Background: In 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.
Methods: Chronic 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.
Results: Rebound 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.
Conclusion: RF 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.
Keywords: post-inhibitory rebound firing, dorsal root ganglia, chronic compression, T-type Ca²⁺ currents