ライフサイエンスコーパス: locomotor

1 ent the first quantitative analysis into the locomotor abilities of a stem-archosaur applying 3D mode

2 we examine the temporal relationship between locomotor ability, brain microstructure, functional brai

3 pression of a negatively reinforced signaled locomotor action known as signaled active avoidance; thi

4 does not drive the expression of a signaled locomotor action mediated by the midbrain.

5 ation and involved in generating most of the locomotor actions that underlie fly behaviors.

6 ctive D(3)R antagonist PG01037 enhanced, the locomotor-activating effects of both acute cocaine admin

7 ic G(q)-DREADD activation increased both the locomotor-activating effects of low dose ethanol and the

8 reater selectivity for DAT over SERT retains locomotor activation in DAT Val559 mice.

9 nd methylphenidate, which induce significant locomotor activation, cocaine administration to these mi

10 jecting medium spiny neurons (iMSNs) impairs locomotor activities in a task-specific manner.

11 60 uM reduced fat accumulation and increased locomotor activity (an indicator of energy expenditure)

12 molecular clock, in generating the mammalian locomotor activity (LMA) circadian rhythm.

13 lness and produces sustained arousal, higher locomotor activity (LMA), and hyperthermia, which are co

14 Furthermore, a decreased spontaneous locomotor activity and absent thermogenic reaction to th

15 ating mice during maternal care and analysed locomotor activity and anxiety-like behaviour in the off

16 tantly, we showed that wild-type S1R rescues locomotor activity and ATP levels of flies expressing th

17 Locomotor activity and body temperature in combination p

18 g cis-element in daily maintenance of animal locomotor activity and body temperature rhythmicity.

19 2R knockout mice, this mutant restored basal locomotor activity and cocaine-induced locomotor activit

20 g in rodents which correlated with increased locomotor activity and HFO power in the OB.

21 ngth of the circadian free-running period of locomotor activity and normal sleep patterns in male mic

22 VTA counteracted two drug-seeking behaviors, locomotor activity and place preference.

23 by a significant improvement in spontaneous locomotor activity and reduced anxiety-like behavior.

24 ian neurons (dTRAPPC9) resulted in increased locomotor activity and reduced sleep, concordant with th

25 (DN) subunits, leads to changes in circadian locomotor activity and shortens lifespan.

26 and characterized in Drosophila by assessing locomotor activity and sleep upon knockdown of those gen

27 Monitoring System (IRAMS) to measure murine locomotor activity as a surrogate measure of disease sev

28 ncing, and primary rewarding effects using a locomotor activity assay, an intracranial self-stimulati

29 It does not affect the locomotor activity at doses several folds higher than it

30 The net effects of this modulatory system on locomotor activity can vary between different vertebrate

31 LPS suppression of locomotor activity correlated with blood glucose concent

32 PD altered several behavioural (reversal of locomotor activity impairment; cognitive impairment; del

33 s platform by characterizing ethanol-induced locomotor activity in a dose-dependent manner as well as

34 basal locomotor activity and cocaine-induced locomotor activity in a manner indistinguishable from wi

35 ecessary for reduced methamphetamine-induced locomotor activity in C57BL/6J congenic mice harboring D

36 underlying decreased methamphetamine-induced locomotor activity in mice.

37 gamma power, and these rats showed enhanced locomotor activity in novel environment.

38 ator alone is sufficient to rescue circadian locomotor activity in the absence of the other.

39 th sexes exposed to + Nic exhibited elevated locomotor activity in the elevated plus maze and altered

40 , colonized E2-exposed larvae showed reduced locomotor activity in the light, in contrast to axenic E

41 ffort exertion through regulation of general locomotor activity levels.

42 Here we evoke fictive locomotor activity of various frequencies in upright spi

43 not interact with the effects of alcohol on locomotor activity or loss-of-righting reflex.

