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 Mg 2+ 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 −] 0 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 −] 0 and thought to result from increased intemeuron 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 Mg 2+ 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 bothN-methyl- d-aspartate and non-N-methyl- d-aspartate receptors. Thus, theN-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 nonN-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 Mg 2+ (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 Mg 2+ appears to be caused by both pre- and postsynaptic factors. These include: (1a) reduction of evoked transmitter release; the reduction of the dorsal root potential by 1.0 mM Mg 2+ was partly reversed by doubling [Ca 2+] 0; (2a) block of theN-methyl- d-aspartate receptor ion channels; (3a) decrease of GABA-depolarization of primary afferent fiber terminals; GABA-depolarizations of terminals were depressed by 1.0 mM Mg 2+; and (4a) decreased release of K + by afferent volleys; exposure to 1.0 mM Mg 2+ reduced the increment in [K +] 0 produced by repetitive afferent stimulation. d-(−)-2-amino-5-phosphonovalerate had only minimal effects on dorsal root potentials in 1.0 mM Mg 2+ presumably because theN-methyl- d-aspartate receptor-ion channel complex is largely inactivated by the Mg 2+. In contrast, kynurenate and 6-cyano-7-nitroquinoxaline-2,3-dione substantially diminished dorsal root potential amplitude and duration.