Partial Peripheral Nerve Injury Promotes a Selective Loss of GABAergic Inhibition in the Superficial Dorsal Horn of the Spinal Cord

By K. Moore, T. Kohno, L. Karchewski, J. Scholz, H. Baba, Clifford J. Woolf. Journal of Neuroscience, 2002

885 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/e3c09d7320cd309f40afaedfe494d8981274676f

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. R. Ji
2. Clifford J. Woolf
3. Z. Zhuang
4. R. Kuner
5. Jürgen Sandkühler
6. A. Todd
7. P. Gerner
8. R. Meyer

In Molecular Biology

1. Clifford J. Woolf
2. R. Ji
3. Jürgen Sandkühler
4. R. Kuner
5. R. Meyer
6. J. Campbell
7. R. Baron
8. Z. Zhuang

In Physiology

1. Clifford J. Woolf
2. R. Ji
3. Jürgen Sandkühler
4. R. Kuner
5. Z. Zhuang
6. M. Malcangio
7. A. Todd
8. R. Baron

Citations in the corpus

• Cytokine Mechanisms of Central Sensitization: Distinct and Overlapping Role of Interleukin-1β, Interleukin-6, and Tumor Necrosis Factor-α in Regulating Synaptic and Neuronal Activity in the Superficial Spinal Cord (2008, background): “First, inhibitory neurons in the lamina II may undergo apoptosis after nerve injury, leading to a loss of GABA currents (Moore et al., 2002) (but see Polgar et al., 2005).”
• The synapsins: key actors of synapse function and plasticity. (2010, background): “development of neuropathic pain has been associated with the concomitant effect of excessive glutamatergic transmission and defective GABAergic inhibitory control, which lead to neuronal death in this region of the spinal cord (Moore et al., 2002; Scholz et al., 2005).”
• Neuronal circuitry for pain processing in the dorsal horn (2010, background): “Moore et al.(108) found a reduction in the proportion of lamina II neurons with primary afferent-evoked inhibitory postsynaptic currents following chronic constriction injury (CCI) or spared nerve injury (SNI).”
• Glia and pain: Is chronic pain a gliopathy? (2013, neutral): “[8,44,169,294].”
• Neural plasticity after peripheral nerve injury and regeneration. (2007, background): “There is also an attenuation of inhibitory GABAergic tone in the substantia gelatinosa interneuron pool (Laird and Bennett, 1992), and changes in the postsynaptic response to GABA and glycine that become less inhibitory on some neurons of lamina I (Moore et al., 2002), although the expression of GAB”
• Central sensitization: Implications for the diagnosis and treatment of pain (2010, background): “by reducing inhibition [12,103,168,180,165,208,226] or increasing membrane excitability can recruit these normal subthreshold inputs to suprathreshold action potentials, producing profound changes in functional properties [270].”
• Central mechanisms of pathological pain (2010, background): “It has been proposed that a selective loss of GABAergic interneurons in the spinal dorsal horn after nerve injury causes an imbalance between excitation and inhibitio”
• Models and mechanisms of hyperalgesia and allodynia. (2009, background): “The proportion of neurons in superficial spinal dorsal horn in vitro that express primary afferent-evoked inhibitory postsynaptic currents is diminished in animals with chronic constriction injury and spared nerve injury but not in animals with a sciatic nerve transection (362).”
• Cellular and Molecular Mechanisms of Pain (2009, neutral): “Although Moore et al. (2002) suggested that the disinhibition results from peripheral nerve injury-induced death of GABAergic interneurons, this claim has been contested (Polgar et al., 2005).”
• Mechanisms of neuropathic pain. (2006, background): “Further evidence indicates that nerve injury induces a selective apoptosis of inhibitory GABAergic interneurons (Moore et al., 2002).”
• Phantom limb pain: a case of maladaptive CNS plasticity? (2006, neutral): “Inhibitory GABA (γ-aminobutyric acid)-containing and glycinergic interneurons in the spinal cord could be destroyed by rapid ectopic discharge or other effects of axotom”
• Biological experimental demonstration of bifurcations from bursting to spiking predicted by theoretical models (2014, background): “[50–55], that can induce spontaneous electrophysiological activity at the injury site.”
• ERK is sequentially activated in neurons, microglia, and astrocytes by spinal nerve ligation and contributes to mechanical allodynia in this neuropathic pain model (2005, methodology): “Since total ERK levels did not change significantly after inflammation and nerve injury (Ji et al., 2002a,b; Moore et al., 2002), we used total ERK levels as loading control, and pERK1 and pERK2 levels were normalized against total ERK1 and ERK2 levels and expressed as fold increase, compared to…”
• MAP kinase and pain (2008, background): “Since disinhibition also occurs in conditions such as nerve injury (Moore et al., 2002; Coull et al., 2003), this mechanism may account for ERK activation by low-threshold stimulation after nerve injury.”