44 We reveal that circadian rhythms in host locomotor activity patterns and body temperature become

45 While 14a increased locomotor activity relative to vehicle, it was significa

46 mple tracking system for assaying Drosophila locomotor activity rhythms and thought that it might als

47 According to our more extensive locomotor activity testing data, cebranopadol itself als

48 We further mapped discrete parameters of locomotor activity to epilepsy-like and anxiety-like beh

49 Locomotor activity was assessed in colonized and axenic

50 stent wakefulness with mania-like qualities: locomotor activity was increased; sensitivity to D-amphe

51 Locomotor activity was measured using the open-field tes

52 owever, after amphetamine injection, greater locomotor activity was observed in Het mice compared wit

53 ncreased metabolism, energy expenditure, and locomotor activity, along with increased body temperatur

54 e phenotypes, including a reduction in adult locomotor activity, alterations in visceral adipose tiss

55 the LNvs influence: temporal organization of locomotor activity, analyzed in males, and sleep, analyz

56 fixed-interval (FI) schedule of food reward, locomotor activity, and anxiety-like behavior], dopamine

57 n LNds, the clock neurons that drive evening locomotor activity, and AstC-R2 is required in these neu

58 working memory, sensorimotor gating, native locomotor activity, and dopaminergic innervation.

59 d broadband gamma frequency power, increased locomotor activity, and impaired novel object recognitio

60 marker of psychotic-like behavior), memory, locomotor activity, and the density of cell-surface and

61 tal TLR7-activated mice have normal baseline locomotor activity, but are hyperresponsive to stimuli i

62 phenotyping studies revealed alterations in locomotor activity, energy expenditure, and daily food i

63 WD also decreased locomotor activity, expression of the D2 receptor and ty

64 rats displayed blunted d-Amphetamine-induced locomotor activity, insensitivity to d-Amphetamine poten

65 h, and animals were assessed for changes in locomotor activity, learning, and memory 6 weeks later.

66 tic Mecp2 mutant mice significantly improved locomotor activity, lifespan and gene expression normali

67 fects of PF-5190457 combined with alcohol on locomotor activity, loss-of-righting reflex (a measure o

68 KO) male mice show increased novelty-induced locomotor activity, lower baseline anxiety, and motivati

69 any difference in basal motor coordination, locomotor activity, or conditioned place preference comp

70 mPFC-AcbSh pathway had no effect on running, locomotor activity, or feeding under ad libitum conditio

71 lateral brain ventricle results in increased locomotor activity, stereotypical behavior, and decrease

72 mutant adults are viable but display reduced locomotor activity, susceptibility to starvation, elevat

73 and evening oscillators eliminates circadian locomotor activity, the molecular clock in either oscill

74 neous Kcnn2 mutations show abnormal gait and locomotor activity, tremor and memory deficits, but huma

75 dent signaling and increased cocaine-induced locomotor activity, whereas overexpression of GIRK2 incr

76 ine synthesis capacity (Cohen's d = 2.5) and locomotor activity.

77 sufficient to cause a decrease in MA-induced locomotor activity.

78 s raised by dams exposed to LB showed higher locomotor activity.

79 udies in rodents where Mc4r agonists reduced locomotor activity.

80 im-short and cold is abrogated have abnormal locomotor activity.

81 d body neurons important for ethanol-induced locomotor activity.

82 any changes in response latencies or general locomotor activity.

83 thermal thresholds, motor coordination, nor locomotor activity.

84 tical to the circadian rhythms in Drosophila locomotor activity.

85 d intake, intestinal nutrient absorption and locomotor activity.

86 d acute inhibition of Mc4r signaling reduces locomotor activity.

87 t of adult mice as well as increased general locomotor activity; however, reward behaviors were simil

88 rd and unilateral/bilateral contributions to locomotor adaptation are also context dependent in healt

89 both groups, there was a persistence of the locomotor after-effect only in patients (P < 0.05).

90 previously experienced as moving generates a locomotor after-effect-the so-called 'broken escalator'

91 The motor responses that occur during locomotor after-effects have been mapped theoretically u

92 Although trunk and gait velocity locomotor after-effects were present in both groups, the

93 icle developed severe memory deficit without locomotor alteration, accompanied by a decrease of NMDAR

94 r, increased stress sensitivity, and reduced locomotor and exploratory activity.

