ライフサイエンスコーパス: locomotor

1 t development of spinal axons as well as the locomotor abilities observed in adult mice are independe

2 After lesions of the CNS, locomotor abilities of animals (mainly cats) are often a

3 method (ladder treadmill [LTM]) to study the locomotor ability of cats with an intact spinal cord or

4 cterized by their ability to perform complex locomotor actions in the absence of full consciousness.

5 K channels in DA neurons exhibited increased locomotor activation in response to acute cocaine admini

6 Methylone produced significant locomotor activation, which was correlated with plasma m

7 ly measures standing, feeding, drinking, and locomotor activities from 3D trajectories.

8 LG-IH also altered metabolic expenditure and locomotor activities in male offspring, and increased nu

9 were associated with the morning or evening locomotor activities occurred ~4 hours before their resp

10 eeding, and drinking were validated, but not locomotor activities.

11 regions of rat mPFC, in appetitive trace and locomotor activity (LMA) procedures.

12 EEG, EMG, body temperature (Tb), and locomotor activity (LMA) were recorded in Taar1 KO, OE,

13 as adjusted their energy expenditure, Tb and locomotor activity according to season and also time of

14 et restfulness were characterised by minimal locomotor activity and a low theta/delta ratio in the lo

15 necessary and sufficient for normal evening locomotor activity and daytime sleep profiles, respectiv

16 f qrfp or its receptors results in increased locomotor activity and decreased sleep during the day.

17 epileptogenesis were associated with altered locomotor activity and distorted circadian rhythm.

18 liver microsomes and compared to cocaine in locomotor activity and drug discrimination paradigms in

19 10-30 mg/kg i.p.) dose-dependently increased locomotor activity and electrical brain-stimulation rewa

20 in both HFD and/or OVX groups, and decreased locomotor activity and energy expenditure after OVX can

21 uate the participation of D2R in spontaneous locomotor activity and motor learning.

22 Viability and behavioral alteration in the locomotor activity and place preference, after IL treatm

23 w that 5-HT and octopamine jointly influence locomotor activity and quiescence in feeding and fasting

24 rosophila also resulted in severely impaired locomotor activity and reduced lifespan, mirroring patie

25 cemaker neurons to brain areas that regulate locomotor activity and sleep.

26 nsequently, the mutant mice were impaired in locomotor activity and spatial memory and were resistant

27 ly I:C and postnatal LPS produced changes in locomotor activity and temperature patterns, increases i

28 in confer an approximately 24-hr rhythm onto locomotor activity are unclear, but involve the neuropep

29 cocaine injections (20 mg/kg) paired with a locomotor activity chamber (Paired) or home cage (Unpair

30 EEG, EMG, body temperature, and locomotor activity data were collected continuously duri

31 ind that the overexpression of QRFP inhibits locomotor activity during the day, whereas mutation of q

32 ar (dHb-IPN) pathway expedites the return of locomotor activity following an unexpected negative stim

33 DH44 PI-Hugin SEZ circuit controls circadian locomotor activity in a daily cycle but has minimal effe

34 Locomotor activity in an open field was also elevated.

35 that electromyograms (EMGs) obtained during locomotor activity in mice were effective for identifica

36 in real-time place preference and increased locomotor activity in open-field testing.

37 ally, Gal-1 deficiency did not change normal locomotor activity in post-natal animals.

38 admill, we show that vestibular influence on locomotor activity is modulated independently in each li

39 During walking, the vestibular influence on locomotor activity is phase-dependent and modulated in b

40 , we find that QRFP overexpression decreases locomotor activity largely in a light-specific manner.

41 nduced behaviour in C. elegans and increased locomotor activity levels when injected into the central

42 Locomotor activity or food reinforced operant responding

43 reinstatement to cocaine, but did not affect locomotor activity or reinstatement to sucrose seeking.

44 During ad libitum feeding, locomotor activity resumed its arrhythmic state, but per

45 Light pulses delay locomotor activity rhythm during the early night and adv

46 est period induces phase delays of circadian locomotor activity rhythm.

47 re sufficient to drive motivated feeding and locomotor activity similar to LHA (GABA) neurons, but wi

48 ng self-administration of 0.2% saccharin and locomotor activity tests.

