Hyperexcitability in sensory neurons of rats selected for high versus low neuropathic pain phenotype

Effects of activation of group III metabotropic glutamate receptors on spinal synaptic transmission in a rat model of neuropathic pain

“…Our results are consistent with those of previous studies that found augmented glutamatergic EPSCs from primary afferents in other animal models of neuropathic pain (Kohno et al, 2003, Wang et al, 2007). Augmented glutamatergic input after nerve injury could result from increased excitability of primary afferent nerves and ectopic discharges from injured afferent nerves or DRG neurons (Matzner and Devor, 1994, Liu et al, 2001). Furthermore, the reciprocal interaction between primary afferents and GABAergic interneurons in the spinal cord is important for nociceptive processing in the spinal cord.…”

Sodium Channels and Mechanisms of Neuropathic Pain

“…Such "pain susceptibility genes" must be distinguished from "disease susceptibility genes," mutations that predispose to the acquisition of particular types of nerve pathology that may be painful. 29,33 It has recently been reported that a gain-of-function mutation in the Na v 1.7 Na ϩ channel increases the repetitive firing capability of some DRG neurons, causing pain symptoms in erythromelalgia. 17,49 …”

The heart‐rate‐reducing agent, ivabradine, reduces mechanical allodynia in a rodent model of neuropathic pain

“…It results from increased excitability in the pain signalling system. In some situations, this may be initialized (Wall and Devor, 1983;Liu et al, 2001) and maintained (Gracely et al, 1992;Pitcher and Henry, 2008;Costigan et al, 2009;Stemkowski and Smith, 2012b) by aberrant activity in primary afferent neurons. Dorsal root ganglia (DRG) are thought to be a major source of this activity (Wall and Devor, 1983;Amir et al, 1999;Liu et al, 2001).…”