Reduction of anion reversal potential subverts the inhibitory control of firing rate in spinal lamina I neurons: towards a biophysical basis for neuropathic pain.
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Expanding Spectrum of Sodium Potassium Chloride Co-transporters in the Pathophysiology of DiseasesSerotonergic modulation of post-synaptic inhibition and locomotor alternating pattern in the spinal cordInhibitory synaptic plasticity: spike timing-dependence and putative network function.Microglia and spinal cord synaptic plasticity in persistent painSpontaneous excitation patterns computed for axons with injury-like impairments of sodium channels and Na/K pumpsNeuronal Chloride Regulation via KCC2 Is Modulated through a GABAB Receptor Protein Complex.Chloride regulation in the pain pathwayAcetazolamide and midazolam act synergistically to inhibit neuropathic pain.Central sensitization: implications for the diagnosis and treatment of pain.A sensitive membrane-targeted biosensor for monitoring changes in intracellular chloride in neuronal processes.Computational modeling reveals dendritic origins of GABA(A)-mediated excitation in CA1 pyramidal neurons.Ovariectomy modulation of morphine analgesia of neuropathic pain is associated with the change of K(+)-Cl(-) cotransporter 2 protein level in spinal dorsal horn.Efficacy of synaptic inhibition depends on multiple, dynamically interacting mechanisms implicated in chloride homeostasis.Osmoregulation requires brain expression of the renal Na-K-2Cl cotransporter NKCC2Neurosteroids and GABA-A Receptor Function.Modulation of spinal GABAergic analgesia by inhibition of chloride extrusion capacity in mice.Transformation of the output of spinal lamina I neurons after nerve injury and microglia stimulation underlying neuropathic pain.Combined Changes in Chloride Regulation and Neuronal Excitability Enable Primary Afferent Depolarization to Elicit Spiking without Compromising its Inhibitory EffectsActivation of 5-HT2A receptors upregulates the function of the neuronal K-Cl cotransporter KCC2.GABA is excitatory in adult vasopressinergic neuroendocrine cells.Neuroinflammation, neuroautoimmunity, and the co-morbidities of complex regional pain syndrome.Motor Cortex Excitability and BDNF Levels in Chronic Musculoskeletal Pain According to Structural PathologyThe α5 subunit containing GABAA receptors contribute to chronic pain.Morphine hyperalgesia gated through microglia-mediated disruption of neuronal Cl⁻ homeostasis.P2X4R+ microglia drive neuropathic pain.Dysfunctional astrocytic and synaptic regulation of hypothalamic glutamatergic transmission in a mouse model of early-life adversity: relevance to neurosteroids and programming of the stress response.Inhibition of carbonic anhydrase augments GABAA receptor-mediated analgesia via a spinal mechanism of action.Is BDNF sufficient for information transfer between microglia and dorsal horn neurons during the onset of central sensitization?The discovery and development of analgesics: new mechanisms, new modalities.Spatial and temporal dynamics in the ionic driving force for GABA(A) receptors.The many forms and functions of long term plasticity at GABAergic synapses.Deconstructing the neuropathic pain phenotype to reveal neural mechanisms.Microglia and intractable chronic pain.Microglia control neuronal network excitability via BDNF signalling.Inhibitory regulation of the pain gate and how its failure causes pathological pain.Identification of sodium channel isoforms that mediate action potential firing in lamina I/II spinal cord neurons.Synaptic conversion of chloride-dependent synapses in spinal nociceptive circuits: roles in neuropathic pain.The role of slow and persistent TTX-resistant sodium currents in acute tumor necrosis factor-α-mediated increase in nociceptors excitability.The Role of K(+)-Cl(-)-Cotransporter-2 in Neuropathic Pain.Neurosteroidogenesis is required for the physiological response to stress: role of neurosteroid-sensitive GABAA receptors.
P2860
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P2860
Reduction of anion reversal potential subverts the inhibitory control of firing rate in spinal lamina I neurons: towards a biophysical basis for neuropathic pain.
description
2006 nî lūn-bûn
@nan
2006年の論文
@ja
2006年論文
@yue
2006年論文
@zh-hant
2006年論文
@zh-hk
2006年論文
@zh-mo
2006年論文
@zh-tw
2006年论文
@wuu
2006年论文
@zh
2006年论文
@zh-cn
name
Reduction of anion reversal po ...... al basis for neuropathic pain.
@en
type
label
Reduction of anion reversal po ...... al basis for neuropathic pain.
@en
prefLabel
Reduction of anion reversal po ...... al basis for neuropathic pain.
@en
P2860
P356
P1433
P1476
Reduction of anion reversal po ...... al basis for neuropathic pain.
@en
P2093
Steven A Prescott
P2860
P2888
P356
10.1186/1744-8069-2-32
P577
2006-10-13T00:00:00Z
P5875
P6179
1011614556