Membrane properties and synaptic potentials in rat sympathetic preganglionic neurons studied in horizontal spinal cord slices in vitro

Abstract

Intracellular recordings were made from neurons in the intermediolateral column and adjacent white matter in horizontal slices of upper thoracic spinal cord from rats aged 21–28 days. Membrane properties were studied in the presence of picrotoxin (100 μM) to block ongoing inhibitory synaptic potentials. 37 neurons were identified as sympathetic preganglionic 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 MΩ ( n = 14). Following a hyperpolarising voltage step, a transient outward current was activated which had a time constant of decay of approx. 400 ms. The inflection in the repolarising phase of the action potential and the following prolonged AHP were both abolished by Cd 2+ (50 μM). The current underlying the AHP had two components with kinetic properties similar to the two calcium-activated potassium conductances, gKCa1, and gKCa2, characterized in other autonomic neurons. Noradrenaline (10–100 μM) 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 approx. 150 ms. All effects of noradrenaline were blocked by phentolamine (10 μM). Graded stimulation of the lateral funiculus 0.5–1 mm rostral to the recording site evoked in all cells monosynaptic fast excitatory synaptic potentials (fEPSPs) which were graded in amplitude. fEPSPs decayed with a time constant identical to the cell input time constant and were reduced in amplitude by CNQX (10–20 μM). In 7 cells, higher 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 reduced by α-adrenoceptor antagonists. The AHP was not blocked when the action potential was initiated during the slow EPSP. We conclude that excitatory bulbospinal inputs to SPNs involve at least one fast transmitter which is likely to be glutamate and one slow transmitter which is not noradrenaline.