49 Through non-linear conversion of locomotor activity to "Locomotor Inactivity During Sleep

50 LS3 suppresses locomotor activity via a BK channel-specific mechanism i

51 In addition, cocaine-induced locomotor activity was used as a general 'read out' of m

52 Phase shifts of locomotor activity were analyzed in grass rats transferr

53 ained improvements in motor coordination and locomotor activity were observed, even after onset of ne

54 dystonic movements or postures or change in locomotor activity were observed.

55 Several parameters of locomotor activity were shifted early in the disease tim

56 or behavior; while LHA (Gal) neurons induced locomotor activity without compulsivity.

57 anges (PS bouts, SWS time, body temperature, locomotor activity) persisted after the CSDS regimen had

58 record electroencephalogram, electromyogram, locomotor activity, and body temperature, and the effica

59 ed ventricles and impaired social behaviour, locomotor activity, and learning and memory.

60 further differed in body weight, spontaneous locomotor activity, and prepulse inhibition of startle.

61 cephalography (EEG), electromyography (EMG), locomotor activity, and subcutaneous temperature.

62 ctivity-promoting E cells paralleled evening locomotor activity, and the LUC profile from sleep-promo

63 and partial agonist RO5263397 on sleep/wake, locomotor activity, body temperature, and cataplexy were

64 e did not affect general or morphine-induced locomotor activity, but markedly increased cocaine-induc

65 (GABA) neuronal activation similarly induced locomotor activity, but with striking differences in mod

66 nd SCN input and, when activated, suppresses locomotor activity, consistent with the behavioral hyper

67 der, older age (> 7 postnatal weeks), higher locomotor activity, daytime recordings, and recent blood

68 ic neurons of Drosophila and observe reduced locomotor activity, impaired survival and an age-depende

69 place within the neural network controlling locomotor activity, including spinal interneurons.

70 Rats exhibited increases in spontaneous locomotor activity, measured by implanted radiotelemetry

71 piny neurons (iMSNs) is sufficient to impair locomotor activity, phenocopying DA depletion models of

72 e report the use of animal models, including locomotor activity, protection, and rescue experiments i

73 Locomotor activity, Tb (measured in the rumen) and the l

74 e also show that QRFP overexpression reduces locomotor activity, whereas animals that lack QRFP signa

75 irect comparison of luciferase activity with locomotor activity, which was assayed in the same flies

76 This effect was not explained by a change in locomotor activity, which was unaffected by STN-HFS.

77 tudies, GluN2B inhibitors reduce MA-mediated locomotor activity, without affecting basal activity.

78 s food intake and body weight and normalizes locomotor activity.

79 reduces AMPH-stimulated dopamine efflux and locomotor activity.

80 lmitate, decreased food intake and increased locomotor activity.

81 or does it translate to a non-weight-bearing locomotor activity.

82 progressive ratio test but had no effect on locomotor activity.

83 chitecture that may account for the enhanced locomotor activity.

84 a high-fat diet, while not altering general locomotor activity.

85 in mice, decreasing methamphetamine-induced locomotor activity.

86 ected 0.2% saccharin self-administration nor locomotor activity.

87 ress-induced potentiation of cocaine-induced locomotor activity.

88 the overall effect to a 19.2% improvement of locomotor activity.

89 ircadian rhythmicity of body temperature and locomotor activity.

90 tor outputs to modulate circadian control of locomotor activity.

91 d circadian behavioral rhythms and decreased locomotor activity.

92 Seventeen subjects performed a multisession locomotor adaptation experiment in the laboratory, toget

93 lizer fMRI scans, after the baseline and the locomotor adaptation sessions.

94 focused on the role of cutaneous feedback in locomotor adaptation that takes place over minutes of tr

95 n long-term motor memories in the context of locomotor adaptation using resting-state fMRI.

96 ntly in other kinds of adaptation such as in locomotor adaptation.

97 and cerebellar-basal ganglia networks after locomotor adaptation.

98 cle activity and kinematics) associated with locomotor adaptation.

