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 GABAA 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. 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.(ABSTRACT TRUNCATED AT 250 WORDS)
Department of Neurology, University of Miami School of Medicine, FL.
J C
JC
Hackman
R A
RA
Davidoff
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D000200:Action Potentials / Q000187:drug effects; D000818:Animals; D001640:Bicuculline / Q000494:pharmacology; D005971:Glutamates / Q000502:physiology*; D018698:Glutamic Acid; D007736:Kynurenic Acid / Q000494:pharmacology; D008274:Magnesium / Q000494:pharmacology*; D009475:Neurons, Afferent / Q000502:physiology; D010852:Picrotoxin / Q000494:pharmacology; D011188:Potassium / Q000502:physiology*; D015221:Potassium Channels / Q000502:physiology; D011810:Quinoxalines / Q000494:pharmacology; D011894:Rana pipiens / Q000502:physiology*; D011963:Receptors, GABA-A / Q000187:drug effects / Q000502:physiology; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate / Q000187:drug effects / Q000502:physiology; D017981:Receptors, Neurotransmitter / Q000187:drug effects / Q000502:physiology; D013126:Spinal Nerve Roots / Q000187:drug effects / Q000502:physiology*; D009435:Synaptic Transmission / Q000187:drug effects; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D015763:2-Amino-5-phosphonovalerate; D018750:6-Cyano-7-nitroquinoxaline-2,3-dione; D001640:Bicuculline; D005971:Glutamates; D018698:Glutamic Acid; D007736:Kynurenic Acid; D008274:Magnesium; D010852:Picrotoxin; D011188:Potassium; D015221:Potassium Channels; D011810:Quinoxalines; D011963:Receptors, GABA-A; D017470:Receptors, Glutamate; D016194:Receptors, N-Methyl-D-Aspartate; D017981:Receptors, Neurotransmitter; D005680:gamma-Aminobutyric Acid