95 ized to the primary focal site, and impaired locomotor and exploratory behavior for up to 1 month pos

96 e for testing the effect of C6 deficiency on locomotor and histological recovery after SCI, and highl

97 Indeed, a high sugar diet improves locomotor and lifespan defects caused by TDP-43 proteino

98 to uncertainty subsequently showed a higher locomotor and NAcc DA response to amphetamine and self-a

99 al enrichment (EE) similarly ameliorates the locomotor and social behavioral deficits in MeCP2 T158A

100 etween those who "get on with it," so-called locomotors, and those who prefer to ensure they "do the

101 leakage test, neurological examination with locomotor assessment, whole-body MRI, motor and somatose

102 ending motor system that commands left-right locomotor asymmetries in mammals.

103 rengthen the idea that dopamine can modulate locomotor behavior both via ascending projections to the

104 f branched muscles, and this correlates with locomotor behavior deficit.

105 at dopamine neurotransmission sensitizes the locomotor behavior elicited by activation of M2 neurons.

106 Here, we analyze the locomotor behavior of severely ataxic reeler mutants and

107 ter of intense debate regarding the species' locomotor behavior, phylogenetic position, insular paleo

108 ion to reticulospinal neurons that modulates locomotor behavior.

109 or these neurons in specific forms of innate locomotor behavior.

110 We investigated how postural-locomotor behaviors may influence vocal development, and

111 c dopaminergic neurons are known to modulate locomotor behaviors through their ascending projections

112 No changes in locomotor behaviors were observed in Het mice; however,

113 xperimental proof of concept that changes in locomotor behaviour and selective breeding might be infe

114 However, estimating the locomotor behaviour of a fossil species remains a challe

115 Inferring the locomotor behaviour of the last common ancestor (LCA) of

116 es associated with neuronal differentiation, locomotor behaviour, schizophrenia and AD.

117 tors, such as an individual's characteristic locomotor behaviour.

118 the lethal neurodegeneration, normalized the locomotor behavioural defects and ameliorated the viscer

119 mulation, a second MLR stimulation stops the locomotor bout if it is of lower intensity than the init

120 a small brainstem structure considered as a locomotor center, is sensitive to reward and sends excit

121 ly of the motor cortex and other supraspinal locomotor centers.

122 However, it remains unclear how the locomotor central pattern generator (CPG) processes desc

123 k, situated in the spinal cord, known as the locomotor central pattern generator (CPG).

124 and provide support for the concept that the locomotor central pattern generator is a modular network

125 To our knowledge, no reconstructions of the locomotor characteristics of stem amniotes based on mult

126 tion causes able-bodied individuals to adopt locomotor characteristics that resemble those of unilate

127 centers with each other and with the spinal locomotor circuits are poorly understood.

128 ole of the Dmrt3 interneurons in spinal cord locomotor circuits as well as molecular and functional i

129 populations and the formation of the spinal locomotor circuits downstream of the Onecut transcriptio

130 ast instructions sent by the brain to spinal locomotor circuits.

131 s differed between measurement sites but not locomotor condition.

132 nctional link between energy homeostasis and locomotor control systems.

133 c CB1KOs display normal cerebellum-dependent locomotor coordination and learning.

134 ouse system to quantify specific deficits in locomotor coordination in mildly ataxic Purkinje cell de

135 onstrating that these neurons participate in locomotor coordination.SIGNIFICANCE STATEMENT In this wo

136 We also found a locomotor correlate of this drop.

137 Many pair-wise differences of locomotor costs between similarly-sized species are cons

138 us to map the transverse distribution of the locomotor CPG and highlight the pattern of dynamic recru

139 riments have demonstrated that the mammalian locomotor CPG is distributed throughout the ventral port

140 tions during locomotion and suggest that the locomotor CPG is not a static network, but rather the sp

141 ed by the average head trajectory across the locomotor cycle.

142 ctivation, each timed at a specific phase of locomotor cycles and associated with a stable muscle syn

143 neurons induces abnormal eye morphology and locomotor defects in a dose-dependent manner.

144 due to integrin dysregulation, which causes locomotor defects in the animals.

145 phila and mouse models exhibit age-dependent locomotor defects, dopaminergic neuronal loss, periphera

146 vely suppresses dopaminergic neuron loss and locomotor deficits and is associated with reduced protei

147 The contribution of somatosensation to locomotor deficits in below-knee amputees (BKAs) has not

148 o not exhibit dystonia, they show pronounced locomotor deficits reflecting derangements in the cerebe

149 y, PFK overexpression rescues TDP-43 induced locomotor deficits.