99 lts highlight the subject-specific nature of locomotor adaptations and how averaging data across subj

100 kdown in mouse NAc regulates cocaine-induced locomotor and place conditioning behavior.

101 s able to partially ameliorate the lifespan, locomotor, and oxidative stress phenotypes.

102 Feeding stages show regressed locomotor appendages.

103 zation (dpf) were evaluated using a standard locomotor assay.

104 ical stimulation-based therapy to accelerate locomotor-based rehabilitation.

105 cally injured animals prevented a decline in locomotor behavior and bladder physiology outcomes assoc

106 ptor in AIY neurons to promote low-amplitude locomotor behavior characteristic of well fed animals.

107 etatarsal heads has been used to reconstruct locomotor behavior in fossil hominins, but few studies h

108 uired for spinal axon development and normal locomotor behavior in mice.

109 nerative rules have been found in vertebrate locomotor behavior in several contexts (pharmacological

110 induced a strong suppression of spontaneous locomotor behavior in the open field with rapid kinetics

111 t the striking difference in compulsive-like locomotor behavior is also based on differential VTA inn

112 We further analyzed locomotor behavior to understand how differential VTA co

113 the decerebrate mouse is ideal for examining locomotor behavior using intracellular recording approac

114 WAVE1 D2-KO mice, cocaine-induced sensitized locomotor behavior was not maintained in WAVE1 D1-KO mic

115 uced rearing time in an open field), whereas locomotor behavior was unaffected by 2 weeks of Tat indu

116 targeted H3K9/14ac increased cocaine-induced locomotor behavior, as well as resilience to social stre

117 -MSNs (direct pathway) resulted in decreased locomotor behavior, reduced weight gain, and early postn

118 a striking impact on the phase of circadian locomotor behavior.

119 d of clock gene expression in the SCN and in locomotor behavior.

120 nd essential for the generation of circadian locomotor behavior.

121 gin and reference for the measurement of fly locomotor behavior; speed, walking direction and trunk o

122 f LHA (GABA) neurons induced compulsive-like locomotor behavior; while LHA (Gal) neurons induced loco

123 slincR resulted in altered neurologic and/or locomotor behavioral responses.

124 high-content profiling of Drosophila larval locomotor behaviors for over 100 genotypes.

125 ty in the brain associated with a variety of locomotor behaviors.

126 Circadian locomotor behaviour is controlled by a pacemaker circuit

127 nges, increased SSp regularity and disrupted locomotor behaviour.

128 content, quantitative phenotyping of larval locomotor behaviours provides a framework for system-lev

129 the involvement of each C. elegans neuron in locomotor behaviours.

130 ributes to feedforward control of subsequent locomotor bouts.

131 and decreased the amplitude of drug-induced locomotor bursting, effects that were dependent on the p

132 cular phase, burst skew and amplitude of the locomotor bursts.

133 rvated the pedunculopontine nucleus, a known locomotor center, and stimulation of the dopaminergic re

134 It may act by shielding brainstem and spinal locomotor centers from abnormal cortical input after str

135 x were used to compare the EMG and kinematic locomotor characteristics during walking on the FTM and

136 the FTM and the LTM, the changes in averaged locomotor characteristics must reflect the specificity o

137 raining maximizes the contribution of spinal locomotor circuits as well as remnant supraspinal inputs

138 e sensory prediction errors that then modify locomotor circuits to effect motor recovery.

139 st that dI3 interneurons compare inputs from locomotor circuits with sensory afferent inputs to compu

140 n the diversity of the neurons within spinal locomotor circuits.

141 tomation and a stronger dissociation between locomotor control and awareness than matched controls wh

142 n additional peripheral mechanism for graded locomotor control at the neuromuscular junction.

143 earning effects are associated with separate locomotor control networks and that intersubject variabi

144 rain causally related to sensory processing, locomotor control, courtship, aggression, and sleep.

145 comotor region (MLR) plays a crucial role in locomotor control.

146 many other aspects of sensory processing and locomotor control.

147 directly required as an integral part of the locomotor coordination machinery, the development of the

148 eurons be recruited at various phases of the locomotor cycle.

149 in dopaminergic neuronal loss, a progressive locomotor defect, abnormal aggregates in the ER and incr

150 of amyloid beta (Abeta) peptides, reversing locomotor defects, and extending lifespan.

