraspinal projection.

209 nt of spinal sensorimotor circuits occurs as supraspinal projections are integrated.

210 aginous fishes and described their brainstem supraspinal projections because most nuclei in the retic

211 umber and neurogenic pattern of neurons with supraspinal projections in the superficial dorsal horn (

212 and are presumably mediated by the numerous supraspinal projections of these neurons.

213 ina I and 0.24 neurons in lamina II that had supraspinal projections per 10-microm transverse section

214 orrelates with the arrival and maturation of supraspinal projections to the spinal cord.

215 The generation of all SDH neurons with supraspinal projections was completed on embryonic day 1

216 In the SDH, 52% of the neurons with supraspinal projections were found to project to rostral

217 ductal gray (vlPAG) is known to be a crucial supraspinal region for initiating descending pain inhibi

218 ty in viral labeling from the spinal cord to supraspinal regions became apparent with increasing surv

219 ng mu opioid receptors (muORs) in spinal and supraspinal regions of the CNS.

220 , which in turn is controlled by inputs from supraspinal regions.

221 rons can act as functional relays to restore supraspinal regulation of denervated SPNs, thereby contr

222 The supraspinal regulation of genital reflexes is poorly und

223 aterally in ventrolateral pathways, and that supraspinal relays were not required for CPSA excitation

224 C1 was used to determine the contribution of supraspinal relays.

225 gh peripheral and spinal mechanisms, but its supraspinal role is unknown.

226 These minimal delays all but rule out a supraspinal route for these interlimb reflexes.

227 een documented in the peripheral, spinal and supraspinal segments of the micturition reflex in diseas

228 play in the self-organization of spinal and supraspinal sensorimotor circuits.

229 Supraspinal serotonergic axons crossed the transection g

230 hat these spinal reflexes can be modified by supraspinal signals in accordance with different motor b

231 affects processing of peripheral, spinal and supraspinal signals in the spinal cord.

232 are known to establish functional relays for supraspinal signals, and they display a greater growth r

233 brainstem nucleus raphe magnus (NRM), a key supraspinal site for opioid analgesia.

234 in the rostral ventromedial medulla (RVM), a supraspinal site involved in the processing of painful s

235 not intrathecal administration, suggesting a supraspinal site of action.

236 ending inhibition of dorsal horn cells via a supraspinal site of action.

237 ited unchanged antihyperalgesia indicating a supraspinal site of action.

238 was detected in spinal neurons projecting to supraspinal sites (brainstem and hypothalamus), in prega

239 Some of this input is relayed directly to supraspinal sites by projection neurons, whereas much of

240 r, the relative importance of the spinal and supraspinal sites in the analgesic action of systemic op

241 e the importance of neural activity at these supraspinal sites in the expression of abdominal hyperse

242 after persistent inflammation, although the supraspinal sites of origin of each pathway are likely f

243 y mediated by their extensive projections to supraspinal sites such as the ventrolateral medulla, the

244 Substance P (SP) is known to act at supraspinal sites to influence pain sensitivity as well

245 e 55%) of Fos-positive neurons projecting to supraspinal sites were also located in the region of the

246 opioid receptor agonists at both spinal and supraspinal sites.

247 esia locally, and also through activation of supraspinal sites.

248 n of M(2) and M(4) mAChRs at both spinal and supraspinal sites.

249 on of plasticity at multiple spinal cord and supraspinal sites.

250 nt autoreceptors, inhibiting transmission in supraspinal sites.

251 Thus, supraspinal sources of dorsal horn VRL-1 immunoreactivit

252 dense enkephalinergic (ENK) innervation from supraspinal sources, including the rostral ventrolateral

253 ) and explored the relative contributions of supraspinal, spinal and peripheral sites to the actions

254 ves spinal sensitization and activates spino-supraspinal-spinal loops leading to descending inhibitor

255 t, isobolographic analysis revealed that the supraspinal/spinal antinociceptive interaction for both

256 in potency against acute nociception without supraspinal/spinal antinociceptive synergy.

257 In sham-operated rats supraspinal/spinal co-administration of morphine produce

258 iceptive potency of i.th. morphine, restored supraspinal/spinal morphine antinociceptive synergy and

259 ulate the NMDA receptor, result in a loss of supraspinal/spinal morphine synergy and may thus account

260 dmill (FTM), which imposes little demands on supraspinal structures as is the case when walking on ta

261 ry feedback, central pattern generators, and supraspinal structures can all evoke presynaptic inhibit

262 force fields generated by the activation of supraspinal structures could result from combinations of

263 es occur centrally in the spinal cord or the supraspinal structures following amputation.

264 unctional imaging studies suggest a role for supraspinal structures in this response.

265 of prominent bursts reflecting modulation by supraspinal structures involved in shaping central respi

266 position and motion, it is less clear which supraspinal structures mediate the signals that ultimate

267 It is believed that supraspinal structures mediate these adaptations, wherea

268 nput from the urinary bladder through either supraspinal structures or direct intraspinal pathways.

269 Reticulospinal neurons, situated between the supraspinal structures that initiate motor movements and

270 e know that plastic reorganization occurs in supraspinal structures with residual descending tracts.

271 related to pain and SCS in the dorsal horn, supraspinal structures, and the Pain Matrix.

272 muli induce pain modulation by activation of supraspinal structures.

273 facilitatory and inhibitory modulation from supraspinal structures.

274 onsible for respiratory rhythm reside in the supraspinal structures.

275 the acute stress effects are dependent on a supraspinal substrate.

276 d neurons may receive direct input both from supraspinal systems and from nociceptive and non-nocicep

277 ually held and a cool heat setting was used, supraspinal systems facilitated the response (Experiment

278 rategies will likely require both spinal and supraspinal targets.

279 outing of the optic nerve after crush and of supraspinal tracts after spinal cord injury.

280 o the SC environment which is rarely seen in supraspinal tracts.

281 ur during normal development, as a result of supraspinal trauma, and during skill acquisition change

282 In addition, when the supraspinal tremor input to one muscle was weak or absen

283 s determined by the relative strength of the supraspinal tremor input to the motoneuron pools.