SPIKE-EVOKED SUPPRESSION AND BURST PATTERNING IN DORSAL-ROOT GANGLIONNEURONS OF THE RAT

Authors
Citation
R. Amir et M. Devor, SPIKE-EVOKED SUPPRESSION AND BURST PATTERNING IN DORSAL-ROOT GANGLIONNEURONS OF THE RAT, Journal of physiology, 501(1), 1997, pp. 183-196
Citations number
37
Categorie Soggetti
Physiology
Journal title
ISSN journal
00223751
Volume
501
Issue
1
Year of publication
1997
Pages
183 - 196
Database
ISI
SICI code
0022-3751(1997)501:1<183:SSABPI>2.0.ZU;2-8
Abstract
1. A low level of spontaneous impulse discharge is generated within do rsal root ganglia (DRGs) in intact animals, and this activity is enhan ced following nerve injury. Many physiological stimuli present in vivo are capable of augmenting this ectopic discharge. Whatever their caus e, episodes of sharply accelerated DRG firing tend to be followed by ' after-suppression' during which discharge falls below baseline rate. I n this study we examined the process of postexcitation suppression of firing rate, and how it shapes spike patterning in primary sensory neu rons. 2. We recorded intracellularly from sensory neurons in excised r at DRGs in vitro. Trains of spikes triggered by intracellular current pulses evoked a prolonged hyperpolarizing shift. This shift appeared t o be due to activation of a Ca2+-dependent K+ conductance (g(K(Ca))). Spikes evoked by just-suprathreshold pulses triggered a hyperpolarizin g shift and spike cessation. As the shift decayed, spiking was restore d. The net result was bursty (on-off) discharge, a previously unexplai ned peculiarity of ectopic discharge in some DRG neurons in vivo. 3. C onditioning nerve tetani delivered to axons of neurons which share the DRG with the impaled neuron evoked transient depolarization ('cross-d epolarization'). However, when stimulus strength was increased so as t o include the axon of the impaled neuron, the net result tvas a hyperp olarizing shift. Nerve stimulation that straddled the threshold of the axon of the impaled neuron drove it intermittently, but it always dro ve axons of at least some neighbouring neurons. The result was dynamic modulation of the membrane potential of the impaled neuron as cross-d epolarization and spike-evoked hyperpolarizing shifts played off again st one another. Membrane potential shifted in the hyperpolarizing dire ction whenever the axon was activated, and shifted in the depolarizing direction whenever it was silent. Dynamic modulation of this sort pro bably also occurs in vivo when stimuli are drawn over the surface of t he skin.