151 that loss of Atg9 led to shortened lifespan, locomotor defects, and increased susceptibility to stres

152 iated with seizure susceptibility and severe locomotor defects.

153 n of trpml(+) in phagocytic glia rescued the locomotor deficit by removing early dying neurons, there

154 The increased locomotor deficit was associated with specific reduction

155 Usp8 protected from alpha-synuclein-induced locomotor deficits and cell loss.

156 adaptor SRSF1 prevents neurodegeneration and locomotor deficits in a Drosophila model of C9ORF72-rela

157 Mutant mice developed greater locomotor deficits in open-field tests than wild-type mi

158 shows robust neurodegeneration, early-onset locomotor deficits, and abundant alpha-synuclein aggrega

159 at the anatomo-physiological features of the locomotor drive are well conserved in vertebrates.

160 efficacy of motor commands and adapts future locomotor drive for tens of seconds.

161 ming across early development, but only when locomotor-driven stabilization and control of movement i

162 To test the sufficiency of locomotor-driven stabilization and the developing contro

163 o which both central efferent expiratory and locomotor drives converge, presumably facilitating the c

164 Locomotor dysfunction in a TDP-43 ALS fly model is also

165 tural integrity of adult neurons, alleviates locomotor dysfunction, and extends lifespan.

166 obust Abeta accumulation, neurodegeneration, locomotor dysfunction, and reduced lifespan.

167 anatomical and physiological determinants of locomotor economy (e.g., limb length and posture) and en

168 ted gait use of cursorial animals to enhance locomotor economy, bipedal jerboa (family Dipodidae) gai

169 In contrast, locomotor effects of heroin were abolished, and heroin-i

170 Locomotor effects were blocked by pretreatment with the

171 timulated dopamine overflow and AMPH-induced locomotor effects.

172 These novel results indicate (i) locomotor EMG activity might be an early measure of dise

173 Locomotor EMGs could have potential use as a clinical di

174 ht support and propulsion would have reduced locomotor endurance in the earliest hominins and likely

175 abain increased burst frequency and extended locomotor episode duration, whereas monensin slowed and

176 e light was turned off motoneuron firing and locomotor frequency both transiently increased.

177 lockade of D1 receptors in the MLR decreased locomotor frequency, but did not disrupt the SNc-evoked

178 ief from hypoxia and improves motoneuron and locomotor function after SCI.

179 TERPRETATION: MLR-HFS can improve disordered locomotor function in a rodent stroke model.

180 linical trials, we show improved sensory and locomotor function in adult (6 months) and elderly (18 m

181 o promote axonal regeneration and to improve locomotor function in the rat with spinal cord injury (S

182 major deterrent to predators and enhance the locomotor function of fins.

183 We optogenetically dissect the locomotor function of the three neurochemically distinct

184 e, thereby promoting axonal regeneration and locomotor function recovery.

185 es (5kU of SOD1/kg) improved the recovery of locomotor functions in rats with moderate SCI, along wit

186 ontributes to the control of visually guided locomotor gait modifications by constructing an estimati

187 i or Vibrio cholerae was sufficient to block locomotor hyperactivity at 10 dpf.

188 T and coat state, and attenuated OBX-induced locomotor hyperactivity.

189 pacity of a donor cell population to promote locomotor improvement after SCI.

190 c donor cell differentiation, and functional locomotor improvements.

191 -linear conversion of locomotor activity to "Locomotor Inactivity During Sleep" (LIDS), movement patt

192 s via interhemispheric inhibition, and demix locomotor instructions to independently drive turning an

193 the role of motoneuron firing during ongoing locomotor-like activity in neonatal mice expressing arch

194 pattern generator (CPG) during drug-induced locomotor-like activity.

195 frequency, and perturbed the phasing of the locomotor-like rhythm.

196 the first study to quantify the terrestrial locomotor morphology, energetics and kinematics in a spe

197 ord for the existence of bimodal respiratory-locomotor motoneurons and interneurons onto which both c

198 ion of muscle contraction underpins variable locomotor movements or gaits.

