EFFECTS OF POTASSIUM-IONS ON ACTION-POTENTIAL CONDUCTION IN A-FIBERS AND C-FIBERS OF RAT SPINAL NERVES

Citation
Jm. Peacock et R. Orchardson, EFFECTS OF POTASSIUM-IONS ON ACTION-POTENTIAL CONDUCTION IN A-FIBERS AND C-FIBERS OF RAT SPINAL NERVES, Journal of dental research, 74(2), 1995, pp. 634-641
Citations number
39
Categorie Soggetti
Dentistry,Oral Surgery & Medicine
Journal title
ISSN journal
00220345
Volume
74
Issue
2
Year of publication
1995
Pages
634 - 641
Database
ISI
SICI code
0022-0345(1995)74:2<634:EOPOAC>2.0.ZU;2-6
Abstract
Potassium ions in dentifrices for treating 'hypersensitive' dentin are believed to act directly on intradental nerves by raising extracellul ar potassium ion concentration ([K+](o)) sufficiently to prevent actio n potential generation by axonal accommodation. However, the [K+](o) n ecessary to block nerve conduction is not precisely known, nor is it c ertain that K+ can diffuse from a dentifrice in sufficient amounts to inactivate intradental nerves. To establish more accurately the [K+](o ) required to block nerve conduction under controlled conditions, we s tudied the effects of increased [K+](o) on the sizes of compound actio n potentials (CAP) recorded from rat spinal nerves in vitro. [K+](o) w as increased by the addition of either KC1 or KNO3 to Krebs' solutions applied to the central portion of the nerves. CAP attenuation increas ed in a dose-dependent manner as [K+](o) was raised in the 8 to 64 mmo l/L range, and complete block was generally produced with solutions co ntaining at least 32 mmol/L K+. CAP attenuation was reversible, and re covery times increased with increasing [K+](o). The effects of KC1 and KNO3 solutions were the same for all [K+](o) tested. Half-maximal (50 %) reduction in the A beta-fiber component of the CAP occurred with 17 .4 mmol/L K+, and with 17.8 mmol/L and 19.3 mmol/L K+, respectively, f or the A delta- and C-fiber components. Control experiments with gluco se and choline chloride confirmed that the conduction block observed w ith increased [K+](o) was not due to increased solution osmolarity or ionic strength. Assuming that intradental axons are as sensitive to al tered [K+](o) as spinal nerve axons, we suggest that for K+ in dentifr ices to block intradental nerve conduction: (1) [K+](o) in excess of 8 mmol/L would have to be achieved around nerve axons in the inner dent in or peripheral pulp, and (2) increases in [K+](o) of these magnitude s would have to be maintained in order for inzatradental nerve inactiv ation to be sustained.