Intracellular recordings were made from hindlimb motoneurons in decerebrate cats to study how synaptic inputs could affect the threshold at which plateau potentials are activated with current injections through the recording microelectrode in the cell body. This study was prompted by recent evidence that the noninactivating inward currents that regeneratively produce the plateau potentials arise (partly) from dendritic conductances, which may be relatively more accessible to synaptic input than to current injected into the soma. Initially, cells were studied by injecting a slow triangular current ramp intracellularly to determine the threshold for activation of the plateau. In cells where the sodium spikes were blocked with intracellular QX314, plateau activation was readily seen as a sudden jump in membrane potential, which was not directly reversed as the current was decreased. With normal spiking, the plateau activation (the noninactivating inward current) was reflected by a steep and sustained jump in firing rate that was not directly reversed as the current was decreased. Importantly, the threshold for plateau activation (at 34 Hz on average) was significantly above the recruitment level (13 Hz on average). When tonic synaptic excitation [excitatory postsynaptic potentials (EPSPs)] was provided either by stretching the triceps surae muscle or by stimulating its nerve at a high frequency, the threshold for plateau activation by intracellular current injection was significantly lowered (by 12 Hz or 5.8 mV on average, without and with QX314, respectively). Conversely, tonic synaptic inhibition [inhibitory postsynaptic potentials (IPSPs)], provided by appropriate nerve stimulation, significantly raised the plateau threshold (by 19 Hz or 7.6 mV on average). These effects were graded with the intensity of tonic EPSPs and IPSPs. Strong enough EPSPs brought the plateau threshold down sufficiently that it was activated by the intracellular current soon after recruitment. A further increase in tonic EPSPs recruited the cell directly, and in this case the plateau was activated at or before recruitment. The finding that synaptic excitation can produce plateau activation below the recruitment level is of importance for the interpretation of its function. With this low-threshold activation, the plateau potentials are likely important in securing an effective recruitment to frequencies that produce significant force generation and would subsequently have no further affect on the frequency modulation, other than to provide a steady depolarizing bias that would help to sustain firing (cf. self-sustained firing). Additional jumps in frequency after recruitment (i.e., bistable firing) would not be expected.

Electrical stimulation of the brainstem in paralysed decerebrate cats evokes a centrally generated pattern of motor output (fictive locomotion) that has many of the characteristics of overground locomotion in adult quadripedal mammals (see Rossignol, 1996). During fictive locomotion, motoneurones innervating limb muscles receive alternating excitatory and inhibitory synaptic currents from the central pattern generator (CPG) for locomotion (Jordan, 1983). These result in the rhythmic fluctuations of membrane potential (locomotor drive potentials, LDPs) that underlie the patterned activation of motoneurones during locomotion. The transformation of rhythmic excitatory drive into trains of action potentials is governed by the passive and active membrane properties of motoneurones. It is now known that some of these properties are altered during locomotion. For example, the post-spike afterhyperpolarization (AHP) is reduced in motoneurones during fictive locomotion (Brownstone et al. 1992;Schmidt, 1994) and there is the appearance of a voltagedependent excitatory current (Brownstone et al. 1994). This voltage-dependent excitation results in non-linear responses of motoneurones to depolarizing currents, which may facilitate the recruitment of motoneurones, or augment motoneuronal output evoked by reflex or central excitation (Brownstone et al. 1994;McCrea et al. 1997;Bennett et al. 1998). These changes in motoneurone membrane properties result in increased motoneuronal firing in response to intracellular current injection during fictive locomotion (Brownstone et al. 1992;. The fictive locomotor state thus appears to include processes that increase the excitability of hindlimb motoneurones.The membrane potential at which action potentials are initiated in response to sufficient depolarizing currents (the voltage threshold, V th ) is not a fixed value in motoneurones. For example, V th tends to be higher (more depolarized) in higher rheobase motoneurones (Gustafsson & Pinter, 1984) 1. Experiments were conducted on decerebrate adult cats to examine the effect of brainstemevoked fictive locomotion on the threshold voltage (V th ) at which action potentials were initiated in hindlimb motoneurones. Measurements of the voltage threshold of the first spike evoked by intracellular injection of depolarizing ramp currents or square pulses were compared during control and fictive locomotor conditions. The sample of motoneurones included flexor and extensor motoneurones, and motoneurones with low and high rheobase currents.2. In all 38 motoneurones examined, action potentials were initiated at more hyperpolarized membrane potentials during fictive locomotion than in control conditions (mean hyperpolarization _8.0 ± 5.5 mV; range _1.8 to _26.6 mV). Hyperpolarization of V th occurred immediately at the onset of fictive locomotion and recovered in seconds (typically < 60 s) following the termination of locomotor activity.3. The V th of spikes occurring spontaneously without intracellular current injection was also reduced during loc...

