Abstract
Spontaneous activity originating in the injured nerve or the dorsal root ganglion (DRG) has been implicated in the development and maintenance of neuropathic pain. The inherent characteristics of spontaneous activity and the causal factors that modulate its firing pattern and frequency are not fully understood. We attempted to assess the thermosensitivity of spontaneous activity in dorsal root ganglion (DRG) neurons in normal rats and in rats with chronic compression of the DRG (CCD) in an in vitro nerve-DRG preparation. Extracellular, dorsal root recording from 66 spontaneously active CCD Aβ fibers indicate that: (1) decreasing bath temperature from 37 to 36–26 °C significantly decreased the firing rate (FR) in 85% (56/66) of fibers tested, of which 19 fibers (34%) responded to temperature change at physiological range (36–37 °C), whereas the remaining fibers responded at lower temperature levels (26–36 °C); (2) cooling of the DRG increased the FR in 12% (8/66) of fibers tested; (3) similarly, the firing rate of 21/26 spontaneously active Aβ fibers from normal rats was decreased following temperature decrease; (4) intracellular recordings from 38 normal neurons revealed that cooling the DRG significantly increased the action potential (AP) threshold, AP duration, AP amplitude and afterhyperpolarization (AHP) duration, but decreased AHP amplitude, maximal depolarizing and repolarizing rates. There was no significant change in the rheobase currents or the resting membrane potential. The present study indicates that large sensory neurons with myelinated axons are temperature dependent. It also suggests that maintenance of a stable temperature is critical for reliable characterization of spontaneous activity of sensory neurons.
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