Differential modulation by tetraethylammonium of the processes underlying network bursting in the neonatal rat spinal cord in vitro.
In the rat spinal cord in vitro, block of synaptic inhibition evokes persistent, regular disinhibited bursting which is a manifestation of the intrinsic network rhythmicity and is readily recorded from ventral roots. This model is advantageous to explore the network mechanisms controlling burst periodicity, and duration. We questioned the relative contribution of K+ conductances to spontaneous rhythmicity by investigating the effects of the broad K+ channel blocker tetraethylammonium (TEA). In TEA (10 mM) solution, bursts occurred at the same rate but became substantially longer, thus showing an unusual dissociation between mechanisms of burst periodicity and duration. In the presence of TEA, electrical stimulation of a single dorsal root or N-methyl-D-aspartate application (5 microM) could, however, fasten bursting associated with immediate decrease in burst length, thus demonstrating maintenance of short-term plasticity. Either riluzole (1 microM) or surgical sectioning that isolated a single spinal segment strongly depressed bursting which could, however, be revived by TEA. In the presence of TEA, the L-type channel blocker nifedipine (20 microM) made bursting faster and shorter. Our data are best explained by assuming that TEA increased network excitability to generate rhythmic bursting, an effect that was counteracted by intrinsic mechanisms, partly dependent on L-type channel activity, to retain standard periodicity. TEA-sensitive mechanisms were, nevertheless, an important process to regulate burst duration. Our results are consistent with the proposal of a hierarchical structural of the central pattern generator in which the circuits responsible for rhythmicity (the clock) drive the discharges of those creating the motor commands (pattern).
Taccola
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Neurobiology Sector, International School for Advanced Studies, via Beirut 2-4, 34014 Trieste, Italy. taccola@sissa.it
Nistri
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A
D000200:Action Potentials / Q000187:drug effects*; D000704:Analysis of Variance; D000818:Animals; D000831:Animals, Newborn; D001640:Bicuculline / Q000494:pharmacology; D004305:Dose-Response Relationship, Drug; D004347:Drug Interactions; D018690:Excitatory Amino Acid Agonists / Q000494:pharmacology; D018691:Excitatory Amino Acid Antagonists / Q000494:pharmacology; D018756:GABA Antagonists / Q000494:pharmacology; D066298:In Vitro Techniques; D053444:Inhibitory Postsynaptic Potentials; D016202:N-Methylaspartate / Q000494:pharmacology; D009415:Nerve Net / Q000187:drug effects*; D009433:Neural Inhibition / Q000187:drug effects; D009474:Neurons / Q000187:drug effects*; D026902:Potassium Channel Blockers / Q000494:pharmacology*; D051381:Rats; D019782:Riluzole / Q000494:pharmacology; D013116:Spinal Cord / Q000166:cytology*; D013331:Strychnine / Q000494:pharmacology; D019789:Tetraethylammonium / Q000494:pharmacology*
D018690:Excitatory Amino Acid Agonists; D018691:Excitatory Amino Acid Antagonists; D018756:GABA Antagonists; D026902:Potassium Channel Blockers; D016202:N-Methylaspartate; D019789:Tetraethylammonium; D019782:Riluzole; D013331:Strychnine; D001640:Bicuculline