Post-Inhibitory Rebound Firing of Dorsal Root Ganglia Neurons.

Abstract

BackgroundIn the central nervous system, post-inhibitory rebound firing (RF) may mediate overactivity of neurons under pathophysiological condition. RF is also observed in dorsal root ganglion (IRA) neurons. However, the functional significance of RF in primary sensory neurons has remained unknown. After peripheral sensory nerve/neuron injury, DRG neurons exhibit hyperexcitability. Therefore, RF may play a role in neuropathic pain.MethodsChronic compression of DRG (CCD) is used as a neuropathic pain model. Rats were divided into 2 groups: Sham and CCD groups. Patch clamp was performed on the whole DRG and cultured DRG neurons to record RF and T-type Ca2+ currents. The blocker of T-type Ca2+ channels, NiCl2, was applied to DRG neurons.ResultsRebound neurons were more excitable than non-rebound neurons. And they discharged RF with prominent after depolarizing potentials, which were blocked by NiCl2. After DRG injury, the proportion of rebound neurons augmented, and rebound neurons’ excitability increased. Meanwhile, the steady-state activation curve of T-type Ca2+ channels was shifted toward the left.ConclusionRF may be related to highly excitable neurons and sensitive to both depolarization and hyperpolarization. T-type Ca2+ channels were critical to RF, potentially enhancing the spontaneous firing of rebound neurons in response to resting membrane potential fluctuations.