150 rehabilitation approaches for patients with locomotor deficits.

151 e ladder test was sensitive enough to detect locomotor deficits.

152 redict survival time and preceded measurable locomotor deficits.

153 2 mo (0.09; 95% CI: -0.02, 0.21; P = 0.115), locomotor development score (2.05; 95% CI: 0.72, 3.38; P

154 ansient effect on linear growth and improved locomotor development.

155 and contribute to the increasing evidence of locomotor diversity within the hominin clade.

156 quires therapists to control the non-trivial locomotor dynamics of patients.

157 d in ichnofossils or unspecific modelling of locomotor dynamics.

158 ults in age-related dopamine neuron loss and locomotor dysfunction in Drosophila melanogaster through

159 aracterized by respiratory chain deficiency, locomotor dysfunction, and decreased lifespan.

160 ccess of rodents and the diversity of rodent locomotor ecologies, we used a large dataset of proximal

161 These data demonstrate that E2 locomotor effects in the light phase are dependent on th

162 aine administration to these mice elicits no locomotor effects, despite retention of conditioned plac

163 n that during stereotyped human self-motion, locomotor efference copies selectively replace vestibula

164 f a feed-forward balance regulation based on locomotor efference copies.

165 ts in walking speed and in the modulation of locomotor electromyograph activity in proximal and dista

166 f force production, is a strong predictor of locomotor energy costs across species of different size

167 nd why persists, impeding reconstructions of locomotor evolution.

168 r leg movements based on their body mass and locomotor experience?

169 onsiderably in how often they employ a given locomotor feature, and how this usage is modulated by od

170 all flies in our dataset use the same set of locomotor features, individual flies vary considerably i

171 out 40% of axons myelinated, and an enhanced locomotor function (score of 6 versus 3 for control grou

172 e the effect of C6 deficiency on recovery of locomotor function and histological injury parameters in

173 Drosophila melanogaster resulted in impaired locomotor function, learning, and short-term memory.

174 Locomotor function, mediated by lumbar neural circuitry,

175 eticulospinal plasticity for the recovery of locomotor functions following spinal hemisection, using

176 ns instruct spinal networks to execute basic locomotor functions, such as gait and speed.

177 In addition, the offspring showed locomotor hyperactivity and working memory deficit not o

178 delivery of Wnt6 to the amygdala ameliorates locomotor impairment and social behavioral deficits in t

179 nduced mortality in flies was accompanied by locomotor impairment, a common phenotype of neurodegener

180 e mice with CCI also exhibited cognitive and locomotor impairment.

181 quantitative foundation for mapping specific locomotor impairments onto distinct neuropathologies in

182 lied on anatomical features alone, ambiguous locomotor information preserved in ichnofossils or unspe

183 anized connectivity provides a mechanism for locomotor initiation and speed control.

184 g an excellent opportunity to understand how locomotor innovation can drive speciation.

185 nvestigate how the integration of visual and locomotor inputs may give rise to such activity in RSC.

186 Our experimental gait analysis of locomotor kinematics across 42 individuals from 15 speci

187 sible gait differences, direct comparison of locomotor kinematics and linear discriminant analysis re

188 We also show that locomotor learning requires active movement: observing a

189 verage the presence at birth of two types of locomotor-like movements, spontaneous kicking and weight

190 Fossorial rodents were also the only locomotor mode to consistently show increased rates of h

191 ll body sizes, allowing them to modify their locomotor mode without requiring major changes to their

192 Ribs and vertebrae are integral to this locomotor mode, but 3D motion of the axial skeleton has

193 Locomotor modes are attracted to landscape basins separa

194 internal or external morphology, with other locomotor modes plotting within a generalist morphospace

195 How locomotor modules develop and to what extent they depend

196 We surmise that mature locomotor modules may derive by combining the multiple p

197 inal neurons act to control the direction of locomotor movements in mammals.