199 ion patterns underlying natural and adaptive locomotor movements poses formidable conceptual and tech

200 s and a progressive increase in the speed of locomotor movements.

201 s with a graded increase in the frequency of locomotor movements.

202 ating from the primal SNc that evokes graded locomotor movements.SIGNIFICANCE STATEMENT The mesenceph

203 l projection of mu-opioid receptor-sensitive locomotor muscle afferents during a 5 km cycling time tr

204 nstrains voluntary neural 'drive' to working locomotor muscle and limits the exercise-induced intramu

205 region evoked dopamine release in brainstem locomotor networks and concurrent reticulospinal activit

206 hat changes in sodium pump activity regulate locomotor networks in the spinal cord of neonatal mice.

207 as a function of the modular organization of locomotor networks through segregation of inhibition, a

208 nal neurons that in turn activate the spinal locomotor networks.

209 he first electrophysiological evidences of a locomotor neuronal system within the MRF in behaving NHP

210 ne per limb) within the spinal cord generate locomotor oscillations and control limb movements.

211 ing the transcriptional activators circadian locomotor output cycles kaput (CLOCK) and brain and musc

212 pared with controls, expression of Circadian Locomotor Output Cycles Kaput (CLOCK) is decreased in ep

213 Mice carrying the circadian locomotor output cycles Kaput delta 19 N-ethyl-N-nitroso

214 e collectively regulated by CLOCK (circadian locomotor output cycles kaput) in circadian rhythms.

215 The CLOCK (circadian locomotor output cycles protein kaput) gene encodes a co

216 hat changes in sodium pump activity regulate locomotor output in the spinal cord of neonatal mice.

217 When more "natural" locomotor output was evoked using dorsal-root stimulatio

218 nsequently evoking a progressive increase in locomotor output.

219 scending dopaminergic inputs that potentiate locomotor output.

220 threatening visual stimuli into directional locomotor output.

221 re, we show that a specific component of the locomotor pattern can be independently manipulated.

222 , and direction of movement, so the specific locomotor pattern generated relies on the diversity of t

223 l mechanism that could help to stabilize the locomotor pattern when changing speed.SIGNIFICANCE STATE

224 correlated with the spatial symmetry of the locomotor pattern, but not with temporal symmetry.

225 easure of disease onset; (ii) alterations in locomotor patterning may reflect changes in neuronal dri

226 Locomotor patterns must be adapted to external forces en

227 dence that inhibition of TDO or KMO improves locomotor performance and ameliorates shortened life spa

228 sexually selected train does not compromise locomotor performance in terms of the metabolic cost of

229 bryonic and brain development, fertility, or locomotor performance of mutant flies or their survival

230 e neuronal signalling genes with significant locomotor phenotypes, and conducted RNAi with ubiquitous

231 conserved in having neuronal expressions and locomotor phenotypes.

232 ly moving rats performing a range of natural locomotor procedures.

233 otor reflexes and interfere with the ongoing locomotor program.

234 reatment represents a therapeutic option for locomotor recovery after NS/PC transplantation, even in

235 e nervous system in transgenic mice enhanced locomotor recovery after sciatic nerve crush, associated

236 ssess the efficacy of OEC transplantation on locomotor recovery after traumatic experimental SCI and

237 rg1 mutants demonstrated reduced spontaneous locomotor recovery compared to injured controls, althoug

238 Significant locomotor recovery in comparison with the control group

239 rmine whether such regular training improves locomotor recovery on the FTM.

240 Interestingly, MaR1 administration improved locomotor recovery significantly and mitigated secondary

241 e lipid content and improves lesion size and locomotor recovery.

242 Ts and confers neuroprotection with improved locomotor recovery.

243 electrical stimulation of the mesencephalic locomotor region (MLR) is known to elicit gait movements

244 The mesencephalic locomotor region (MLR) plays a crucial role in locomotor

245 nts.SIGNIFICANCE STATEMENT The mesencephalic locomotor region (MLR) plays a crucial role in the contr

246 athway-mediated control of the mesencephalic locomotor region (MLR), a brainstem target of BG that is

247 tiated by projections from the mesencephalic locomotor region, the latter through a disinhibitory cir

248 racterized by connectivity to the cerebellar locomotor region.

