DORSAL-ROOT POTENTIALS IN THE ISOLATED FROG SPINAL-CORD - AMINO-ACID NEUROTRANSMITTERS AND MAGNESIUM-IONS

Sucrose gap techniques recorded dorsal root potentials evoked by supramaximal dorsal root stimulation in in vitro, hemisected frog spinal cords. In 0 mM Mg2+ large (mean 13.0 mV), long lasting (mean 8.1 s) dorsal root potentials were recorded which consisted of two components: (1) an early component sensitive to picrotoxin, bicuculline, and low [Cl-]o and presumably produced by activation of GABA(A) receptors; and (2) a long-duration second component enhanced and lengthened by picrotoxin, bicuculline and low [Cl-]o and thought to result from increased interneuron discharges resulting from depression of GABA-mediated pre- and postsynaptic inhibition. Both the early and late components were reduced by over 90% in amplitude and duration by 20 mM Mg2+ or by kynurenate and bicuculline. The early component of the dorsal root potential may depend mainly upon activation of non-N-methyl-D-aspartate receptors, but the late component requires both N-methyl-D-aspartate and non-N-methyl-D-aspartate receptors. Thus, the N-methyl-D-aspartate antagonist D-(-)-2-amino-5-phosphonovalerate caused only a modest reduction in the amplitude of the early dorsal root potential component while the non N-methyl-D-aspartate antagonist 6-cyano-7-nitroquinoxaline-2,3-dione caused a much more substantial reduction. Exposure of the spinal cord to a "physiological" concentration of Mg2+ (1.0 mM) greatly reduced the duration and somewhat reduced the amplitude of the dorsal root potential. The reduction of dorsal root potentials by 1.0 mM Mg2+ appears to be caused by both pre- and postsynaptic factors. These include: (1) reduction of evoked transmitter release; the reduction of the dorsal root potential by 1.0 mM Mg2+ was partly reversed by doubling [Ca2+]o; (2) block of the N-methyl-D-aspartate receptor ion channels; (3) decrease of GABA-depolarization of primary afferent fiber terminals; GABA-depolarizations of terminals were depressed by 1.0 mM Mg2+; and (4) decreased release of K+ by afferent volleys; exposure to 1.0 mM Mg2+ reduced the increment in [K+]o produced by repetitive afferent stimulation. D-(-)-2-amino-5-phosphonovalerate had only minimal effects on dorsal root potentials in 1.0 mM Mg2+ presumably because the N-methyl-D-aspartate receptor-ion channel complex is largely inactivated by the Mg2+. In contrast, kynurenate and 6-cyano-7-nitroquinoxaline-2,3-dione substantially diminished dorsal root potential amplitude and duration.