Pharmacological block of the electrogenic sodium pump disrupts rhythmic bursting induced by strychnine and bicuculline in the neonatal rat spinal cord. Ballerini, Laura, Enrico Bracci and Andrea Nistri. Biophysics Sector, International School for Advanced Studies (S.I.S.S.A.), via Beirut 4, 34014 Trieste, Italy.
APStracts 3:0188N, 1996.
1. The cellular mechanisms underlying rhythmic bursts induced in the isolated neonatal rat spinal cord by bath application of strychnine and bicuculline (which block glycine and GABAA receptor mediated inhibition, respectively) were probed with pharmacological tools. Such spontaneous bursts were recorded either intracellularly from lumbar motoneurons or extracellularly from ventral roots. As previously described, these network driven events consisted of large amplitude depolarizations arising abruptly from baseline with a highly regular period (on average 28 s). Burst episodes (lasting on average 7 s) comprised several oscillations and appeared synchronously on flexor and extensor motoneuron pools of both sides of the spinal cord. Their diffuse location made convenient to use bath-applied substances in the attempt to block selectively distinct membrane processes operating through the network. Application of apamin (0.4 (M) shortened both cycle period and burst duration without changing their regular rhythmicity. Similar results were obtained with carbachol (10 (M). Cs+ (4 mM) reversibly hyperpolarized the motoneuron membrane potential and largely increased burst duration which was characterized by a long series of repetitive oscillatory waves. Cycle period and rhythmicity remained unaltered. Ouabain (10 (M), strophanthidin (4 (M) or K+-free solutions disrupted rhythmic bursting which was fragmented into irregularly occurring paroxysmal activity mixed with short depolarizing events, still developing simultaneously on both sides of the spinal cord. Bursting activity eventually ceased after about 30-40 min application of ouabain or strophanthidin. Prolonged washout of strophanthidin or K+-free solutions re-established regular bursting patterns while no recovery from ouabain was observed. At the time of strong depression of bursting it was still possible to evoke bursts by single electrical pulses applied to the segmental dorsal root. Antidromic spikes of motoneurons could still be evoked by ventral root stimulation. These results demonstrate that, in a spinal bursting network mainly made up by excitatory processes, blockers of slow Ca2+ dependent K+ currents, such as apamin or carbachol, or of the slow inward rectifier, such as Cs+, did not suppress rhythmicity, suggesting that these conductances simply contributed to control cycle period and/or burst duration. Conversely, pharmacological blockers of the electrogenic Na+ pump such as ouabain, strophanthidin or K+-free solutions severely disrupted all characteristics of rhythmic bursting. It is proposed that the operation of the electrogenic Na+ pump of premotoneurons was a crucial element for rhythmic bursting.

Received 19 June 1996; accepted in final form 5 September 1996.
APS Manuscript Number J485-6.
Article publication pending J. Neurophysiol.
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 7 October 1996