SUMMARY1. In the preceding paper (Crone, Hultborn, Kiehn, Mazieres & Wigstr6m, 1988) it was shown that a short-lasting synaptic excitation ('on' stimulus) of extensor motoneurones (primarily triceps surae) in the decerebrate cat often resulted in a maintained excitability increase, which could be reset by a short-lasting inhibitory stimulus train ('off' stimulus). In the present experiments intracellular recording from triceps surae motoneurones and the electroneurogram (ENG activity) from triceps surae nerve branches were performed in parallel.2. Sustained firing of individual triceps surae motoneurones was most often recorded in parallel with the maintained ENG activity following a synaptic 'on' stimulus. When the motoneurone was silenced, by a hyperpolarizing current through the microelectrode, there was no sign of on-going synaptic excitation during the maintained ENG activity following an 'on' stimulus. It was therefore suggested that voltage-dependent intrinsic properties of the motoneurones themselves could be responsible for the maintained firing.3. In confirmation of this hypothesis it was found that short-lasting depolarizing current pulses through the recording microelectrode could trigger a self-sustained firing in the motoneurone provided that the bias current (i.e. the holding potential) was kept within certain limits. Hyperpolarizing current pulses terminated the firing. When the spike-generating mechanism was inactivated (by long-lasting excessive depolarization) similar depolarizing and hyperpolarizing current pulses could initiate and terminate plateau potentials in the motoneurones. By grading the depolarizing current pulses it was found that the plateau potentials were of all-or-none character, typically around 10 mV in amplitude. The two levels of excitability which can be triggered by short-lasting excitation and inhibition of the motoneurones is referred to as 'bistable' behaviour of the motoneurones. 4. After an acute spinal transection, in the unanaesthetized cat, the bistable behaviour of the motoneurones disappeared. However, it reappears following intravenous injection of the serotonin precursor 5-hydroxytryptophan (50-120 mg/kg).* To whom reprint requests should be sent.

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SUMMARY1. The effect of serotonin on the firing properties of motoneurones was studied in transverse sections of the adult turtle spinal cord in vitro with intracellular recording techniques.2. In normal medium, turtle motoneurones adapt from an initial high frequency to a low steady firing during a depolarizing current pulse. In the presence of serotonin (4-100 JtM) motoneurones responded with accelerated firing and a frequency jump during a depolarizing current pulse followed by an after-depolarization outlasting the stimulus. From a depolarized holding potential motoneuronal activity was shifted between two stable states by brief depolarizing and hyperpolarizing current pulses. As an expression of this bistable firing behaviour, the frequency-current relation in response to a triangular current injection was counter-clockwise in serotonin while clockwise in normal medium.3. The delay to onset of the frequency jump was shortened as the amplitude of the activation pulse was increased. From a positive holding potential the afterdepolarization exceeded spike threshold and its duration increased with an increase in steady bias current. The effect of serotonin on turtle motoneurones could be blocked by methysergide (10,UM).4. When action potentials were depressed by tetrodotoxin, a voltage-dependent, non-inactivating plateau potential, intrinsic to the motoneurone, was revealed. Activation of this voltage plateau provides the motoneurones with two stable states of firing. The apparent input resistance was 2-4-fold lower during the plateau than at rest.5. The serotonin-induced plateau potential was Ca2"-dependent and was blocked when Ca2+ was replaced by either Co2+ (3 mM) or Mn21 (3 mM).6. The Ca2+ plateau was blocked by nifedipine (1-15 /IM). 7. Serotonin reduced the slow after-hyperpolarization following action potentials.The change in balance between inward and outward currents seems to be sufficient to reveal the plateau response.8. Although a small plateau response was induced by Bay K 8644 (1-15 /LM), this L-channel agonist could not reproduce the pronounced effect of serotonin.* To whom reprint requests should be sent.J. HOUNSGAARD AND 0. KIEHN 9. It is concluded that serotonin induces a Ca2+-dependent and nifedipinesensitive plateau potential in turtle motoneurones primarily by reducing a K+-current responsible for the slow after-hyperpolarization.

Many limb movements are composed of alternating flexions and extensions. However, the underlying spinal network mechanisms remain poorly defined. Here, we show that the intensity of synaptic excitation and inhibition in limb motoneurons varies in phase rather than out of phase during rhythmic scratchlike network activity in the turtle. Inhibition and excitation peak with the total neuron conductance during the depolarizing waves of scratch episodes. Furthermore, spike activity is driven by depolarizing synaptic transients rather than pacemaker properties. These findings show that balanced excitation and inhibition and irregular firing are fundamental motifs in certain spinal network functions.

SUMMARY1. The ability of dendrites in turtle motoneurones to support calcium spikes and calcium plateaux was investigated using differential polarization by applied electric fields.2. Electric fields were generated by passing current through transverse slices of the turtle spinal cord between two plate electrodes. The linear extracellular voltage gradient generated by the field implied that the tissue was ohmic and homogeneous.3. The transmembrane potential at the cell body of motoneurones was measured as the voltage difference between an intracellular and an extracellular microelectrode.4. In normal medium an applied field induced synaptic activity as well as intrinsic polarization of motoneurones. Synaptic activity was suppressed by tetrodotoxin (TTX, 1 JtM).5. In the presence of TTX and tetraethylammonium (TEA, 1-5 mM), applied fields evoked multicomponent Ca2+ spikes in both the soma-hyperpolarizing and soma-depolarizing direction of the field. The different components of Ca2+ spikes were discrete and additive. High amplitude components had higher threshold and faster time course and were followed by larger after-hyperpolarizations, than low amplitude components. The frequency of field-evoked regenerative responses was relatively insensitive to somatic bias current.6. TTX-resistant Ca2+-mediated plateau potentials promoted by apamin were evoked by differential polarization in both the soma-depolarizing and somahyperpolarizing direction.7. It is concluded that Ca2+ channels responsible for Ca2+ spikes and Ca2+ plateaux are present in dendrites of spinal motoneurones of the turtle.