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The isolated thoracic cord of a neonatal rat in vitro generates tonic sympathetic activities in the splanchnic nerves. This tonic sympathetic nerve discharge (SND) has a prominent quasi-periodic oscillation at approximately 1-2 Hz. Bath application of bicuculline and strychnine, which removes endogenous GABA(A) and glycine receptor activities, transforms the quasi-periodic tonic SND into synchronized bursts (bSND). Picrotoxin, another GABA(A) receptor antagonist, also induces bSND. Serial transections of the thoracic cord (T1-12) were performed to identify the cord segments responsible for these tonic and bursting SNDs. Removal of T1-5 did not affect tonic SND. Nerve-cord preparation with either T6-8 or T10-12 segments could generate a substantial amount of tonic SND that retained comparable oscillating patterns. On the other hand, removal of T1-5 significantly reduced bSND amplitude without affecting its rhythmicity. Either T6-8 or T10-12 segments alone could generate bSND. Mid-point transection of T6-12 at T9 might split bSND rhythmogenesis, leading to the occurrence of bSND that could be attributed to two independent oscillators. Our results demonstrated that three segments within the T6-12 cord were sufficient to generate a rudimentary tonic and bursting SNDs. The thoracic cord segments, however, are dynamically interacting so that a full size bSND could only be produced with the intact thoracic cord.

Endogenous neurotransmitter activities underlying the sympathetic nerve discharge (SND) generated by newborn rat spinal cord in vitro were investigated using glutamatergic, glycinergic, and GABAergic antagonists. Under control conditions, the SND power spectrum had two major frequency components: synchronous bursting SND (bSND) with power dominant at