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Volume 17, Number 5, Issue of March 1, 1997 pp. 1633-1641
Copyright ©1997 Society for NeuroscienceEctopic
2-Adrenoceptors Couple to N-Type Ca2+ Channels in Axotomized Rat Sensory Neurons
Received Sept. 12, 1996; revised Dec. 16, 1996; accepted Dec. 23, 1996.
Fuad A. Abdulla and Peter A. Smith Department of Pharmacology, University of Alberta, Edmonton, Alberta, Canada T6G 2H7
Dorsal root ganglion (DRG) neurons from control rats or from rats in which the sciatic nerve had been sectioned were studied by whole-cell recording techniques. Noradrenaline (10-100 µM) activated
-adrenoceptors and increased L-type Ca2+ channel current in control DRG cells, but this had little effect on excitability (the number of action potentials generated by a pulse of current at rheobasic strength). By contrast, in cells from nerve-damaged animals, noradrenaline activated
2-adrenoceptors, suppressed N-type Ca2+ channel current, and increased excitability. In axotomized cells, it also reduced total outward current recorded at +70 mV. Because noradrenaline did not affect total outward current recorded in the presence of the Ca2+ channel blocker Cd2+ (0.5-1 mM), its effects on excitability may result from reduction of Ca2+-sensitive K+-conductance(s) following suppression of N-type Ca2+ channel current. The strongest effects of noradrenaline were seen in small cells and in cells from animals that exhibited autotomy, a self-mutilatory behavior that can accompany peripheral nerve damage. Because many of these small DRG cells may be involved in the transmission of nociceptive information, changes in coupling between Ca2+ channels and adrenoceptors may contribute to the generation of the ectopic sensory nerve activity that has been implicated in the etiology of neuropathic pain.
Key words: pain; nerve injury; spinal ganglion; sodium channel; norepinephrine; acutely dissociated neurons
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