spinal motoneurons
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AbstractBistable motoneurons of the spinal cord exhibit warmth-activated plateau potential driven by Na+ and triggered by a brief excitation. The thermoregulating molecular mechanisms of bistability and their role in motor functions remain unknown. Here, we identify thermosensitive Na+-permeable Trpm5 channels as the main molecular players for bistability in mouse motoneurons. Pharmacological, genetic or computational inhibition of Trpm5 occlude bistable-related properties (slow afterdepolarization, windup, plateau potentials) and reduce spinal locomotor outputs while central pattern generators for locomotion operate normally. At cellular level, Trpm5 is activated by a ryanodine-mediated Ca2+ release and turned off by Ca2+ reuptake through the sarco/endoplasmic reticulum Ca2+-ATPase (SERCA) pump. Mice in which Trpm5 is genetically silenced in most lumbar motoneurons develop hindlimb paresis and show difficulties in executing high-demanding locomotor tasks. Overall, by encoding bistability in motoneurons, Trpm5 appears indispensable for producing a postural tone in hindlimbs and amplifying the locomotor output.

Vibration decreased the responsiveness of Ia afferents from the muscle exposed to vibration, and the duration of depressive effect was modulated by the duration and frequency of the vibration: a longer duration and a higher frequency of vibration led to a longer recovery time of the depression. In addition to this presynaptic effect, it also depressed the responsiveness of spinal motoneurons, indicating postsynaptic inhibition through specific circuits triggered by Ia impulses.

The review surveys various aspects of the plasticity of nerve fibres, in particular the prolonged increase in their excitability evoked by polarization, focusing on a long-lasting increase in the excitability of myelinated afferent fibres traversing the dorsal columns of the spinal cord. We review the evidence that increased axonal excitability (i) follows epidurally applied direct current as well as relatively short (5 or 10 ms) current pulses and synaptically evoked intrinsic field potentials; (ii) critically depends on the polarization of branching regions of afferent fibres at the sites where they bifurcate and give off axon collaterals entering the spinal grey matter in conjunction with actions of extrasynaptic GABAA membrane receptors; and (iii) shares the feature of being activity-independent with the short-lasting effects of polarization of peripheral nerve fibres. A comparison between the polarization evoked sustained increase in the excitability of dorsal column fibres and spinal motoneurons (plateau potentials) indicates the possibility that they are mediated by partly similar membrane channels (including non-inactivating type L Cav++ 1.3 but not Na+ channels) and partly different mechanisms. We finally consider under which conditions trans-spinally applied DC (tsDCS) might reproduce the effects of epidural polarization on dorsal column fibres and the possible advantages of increased excitability of afferent fibres for the rehabilitation of motor and sensory functions after spinal cord injuries.

Abstract As the neuronal site where voltage gated channel density is highest, the axon initial segment (AIS) plays a key role in establishing a neuron’s action potential threshold, i.e. excitability. Among the properties of AIS that gain attention are length (AISl) and distance from the soma (AISd), which are variously found to change together with neuronal excitability following experimentally-induced perturbations in neural activity. The present study was designed to test the possibility that variation in AIS structural parameters regulates the native range in intrinsic excitability for one class of mature neurons. Spinal motoneurons were selected for their naturally large range in excitability and for their experimental accessibility to in vivo study. We began by determining whether AIS length or distance differed for motoneurons in motor pools that exhibit different activity profiles. Motoneurons sampled from the medial gastrocnemius (MG) motor pool exhibited values for average AISd that were significantly more than for motoneurons from the soleus (SOL) motor pool, which is more readily activated in low-level movements. Next, we tested whether AISd covaried with intrinsic excitability of individual motoneurons. Using anesthetized rats, we measured rheobase current intracellularly from MG motoneurons before labeling them for later immunohistochemical study of AIS. This combinatory approach revealed a significant correlation between AISd and rheobase, for 16 motoneurons sampled within the MG motor pool. Among multiple electrophysiological and morphological parameters measured here, AISd stood out as the dominant predictor of motoneuron excitability. These findings suggest an important role for AISd in setting the intrinsic excitability of spinal motoneurons.

Abstract Evolution of the direct connection from primary motor cortex to motoneurons in the spinal cord parallels acquisition of hand dexterity and lateralization of hand preference. Recent studies indicated that the phylogenetically older pathway consisting of multi-synaptic connections from primary motor cortex to spinal motoneurons also participate in controlling dexterous hand movement. However, it remains unknown how the two corticospinal pathways work in concert to control unilateral hand movement with lateralized preference. Using corticospinal functional magnetic resonance imaging, we discovered the asymmetric organization of the two corticospinal networks that modelled monosynaptic or polysynaptic control from primary motor cortices over spinal motoneurons. Moreover, the degree of the involvement of the two corticospinal networks paralleled the lateralization of hand preference. The present results pointed to the functionally lateralized motor nervous system that underlies the behavioural asymmetry of handedness, a uniquely human trait which could have phylogenetically differentiated humans from other primates.

Although slice recordings from spinal motoneurons (MNs) are being widely used, the effects of slicing on the measured MN electrical properties under normal and disease conditions have not been assessed. Using high-fidelity cell models of neonatal WT and SOD cells, we examined the effects of slice thickness, soma position within the slice, and slice orientation to estimate the error induced in measured MN electrical properties from spinal slices. Our results show that most MN electrical properties are not adversely affected by slicing, except for cell time constant, cell capacitance, and Ca2+ PIC, which all exhibited large errors, regardless of the slice condition. Among the examined factors, soma position within the slice appears to be the strongest factor in influencing the magnitude of error in measured MN electrical properties. Transverse slices appear to have the least impact on measured MN electrical properties. Surprisingly, and despite their anatomical enlargement, we found that G85R-SOD MNs experience similar error in their measured electrical properties to those of WT MNs, but their errors are more sensitive to the soma position within the slice than WT MNs. Unless in thick and symmetrical slices, slicing appears to reduce motoneuron type differences. Accordingly, slice studies should attempt to record from MNs at the slice center to avoid large and inconsistent errors in measured cell properties and have valid cell measurements' comparisons. Our results, therefore, offer information that would enhance the rigor of MN electrophysiological data measured from the slice preparation under normal and disease conditions.