Pharmacological block of the electrogenic sodium pump disrupts rhythmic
bursting induced by strychnine and bicuculline in the neonatal rat spinal
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
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