Steven A. Prescott

TL;DR: Evidence is presented for a novel mechanism of disinhibition following peripheral nerve injury that involves a trans-synaptic reduction in the expression of the potassium–chloride exporter KCC2, and the consequent disruption of anion homeostasis in neurons of lamina I of the superficial dorsal horn, one of the main spinal nociceptive output pathways.

TL;DR: It is shown that divisive modulation of firing rate by shunting inhibition requires synaptic noise to smooth the relation between firing rate and somatic depolarization, and its modulatory effects are fully explained only when both synaptic noise and dendritic saturation are taken into account.

TL;DR: Through detailed analysis of the spike-initiating process, the results demonstrate that all three classes of excitability arise from a continuum in the direction and magnitude of subthreshold currents.

TL;DR: The current state of knowledge in this area is summarized with particular attention to how such findings relate to endogenous mechanisms of hyperalgesia and allodynia and potential applications for therapeutics based on modulation of intracellular Cl(-) gradients or pharmacological interventions targeting GABA(A) receptors.

TL;DR: There are multiple physiological cells types in lamina I with specific morphological correlates and distinctive signal processing characteristics that confer significant differences in the transduction of input into spike trains.