198 dopaminergic neurons were found to increase locomotor movements through direct descending projection

199 es demonstrate greater fatigue resistance of locomotor muscle during single-limb and whole-body exerc

200 These findings suggest that locomotor muscle group III/IV afferent feedback in HFrEF

201 These findings indicate that locomotor muscle group III/IV afferent feedback in patie

202 e exercise intolerance in HFrEF is excessive locomotor muscle group III/IV afferent feedback; however

203 on (HFrEF), we investigated the influence of locomotor muscle group III/IV afferent inhibition via lu

204 e concentration, and greater respiratory and locomotor muscle oxygenation, but there were no differen

205 me spinal interneuronal networks that encode locomotor muscle synergies.

206 alterations of locomotor pattern and spinal locomotor network activity, likely resulting from defect

207 excitatory neurons and modulates the lumbar locomotor network independently of the motor cortex and

208 However, the spinal locomotor network requires greater excitability to produ

209 We found that (i) locomotor network vulnerability is established by struct

210 comotion are consistent with a shared spinal locomotor network, with sensory feedback from the limbs

211 ory and descending inputs to activate spinal locomotor neurons.

212 sparate morphologies to accommodate numerous locomotor niches, providing an excellent opportunity to

213 While terrestrial locomotors often contend with permanently deformable sub

214 hree weeks later, rats were tested for their locomotor or nucleus accumbens dopamine (NAcc DA) respon

215 We studied the effect of a circadian locomotor output cycles kaput (CLOCK) mutant (ClkDelta19

216 egulator, the transcription factor circadian locomotor output cycles kaput (CLOCK).

217 ite Collar complex; WCC] and BMAL1/Circadian Locomotor Output Cycles Kaput [CLOCK]).

218 tor-dependent regulation of the intensity of locomotor output is lost.

219 ectively tune neuronal activity and modulate locomotor output patterns.

220 d indicates that few neurons are involved in locomotor outputs across multiple speeds.

221 t pattern of these cells as the frequency of locomotor outputs is altered.

222 he brain to produce a variety of coordinated locomotor outputs.

223 ates and adult mice exhibited alterations of locomotor pattern and spinal locomotor network activity,

224 ricanus exhibits a modern human-like bipedal locomotor pattern, while that of a geologically younger

225 ve and quantitative analyses of the obtained locomotor patterns revealed that behavioral effects were

226 A clear distinction of MoAs based on locomotor patterns was not possible for most compounds.

227 mice lacking D5R exhibited slightly worsened locomotor performance in response to L-DOPA and enhanced

228 s, and demonstrate how morphological traits, locomotor performance, and age-specific survival may tra

229 oupling between morphological plasticity and locomotor performance, highly plastic features did not s

230 ciated with functional trade-offs related to locomotor performance.

231 and did not consistently improve individual locomotor performance.

232 tories with custom software tools to measure locomotor performance.

233 hortening, peripheral glial compression, and locomotor phenotypes, and that reduction in the integrin

234 O) flies lacking O-GlcNAcase activity showed locomotor phenotypes.

235 rate individualized estimates of each fish's locomotor plant and controller, revealing substantial va

236 We measured locomotor play using accelerometers on two consecutive d

237 ogy most like orangutans and consistent with locomotor power-grasping with the fingers, while that of

238 Surprisingly, we observed improved locomotor recovery and spinal cord white matter sparing

239 This is the quickest locomotor recovery recorded for autotomizing animals.

240 -injury confers neuroprotection and enhances locomotor recovery, and also exerts a complex modulation

241 ion.SIGNIFICANCE STATEMENT The mesencephalic locomotor region (MLR) is a brainstem region well known

242 opontine tegmentum (PPT) within the midbrain locomotor region abolishes signaled active avoidance res

243 descending projections to the mesencephalic locomotor region and spinal cord.

244 glia, spinal networks, and the mesencephalic locomotor region, a brainstem region that controls locom

245 , which in turn project to the mesencephalic locomotor region, known to control locomotion in vertebr

246 contrast, M3 receptor blockade destabilizes locomotor-related bursting.

247 eriments allow us to map the distribution of locomotor-related cells across the transverse plane of t

248 es us to use an imaging approach to identify locomotor-related cells across the transverse plane of t

249 hat exhibited knuckle-walking as part of its locomotor repertoire and that was probably later exapted

250 e Sterkfontein Caves practiced two different locomotor repertoires.