Cat hindlimb motoneurons possess noninactivating voltage-gated inward currents that can, under appropriate conditions, regeneratively produce sustained increments in depolarization and firing of the cell (i.e., plateau potentials). Recent studies in turtle dorsal horn neurons and motoneurons indicate that facilitation of plateaus occurs with repeated plateau activation (decreased threshold and increased duration; this phenomenon is referred to as warm-up). The purpose of the present study was to study warm-up in cat motoneurons. Initially, cells were studied by injecting a slow triangular current ramp intracellularly to determine the threshold for activation of the plateau. In cells where the sodium spikes were blocked with intracellular QX314, plateau activation was readily seen as a sudden jump in membrane potential, which was not directly reversed as the current was decreased (cf. hysteresis). With normal spiking, the plateau activation (the noninactivating inward current) was reflected by a steep and sustained jump in firing rate, which was not directly reversed as the current was decreased (hysteresis). Repetitive plateau activation significantly lowered the plateau activation threshold in 83% of cells (by on average 5 mV and 11 Hz with and without QX314, respectively). This interaction between successive plateaus (warm-up) occurred when tested with 3- to 6-s intervals; no interaction occurred at times >20 s. Plateaus initiated by synaptic activation from muscle stretch were also facilitated by repetition. Repeated slow muscle stretches that produced small phasic responses when a cell was hyperpolarized with intracellular current bias produced a larger and more prolonged responses (plateau) when the bias was removed, and the amplitude and duration of this response grew with repetition. The effects of warm-up seen with intracellular recordings during muscle stretch could also be recorded extracellularly with gross electromyographic (EMG) recordings. That is, the same repetitive stretch as above produced a progressively larger and more prolonged EMG response. Warm-up may be a functionally important form of short-term plasticity in motoneurons that secures efficient motor output once a threshold level is reached for a significant period. Finally, the finding that warm-up can be readily observed with gross EMG recordings will be useful in future studies of plateaus in awake animals and humans.

We examined the effects of spontaneous or evoked episodes of rhythmic activity on synaptic transmission in several spinal pathways of embryonic day 9-12 chick embryos. We compared the amplitude of synaptic potentials evoked by stimulation of the ventrolateral funiculus (VLF), the dorsal or ventral roots, before and after episodes of activity. With the exception of the short-latency responses evoked by dorsal root stimulation, the potentials were briefly potentiated and then reduced for several minutes after an episode of rhythmic activity. Their amplitude progressively recovered in the interval between successive episodes. The lack of post-episode depression in the shortlatency component of the dorsal root evoked responses is probably attributable to the absence of firing in cut muscle afferents during an episode of activity.The post-episode depression of VLF-evoked potentials was mimicked by prolonged stimulation of the VLF, subthreshold for an episode of activity. By contrast, antidromically induced motoneuron firing and the accompanying calcium entry did not depress VLF-evoked potentials recorded from the stimulated ventral root. In addition, post-episode depression of VLFevoked synaptic currents was observed in voltage-clamped spinal neurons. Collectively, these findings suggest that somatic postsynaptic activity and calcium entry are not required for the depression. We propose instead that the mechanism may involve a form of long-lasting activity-induced synaptic depression, possibly a combination of transmitter depletion and ligand-induced changes in the postsynaptic current accompanying transmitter release. This activity-dependent depression appears to be an important mechanism underlying the occurrence of spontaneous activity in developing spinal networks.

Stimulation of the superficial peroneal or the sural nerve (3 shocks, 3 ms interval, 1 ms duration, 2.5 × perception threshold) evoked a reflex activation of the tibialis anterior muscle at a latency of approximately 70–95 ms in all of nine healthy human subjects. Stimulation of the medial plantar nerve only rarely produced similar effects. The possibility that a transcortical pathway contributes to these late reflex responses was investigated by combining the cutaneous stimulations and a transcranial magnetic stimulation of the contralateral motor cortex. A significant facilitation of short‐latency peaks in the post‐stimulus time histogram of single tibialis anterior motor units evoked by the transcortical magnetic stimulation was observed in eight out of nine subjects following stimulation of the superficial peroneal or sural nerves at the latency of the long‐latency reflex. In contrast such a facilitation was only rarely seen when the medial plantar nerve was stimulated. With the same timing for the stimuli, the superficial peroneal and sural nerve stimulations also produced a significant increase in the short‐latency, presumed monosynaptic, facilitation of the tibialis anterior H reflex produced by the brain stimulation. Similar facilitatory effects of the cutaneous stimuli could not be demonstrated when the magnetic stimulation of the cortex was replaced with electrical stimulation, implying that cortical excitability is affected by a conditioning cutaneous stimulation. It is suggested that the long‐latency reflexes in the tibialis anterior muscle evoked by activation of cutaneous afferents from the human foot are, at least partly, mediated by a transcortical pathway.