Martin Michaelis

TL;DR: The identification of a specific population of neurons whose firing properties change suddenly and synchronously following axotomy, and whose activity is associated with tactile allodynia, provides a powerful vehicle for defining the specific cascade of cellular and molecular events that underlie neuropathic pain.

TL;DR: It is reported that the ability of primary sensory neurons to sustain repetitive discharge depends on intrinsic resonant properties of the cell membrane and that the prevalence of this characteristic increases after nerve injury, and that selective pharmacological suppression of subthreshold oscillations may offer a means of controlling neuropathic paraesthesias and pain without blocking afferent nerve conduction.

TL;DR: Findings provide the first evidence that after peripheral nerve injury both axotomized as well as intact afferent neurons supplying skeletal muscle but not skin afferents generate ongoing activity within theDRG, probably because of a yet unknown signal in the DRG triggered by axotomy.

TL;DR: It is shown that subthreshold oscillations and burst discharge occur in vivo, as they do in vitro, and that although the first spike in each burst is triggered by an oscillatory sinusoid, firing within bursts is maintained by brief regenerative post-spike depolarizing afterpotentials (DAPs).