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 Supraspinal administration of the NOS inhibitor NOArg lo

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

10 The removal of supraspinal afferents resulted in extremely local effect

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

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

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

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

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

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

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

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

19 hat GA suppresses pain in part by activating supraspinal analgesic circuits.

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 l, correlating with maturation of descending supraspinal and local spinal circuits.

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

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

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

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

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

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

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 ise from primary motor cortex (M1) and other supraspinal areas.

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

44 ns, as well as the involvement of spinal and supraspinal astrocytes in the modulation of pain signall

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

46 The remodeling of supraspinal axonal circuits mediates functional recovery

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 itors acted as a neuronal relay to reconnect supraspinal center and spinal sympathetic neurons below

58 bation, suggesting that both SC circuits and supraspinal centers could contribute to later response c

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

60 ents are typically assumed to originate from supraspinal centers.

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

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

63 on whether spinal networks are connected to supraspinal centres.

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

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

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

67 ings from investigations into the spinal and supraspinal circuitry responsible for the sensation of i

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

69 espread surrounding inhibition may depend on supraspinal circuitry.

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

71 ssessing the functional status of spinal and supraspinal circuits.

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

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

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

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

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

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

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

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

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

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

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

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

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

85 grafted into a spinal cord injury site relay supraspinal control of serotonergic regulation for sympa

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

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

88 To restore supraspinal control of sympathetic preganglionic neurons

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

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

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

92 motor function in the absence of descending supraspinal control.

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

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

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

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

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

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

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

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

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

102 bles were correlated with an estimate of the supraspinal drive, which was measured as the speed of mo

103 late sympathetic discharge in the absence of supraspinal drive.

104 of spinal mechanisms to perform APAs due to supraspinal dysfunction.

105 ing in a cessation of step initiation due to supraspinal dysfunction.

106 have declined, suggesting an involvement of supraspinal dysfunction.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

143 spinal locomotor circuits as well as remnant supraspinal inputs.

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

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

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

147 te axonal regeneration, including those from supraspinal level.

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

149 increased strength is likely modulated at a supraspinal level.

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

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

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

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

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

155 s spinal LTP affects sensory transmission at supraspinal levels.

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

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

158 independently of the motor cortex and other supraspinal locomotor centers.

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

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

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

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

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

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

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

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

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

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

169 450 activity within the RVM is important for supraspinal morphine antinociception.

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

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

172 gene delivery throughout the spinal cord and supraspinal motor centers.

173 is centrally modulated to allow execution of supraspinal motor commands, here we hypothesized a loss

174 is centrally modulated to allow execution of supraspinal motor commands, it may be deficient in freez

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

176 ed by feedforward motor commands conveyed by supraspinal motor pathways.

177 Supraspinal multiplicative opiate analgesic interactions

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

179 ly, as a direct, non-invasive readout of the supraspinal neural contribution to pain sensitivity, it

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

181 bospinal excitatory drive predominately from supraspinal neurons of the rostral ventral respiratory g

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

183 5 days, sympathetic pre-motor neurons (i.e., supraspinal neurons that project to the IML) were identi

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

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

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

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

188 fective spatial learning, impaired gait, and supraspinal nociception.

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

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

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

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

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

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

195 receptors have been demonstrated to mediate supraspinal opioid antinociception.

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

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

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

199 her include excessive ascending signaling to supraspinal pain centers.

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

201 motor excitability, suggesting a maladaptive supraspinal pain modulatory state.

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

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

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

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

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

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

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

209 irreversible interruption of long descending supraspinal pathways in mice.

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

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

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

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

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

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

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

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

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

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

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

221 in lamina I have characteristic patterns of supraspinal projection.

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

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

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

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

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

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

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

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

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

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

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

233 xes in distal and forearm muscles, alongside supraspinal regions, such as the motor cortex and brains

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

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

236 The supraspinal regulation of genital reflexes is poorly und

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

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

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

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

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

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

243 Supraspinal serotonergic axons crossed the transection g

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

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

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

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

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

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

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

251 ited unchanged antihyperalgesia indicating a supraspinal site of action.

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

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

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

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

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

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

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

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

260 nt autoreceptors, inhibiting transmission in supraspinal sites.

261 opioid receptor agonists at both spinal and supraspinal sites.

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

286 ion neurons conveying nociceptive input into supraspinal structures.

287 muli induce pain modulation by activation of supraspinal structures.

288 facilitatory and inhibitory modulation from supraspinal structures.

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

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

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

292 rategies will likely require both spinal and supraspinal targets.

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

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

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

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

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

298 Disrupting supraspinal vasomotor pathways affects basal hemodynamic

299 Neuronal tracing showed that host supraspinal vasomotor pathways regenerated into the graf

300 unction.SIGNIFICANCE STATEMENT Disruption of supraspinal vasomotor pathways results in cardiovascular