251 aine administration, and subsequent enhanced locomotor response and drug seeking behavior after repea

252 sured by electrophysiological recordings and locomotor response to amphetamine.

253 of DA neurons and the associated increase in locomotor response to amphetamine.

254 ated behaviors in the elevated plus maze and locomotor responses to amphetamine were also analyzed.

255 to trigger acute hypothermia, analgesic, and locomotor responses, and that 15 days of access to THC-g

256 ons reduced anxiety-like behavior, increased locomotor responsiveness to cocaine, and improved thermo

257 se perturbations occurred independent of the locomotor rhythm, intralimb coordination, and speed-depe

258 an additional 3 to be involved in regulating locomotor rhythm.

259 Unilateral locomotor rib movements are remarkably similar to the bi

260 e that DA neurons in the hypothalamus play a locomotor role, their precise contributions to behavior

261 ons and cocaine-induced behaviors, including locomotor sensitization and conditioned place preference

262 limbic areas, contributes to cocaine-induced locomotor sensitization and conditioned place preference

263 ulation and behavioral adaptation, including locomotor sensitization and drug preference in rodents.

264 ioral responses to repeated cocaine, such as locomotor sensitization and drug self-administration.

265 Given links between locomotor sensitization and mesolimbic dopamine signalin

266 Locomotor sensitization caused by interrupted morphine e

267 Additionally, nicotine locomotor sensitization correlated with accumbal dopamin

268 malized stereotypies and anxiety and blunted locomotor sensitization in morphine abstinent mice.

269 rotubule polymerization in the NAc inhibited locomotor sensitization to cocaine and contextual reward

270 DMS pathway and attenuates the expression of locomotor sensitization, directly linking OFC-DMS potent

271 s D1R hypersensitivity to facilitate cocaine locomotor sensitization, which by itself was not associa

272 In Gpr88 knockout mice, morphine-induced locomotor sensitization, withdrawal and supra-spinal ana

273 ne self-administration produced psychomotor (locomotor) sensitization, strong motivation to take and

274 cted assays to examine behavioural deficits (locomotor, sensory, memory and learning) and loss of dop

275 In this logic, rovers and locomotors share similarities in goal pursuit, as do sit

276 By quantifying the morphology of the locomotor skeleton of 95 species, we demonstrate that ec

277 The locomotor skeleton of Anolis may have evolved within a s

278 ed of locomotion, while inhibition decreases locomotor speed and ultimately terminates stepping.

279 These deficits in locomotor speed encoding likely severely impact path int

280 form negative chemotaxis by modulating their locomotor speed to avoid locations associated with optog

281 is mediated by two pathways, one controlling locomotor speed via connections to rhythm generating cir

282 he environmental demands, such as changes in locomotor speed.

283 uit modules engaged sequentially to increase locomotor speed.

284 near relationships that peaked at a range of locomotor speeds.

285 Given that shoes affect human locomotor stability and that visual, cognitive and somat

286 ify how body shape and its relationship with locomotor stance (quadruped/biped) changed in ontogeny,

287 e increased versatility for adopting diverse locomotor strategies.

288 We seek to understand how locomotor synergies change during development and traini

289 Despite a dysfunctional locomotor system, patients show normal adaptive learning

290 chanical and neurological constraints of the locomotor system.

291 e tensiometers to evaluate tendon loading in locomotor tasks.

292 ction-related information during challenging locomotor tasks.

293 ol, and planning over the large, intractable locomotor-terrain parameter space to generate robust loc

294 Our current understanding of the locomotor transition from water to land is largely based

295 We still know little about how locomotor transitions emerge from physical interaction w

296 a statistical physics theory of multipathway locomotor transitions in complex terrain.

297 Recent studies revealed that locomotor transitions in complex three-dimensional (3D)

298 We discovered that locomotor transitions of animals and robots self-propell

299 r-terrain parameter space to generate robust locomotor transitions through the real world.

300 ow the technique is feasible for people with locomotor turning problems.

301 s promise in clinical populations to improve locomotor turning; however, the adaptive mechanisms invo