ライフサイエンスコーパス: spinal reflex

1 fter SCI, but could not modulate exaggerated spinal reflex.

2 to "normalize' the excitability of specific spinal reflexes.

3 Operant conditioning of a spinal reflex, a simple learning model, changes the rat

4 les, spastic individuals display hyperactive spinal reflexes and involuntary muscle co-contractions.

5 also been described for other responses like spinal reflexes and other sensory responses.

6 ted that central neurons mediating vestibulo-spinal reflexes and self-motion perception optimally enc

7 bolism, learning and memory, nociception and spinal reflexes, and anxiety and related behaviors.

8 an increase in rate-dependent depression of spinal reflexes, and ground and skill locomotion were im

9 city, increased rate-dependent depression in spinal reflexes, and improved ground and skill locomotio

10 Contrary to evidence from adults that spinal reflexes are inhibited during twitching [9-11], t

11 hat the tail-flick test of pain depends on a spinal reflex because a similar response is observed in

12 esponses elicited after the shortest latency spinal reflexes but prior to the onset of voluntary acti

13 njury, appropriate operant conditioning of a spinal reflex can improve impaired locomotion.

14 r response to bending, suggesting that these spinal reflexes can be modified by supraspinal signals i

15 ole for astrocytic Rac1 signaling within the spinal reflex circuit and the development of SCI-related

16 Spinal reflex circuit development requires the precise r

17 The organization of spinal reflex circuits relies on the specification of di

18 ch was likely to have been generated through spinal reflex circuits, as a template to learn a predict

19 like immunoreactivity; and (3) regulation of spinal reflex circuits, as shown by an increase in alpha

20 ide new insight into the factors controlling spinal reflex conditioning; they suggest that the condit

21 These spinal reflexes could contribute to feedback regulation

22 and survival of SMA mice, partially restores spinal reflexes, illustrating the reversibility of these

23 cessive mono- and polysynaptic low threshold spinal reflexes in rats.

24 of dopamine and D2-like receptor ligands on spinal reflexes in wild-type (WT) and D3-receptor knock-

25 is a dramatic reduction of extensor tone and spinal reflexes, including PLRs.

26 Understanding trunk roles in voluntary and spinal reflex integration after spinal cord injury and i

27 muscle as well as low threshold polysynaptic spinal reflexes involving afferents from other treated m

28 This condition involves an overactive spinal reflex loop that resists the passive lengthening

29 Impairment of the corresponding otolith-spinal reflexes may contribute substantially to falls.

30 ysfunction of lumbar motoneurons and altered spinal reflexes modulation.

31 y information from the urethra that controls spinal reflexes necessary to maintain continence and ach

32 pinal cord injury (SCI), the excitability of spinal reflexes of muscle afferent origins changes, like

33 that the nRO may influence the regulation of spinal reflexes of the pelvic floor.

34 Nerve ligations excluded contributions of spinal reflexes or distal axon reflexes to the distribut

35 assessed by their continued ability to block spinal reflex pathways during the reappearance of sponta

36 Transmission in spinal reflex pathways from the toes to the ankle flexor

37 al evidence, we propose the existence of two spinal reflex pathways involved in micturition: a pathwa

38 wake animals on the excitability of multiple spinal reflex pathways required for normal movement incl

39 y has a potent effect on the excitability of spinal reflex pathways.

40 tance leg control solely relies on dedicated spinal reflex pathways.

41 This priming of spinal reflex sensitivity was measured by both reduction

42 muscle activity for operant conditioning of spinal reflexes still use rigid metal electrodes with co

43 Spinal reflexes stimulate Hill-type muscles that actuate

44 fferent antinociceptive systems to inhibit a spinal reflex, tail withdrawal from radiant heat.

45 idine) receptor-induced antinociception in a spinal reflex test.

46 s, is associated with gradual alterations in spinal reflexes that appear to contribute to skill acqui

47 o depress sensory input but may also amplify spinal reflexes; the mechanisms of this modulation withi

48 omplete spinal cord injury (SCI), changing a spinal reflex through an operant conditioning protocol c

49 lso increased pain-related vocalizations and spinal reflexes through a mechanism that required mGluR5

50 immersion paradigm, which primarily assesses spinal reflexes to painful thermal stimuli.

51 leus and m. gastrocnemius is a short-latency spinal reflex triggered by ankle joint rotation.

52 nship between nociceptive brain activity and spinal reflex withdrawal activity in response to a clini

53 ise the nociceptive-specific brain activity, spinal reflex withdrawal and behavioural activity follow