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

By Jeffrey A. M. Coull, D. Boudreau, Karine Bachand, S. Prescott, Francine Nault, A. Sik, P. Koninck, Y. Koninck. Nature, 2003

1,104 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/cf622903687fe32ea71758126f3ca05060ee6ab1

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. Friedemann Zenke
2. R. Ji
3. Robert Froemke
4. Clifford J. Woolf
5. Jürgen Sandkühler
6. Matthieu Gilson
7. M. Suter
8. Henning Sprekeler

In Molecular Biology

1. Clifford J. Woolf
2. R. Ji
3. Alban Latremoliere
4. M. Suter
5. Jürgen Sandkühler
6. R. Meyer
7. J. Campbell
8. M. Malcangio

In Physiology

1. Clifford J. Woolf
2. Alban Latremoliere
3. R. Ji
4. Jürgen Sandkühler
5. M. Suter
6. T. Berta
7. Maiken Nedergaard
8. M. Malcangio

Citations in the corpus

• Models and mechanisms of hyperalgesia and allodynia. (2009, background): “Thus the level of the chloride concentration gradient across the GABAA receptor expressing postsynaptic cell membrane determines if GABA is hyper- or depolarizing (89).”
• Perturbed Chloride Homeostasis and GABAergic Signaling in Human Temporal Lobe Epilepsy (2007, background): “A similar shift in GABA reversal potential, associated with a loss of KCC2 function, has been observed in pathological conditions including trauma, deafferentation, and paroxysmal activity (Vale and Sanes, 2000; Nabekura et al., 2002; Rivera et al., 2002, 2004; Coull et al., 2003; de Guzman et al., ”
• Mechanisms of neuropathic pain. (2006, background): “Consistent with this finding, knockdown of the expression of KCC2 leads to hyperalgesia (Coull et al., 2003).”
• Inhibitory synaptic plasticity: spike timing-dependence and putative network function (2013, background): “…2009), [e.g., through downregulation of a neuron-specific K+/Cl− co-transporter (KCC2)] is linked to pathologies such as chronic pain, schizophrenia, and epilepsy (Coull et al., 2003; Buzsáki et al., 2007; De Koninck, 2007; Kaila and Miles, 2010; Wamsteeker and Bains, 2010; Huberfeld et al., 2011).”
• 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.”
• Central Sensitization: A Generator of Pain Hypersensitivity by Central Neural Plasticity (2009, positive): “After peripheral nerve injury, BDNF released by activated microglial cells results in a reduction of KCC2 expression in a subset of neurons in the superficial lamina of the dorsal horn.(57,58,203) Consequently, activation of GABAA receptors by GABA result in a diminution or absence of Cl entry into ”
• Cellular and Molecular Mechanisms of Pain (2009, neutral): “For example, peripheral nerve injury profoundly downregulates the K+-Cl− cotransporter KCC2, which is essential for maintaining normal K+ and Cl− gradients across the plasma membrane (Coull et al., 2003).”
• Glia and pain: Is chronic pain a gliopathy? (2013, background): “As shown in Table 4, glia produce both large molecules (cytokines, chemokines, growth factors, and proteases) and small molecules (glutamate, ATP, Dserine, and prostaglandin E2 (PGE2).”