MEMBRANE-PROPERTIES AND SYNAPTIC POTENTIALS IN RAT SYMPATHETIC PREGANGLIONIC NEURONS STUDIED IN HORIZONTAL SPINAL-CORD SLICES IN-VITRO

Intracellular recordings were made from neurons in the intermediolater al column and adjacent white matter in horizontal slices of upper thor acic spinal cord from rats aged 21-28 days. Membrane properties were s tudied in the presence of picrotoxin (100 mu M) to block ongoing inhib itory synaptic potentials. 37 neurons were identified as sympathetic p reganglionic neurons (SPNs) by their electrical behaviour, anatomical location and/or morphology. SPNs had resting potentials of - 57 +/- 2 mV and input resistances of 254 +/- 31 M Omega(n = 14). Following a hy perpolarising voltage step, a transient outward current was activated which had a lime constant of decay of approx. 400 ms. The inflection i n the repolarising phase of the action potential and the following pro longed AHP were both abolished by Cd2+ (50 mu M). The current underlyi ng the AHP had two components with kinetic properties similar to the t wo calcium-activated potassium conductances, gKCa1, and gKCa2, charact erized in other autonomic neurons. Noradrenaline (10-100 mu M) caused a small depolarization and blocked the calcium component of the action potential suppressing the AHP. This revealed an afterdepolarization ( ADP) with an underlying inward current with a decay time constant of a pprox. 150 ms. All effects of noradrenaline were blocked by phentolami ne (10 mu M). Graded stimulation of the lateral funiculus 0.5-1 mm ros tral to the recording site evoked in all cells monosynaptic fast excit atory synaptic potentials (fEPSPs) which were graded in amplitude. fEP SPs decayed with a time constant identical to the cell input time cons tant and were reduced in amplitude by CNQX (10-20 mu M). In 7 cells, h igher stimulus voltages elicited slow EPSPs with a time to peak of 1.1 +/- 0.1 s and a half decay of 2.8 +/- 0.3 s (n = 7) which were not re duced by alpha-adrenoceptor antagonists. The AHP was not blocked when the action potential was initiated during the slow EPSP. We conclude t hat excitatory bulbospinal inputs to SPNs involve at least one fast tr ansmitter which is likely to be glutamate and one slow transmitter whi ch is not noradrenaline.