249 ed by locomotor tasks, termed the cerebellar locomotor region.

250 from baseline resting-state connectivity in locomotor-related networks.

251 these mice have reduced amphetamine-induced locomotor response and striatal dopamine efflux.

252 ts selectively bred for differences in their locomotor response to a novel environment.

253 ule of food reinforcement, yet an attenuated locomotor response to acute cocaine.

254 The acute locomotor response to amphetamine and cocaine similarly

255 We found a sensitized locomotor response to cocaine in rats that gained weight

256 the mouse nucleus accumbens in a sensitized locomotor response to cocaine.

257 ral tegmental area (VTA) showed a sensitized locomotor response when challenged with amphetamine week

258 mphetamine subsequently showed a conditioned locomotor response when challenged with saline in the op

259 ntified true biological effects on zebrafish locomotor response.

260 lumination, zebrafish larvae display a rapid locomotor response.

261 GluA1 and GluN2B, along with markedly higher locomotor responses to intra-VTA infusions of AMPA, sugg

262 eurons, developed heightened cocaine-induced locomotor responses.

263 e neurons exhibit heightened cocaine-induced locomotor responses.

264 riod of MSDR but a long period of single-fly locomotor rhythm (SLR).

265 for the generation and control of the basic locomotor rhythm by activating muscles on either side of

266 While the locomotor rhythm is generated by ipsilateral excitatory

267 d are required for the production of a fluid locomotor rhythm.

268 put of the spinal cord that do not influence locomotor rhythmogenesis.

269 e of the neural circadian pacemakers driving locomotor rhythms are unaffected.

270 ways, whereas allatotropin (AT) only delayed locomotor rhythms at the early night.

271 hing the s-LNvs, the master pacemaker of the locomotor rhythms, from other clock neuron subtypes.

272 ted adult-restricted knockdown of Rnb impair locomotor rhythms.

273 p clock cells and does not require rescue of locomotor rhythms.

274 important regulator of Drosophila circadian locomotor rhythms.

275 regulates PDF responsiveness and behavioral locomotor rhythms.

276 motor output during lumbar afferent-induced locomotor rhythms.

277 inhibition in the expression of AMPH-induced locomotor sensitization and CPP.

278 activity to the NAc only transiently reduced locomotor sensitization and had no effect on drug taking

279 epeated exposure to psychostimulants induces locomotor sensitization and leads to persistent changes

280 NAc selectively inhibited the expression of locomotor sensitization following repeated injections of

281 nhibitor rolipram attenuated cocaine-induced locomotor sensitization in mice.

282 acute cocaine administration and an altered locomotor sensitization profile, as well as increased re

283 ission inhibitor, blunts cocaine seeking and locomotor sensitization, while blocking c-Fos induction

284 motion in mice and reduced oxycodone-induced locomotor sensitization.

285 the mastoid processes were combined with the Locomotor Sensory Organization Test (LSOT) paradigm to c

286 L-37-treated mice had significantly enhanced locomotor skills in an open field using the Basso Mouse

287 neous quantification of parameters including locomotor, sleep consolidation and molecular rhythms in

288 inputs from mechanosensory neurons increase locomotor speed by prolonging fast swimming at the expen

289 d their recruitment pattern as a function of locomotor speed.

290 ite this, relatively basic data, such as the locomotor speeds that animals choose to walk at in the w

291 Here we examined whether distinct locomotor states are encoded differentially in genetical

292 A random search model based on measured locomotor statistics could not reproduce the centered na

293 ated by GIRK channel activation, tempers the locomotor stimulatory effect of cocaine while also modul

294 ccelerated re-entrainment, and an absence of locomotor suppression.

295 Tails are an intricate component of the locomotor system for many vertebrates.

296 Locomotor systems generate diverse motor patterns to pro

297 section at T10 to cope with such a demanding locomotor task; and (3) to regularly train cats for 6 we

298 sly recognized regions that are activated by locomotor tasks, termed the cerebellar locomotor region.

299 Herein we studied locomotor time series of visually isolated Japanese quai

300 modulated across both limbs with changes in locomotor velocity and cadence.