Neuronal bursting induced by NK3 receptor activation in the neonatal rat spinal cord in vitro

Intracellular recording from lumbar motoneurons and extracellular recording from ventral roots of the neonatal rat isolated spinal cord were used to s tudy the mechanisms responsible for the excitation mediated by NK3 tachykin in receptors. The selective NK3 agonists senktide or [MePhe7] neurokinin B induced a slow depolarization with superimposed oscillations (mean period /- SD was 2.8 +/-0.8 s) that, in the majority of cases, showed left-right a lternation at segmental level and were synchronous between L-2 and L-5 of t he same side. During agonist wash out (5-20 min) a delayed form of hyperexc itability emerged consisting of bursts lasting 8 +/-2 s (average interburst interval 55 +/- 21 s) with superimposed oscillations usually with homosegm ental alternation and heterosegmental synchronicity. Such bursting was acco mpanied by depression of GABAergic dorsal root potentials evoked by dorsal root stimulation and of the recurrent inhibitory postsynaptic potential rec orded from motoneurons. Despite bursting, motoneuron membrane potential ret urned to baseline while input resistance was increased. Bursts were a netwo rk-dependent phenomenon triggered by previous NK3 receptor activation becau se bursting was suppressed by glutamate receptor antagonists and was insens itive to motoneuron membrane potential or subsequent application of an NK3 receptor antagonist. NK3 receptors operated synergistically with N-methyl-D -aspartate (NMDA) and 5-hydroxytryptamine (5-HT) to trigger fully alternati ng locomotor-like rhythms while NK3 receptor antagonism disrupted the same rhythm. In summary, in the neonatal rat spinal cord NK3 receptors could tri gger rhythmic activity predominantly with alternation at segmental level bu t with synchronous coupling between ipsilateral motor pools. NK3 receptor a ctivation could also facilitate fictive locomotor patterns induced by NMDA and 5-HT.