ELECTROPHYSIOLOGICAL PROPERTIES OF GUINEA-PIG TRIGEMINAL MOTONEURONS RECORDED IN-VITRO

1. Intracellular recording and stimulation were made from guinea pig t rigeminal motoneurons (TMNs) in brain stem slices. Electrophysiologica l properties were examined and the underlying currents responsible for motoneuron excitability were investigated by the use of current clamp and single electrode voltage clamp (SEVC) techniques. 2. The voltage responses to subthreshold hyperpolarizing or depolarizing current puls es showed voltage- and time-dependent inward rectification. SEVC analy sis demonstrated that the hyperpolarizing inward rectification resulte d from the development of a slowly occurring voltage-dependent inward current activated at hyperpolarized membrane potentials. This current persisted in solutions containing low Ca2+/Mn2+, tetraethylammonium (T EA), and Ba2+, whereas it was reduced by 1-3 mM cesium. The depolarizi ng inward rectification was mediated by a persistent sodium current (I -Na-P) that was completely abolished by bath application of tetrodotox in (TTX). 3. Action potential characteristics were studied by intracel lular stimulation with brief current pulses (<3 ms) in combination wit h ionic substitutions or application of specific ionic conductance blo cking agents. Bath application of TTX abolished the action potential, whereas 1-10 mM TEA or 0.5-2 mM 4-aminopyridine (4-AP) increased, sign ificantly, the spike duration, suggesting participation of the delayed rectifier and A-current type conductances in spike repolarization. SE VC analysis revealed a TEA-sensitive sustained outward current and a f ast, voltage-dependent, transient current with properties consistent w ith their roles in spike repolarization. 4. TMN afterhyperpolarizing p otentials (AHPs) that followed a single spike consisted of fast and sl ow components usually separated by a depolarizing hump [afterdepolariz ation (ADP)]. The fast component was abolished by TEA or 4-AP but not by Mn2+ Co2+, or the bee venom apamin. In contrast, the slow AHP was r eadily reduced by Mn2+, Co2+, or apamin, suggesting participation of a n apamin-sensitive, calcium-dependent K+ conductance in the production of the slow AHP. SEVC analysis and ionic substitutions demonstrated a slowly activating and deactivating calcium-dependent K+ current with properties that could account for the slow AHP observed in these neuro ns. 5. Repetitive discharge was examined with long depolarizing curren t pulses (1 s) and analysis of frequency-current plots. When evoked fr om resting potential (about -55 mV), spike onset from rheobase occurre d rapidly and was maintained throughout the current pulse. At higher c urrent intensities, early and late adaptations in spike discharge were observed. Frequency-current plots exhibited a bilinear relationship f or the first interspike interval (ISI) in similar to 50% of the neuron s tested and in most neurons tested during steady-state discharge (SS) . The mean slopes for the first ISI of the primary and secondary range firings were 56 and 117 Hz/nA and 16 Hz/nA for the primary range duri ng SS discharge. 6. Bath application of inorganic calcium channel bloc kers (Mn2+, Co2+) or apamin increased the maximum SS frequency and slo pe of the frequency-current plots for all neurons tested, suggesting a role for a calcium-dependent K+ conductance in control of repetitive discharge. 7. The present study indicates that intrinsic cellular prop erties, in addition to timing of synaptic inputs, must be considered w hen discussing the factors that control motoneuronal excitability and burst-pattern formation during jaw movements.