BDNF Induced by Treadmill Training Contributes to the Suppression of Spasticity and Allodynia After Spinal Cord Injury via Upregulation of KCC2. (Q48405027)

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scientific article published on 19 December 2014

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English	BDNF Induced by Treadmill Training Contributes to the Suppression of Spasticity and Allodynia After Spinal Cord Injury via Upregulation of KCC2.	scientific article published on 19 December 2014

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25 February 2020

BDNF Induced by Treadmill Training Contributes to the Suppression of Spasticity and Allodynia After Spinal Cord Injury via Upregulation of KCC2 (English)

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Syoichi Tashiro

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Munehisa Shinozaki

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Masahiko Mukaino

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François Renault-Mihara

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Yoshiaki Toyama

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Meigen Liu

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Masaya Nakamura

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19 December 2014

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Neurorehabilitation and Neural Repair

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677-689

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25 February 2020

Effects of locomotor training after incomplete spinal cord injury: a systematic review

1 reference

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Wind-up of stretch reflexes as a measure of spasticity in chronic spinalized rats: The effects of passive exercise and modafinil.

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Mechanical allodynia following contusion injury of the rat spinal cord is associated with loss of GABAergic inhibition in the dorsal horn

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Trans-synaptic shift in anion gradient in spinal lamina I neurons as a mechanism of neuropathic pain

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Down-regulation of the potassium-chloride cotransporter KCC2 contributes to spasticity after spinal cord injury

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The K+/Cl- co-transporter KCC2 renders GABA hyperpolarizing during neuronal maturation

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Spinal cord injury-induced attenuation of GABAergic inhibition in spinal dorsal horn circuits is associated with down-regulation of the chloride transporter KCC2 in rat.

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GABA regulates synaptic integration of newly generated neurons in the adult brain

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The role of cation-dependent chloride transporters in neuropathic pain following spinal cord injury

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BDNF-induced TrkB activation down-regulates the K+-Cl- cotransporter KCC2 and impairs neuronal Cl- extrusion

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Age-dependent spontaneous hyperexcitability and impairment of GABAergic function in the hippocampus of mice lacking trkB.

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BDNF regulates spontaneous correlated activity at early developmental stages by increasing synaptogenesis and expression of the K+/Cl- co-transporter KCC2.

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Mechanism of activity-dependent downregulation of the neuron-specific K-Cl cotransporter KCC2.

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Early exercise in spinal cord injured rats induces allodynia through TrkB signaling.

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Locomotor ability in spinal rats is dependent on the amount of activity imposed on the hindlimbs during treadmill training

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BDNF and learning: Evidence that instrumental training promotes learning within the spinal cord by up-regulating BDNF expression.

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Cannabinoids control spasticity and tremor in a multiple sclerosis model

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Quantitative assessment of tactile allodynia in the rat paw

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A new and sensitive method for measuring thermal nociception in cutaneous hyperalgesia

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Effect of spinal cord injury severity on alterations of the H-reflex

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Quantitative metrics of spinal cord injury recovery in the rat using motion capture, electromyography and ground reaction force measurement.

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Beneficial compaction of spinal cord lesion by migrating astrocytes through glycogen synthase kinase-3 inhibition.

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A selective Sema3A inhibitor enhances regenerative responses and functional recovery of the injured spinal cord

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Diabetes affects the expression of GABA and potassium chloride cotransporter in the spinal cord: a study in streptozotocin diabetic rats

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Allodynia limits the usefulness of intraspinal neural stem cell grafts; directed differentiation improves outcome

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Exercise therapy and recovery after SCI: evidence that shows early intervention improves recovery of function

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TrkB.T1 contributes to neuropathic pain after spinal cord injury through regulation of cell cycle pathways

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Oligomerization of KCC2 correlates with development of inhibitory neurotransmission.

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Activity-dependent increase in neurotrophic factors is associated with an enhanced modulation of spinal reflexes after spinal cord injury

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Early Growth Response 4 Mediates BDNF Induction of Potassium Chloride Cotransporter 2 Transcription

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21 January 2018

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10.1177/1545968314562110

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25 February 2020

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