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The manner in which motoneurons respond to excitatory and inhibitory inputs depends strongly on how their intrinsic properties are influenced by the neuromodulators serotonin and noradrenaline. These neuromodulators enhance the activation of voltage­gated channels that generate persistent (long-lasting) inward sodium and calcium currents (PICs) into the motoneurons. PICs are crucial for initiating, accelerating, and maintaining motoneuron firing. A greater accessibility to state-of-the-art techniques that allows both the estimation and examination of PIC modulation in tens of motoneurons in vivo has rapidly evolved our knowledge of how motoneurons amplify and prolong the effects of synaptic input. We are now in a position to gain substantial mechanistic insight into the role of PICs in motor control at an unprecedented pace. The present review briefly describes the effects of PICs on motoneuron firing and the methods available for estimating them before presenting the emerging evidence of how PICs can be modulated in health and disease. Our rapidly developing knowledge of the potent effects of PICs on motoneuron firing has the potential to improve our understanding of how we move, and points to new approaches to improve motor control. Finally, gaps in our understanding are highlighted and methodological advancements suggested to encourage readers to explore outstanding questions to further elucidate PIC physiology.

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5-HT2 receptors on motoneurones play a critical role in facilitating persistent inward currents (PICs). Although facilitation of PICs can enhance self-sustained firing after periods of excitation, the relationship between 5-HT2 receptor activity and self-sustained firing in human motor units (MUs) has not been resolved. MU activity was assessed from the tibialis anterior of 10 healthy adults (24.9 ± 2.8 years) during two contraction protocols. Both protocols featured steady-state isometric contractions with constant descending drive to the motoneurone pool. However, one protocol also included an additional phase of superimposed descending drive. Adding and then removing descending drive in the middle of steady-state contractions altered MU firing behaviour across the motor pool, where newly recruited units in the superimposed phase were unable to switch off (P = 0.0002), and units recruited prior to additional descending drive reduced their discharge rates (P < 0.0001, difference in estimated marginal means (∆) = 2.24 pulses/s). The 5-HT2 receptor antagonist, cyproheptadine, was then administered to determine whether changes in MU firing were mediated by serotonergic mechanisms. 5-HT2 receptor antagonism caused reductions in MU discharge rate (P < 0.001, ∆ = 1.65 pulses/s), recruitment threshold (P = 0.00112, ∆ = 1.09% maximal voluntary contraction) and self-sustained firing duration (P < 0.0001, ∆ = 1.77s) after the additional descending drive was removed in the middle of the steady-state contraction. These findings indicate that serotonergic neuromodulation plays a key role in facilitating discharge and self-sustained firing of human motoneurones, where adaptive changes in MU recruitment must occur to meet the demands of the contraction. KEY POINTS: Animal and cellular preparations indicate that somato-dendritic 5-HT2 receptors regulate the intrinsic excitability of motoneurones. 5-HT2 receptor antagonism reduces estimates of persistent inward currents in motoneurones, which contribute to self-sustained firing when synaptic inputs are reduced or removed. This human study employed a contraction task that slowly increased (and then removed) the additional descending drive in the middle of a steady-state contraction where marked self-sustained firing occurred when the descending drive was removed. 5-HT2 receptor antagonism caused widespread reductions in motor unit (MU) discharge rates during contractions, which was accompanied by reduced recruitment threshold and attenuation of self-sustained firing duration after the removal of the additional descending drive to motoneurones. These findings support the role that serotonergic neuromodulation is a key facilitator of MU discharge and self-sustained firing of human motoneurones, where adaptative changes in MU recruitment must occur to meet the demands of the contraction.

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BACKGROUND: Lower capacity to generate knee extension maximal voluntary force (MVF) has been observed in individuals affected with patellar tendinopathy (PT) compared to asymptomatic controls. This MVF deficit is hypothesized to emanate from alterations in corticospinal excitability (CSE). The modulation of CSE is intricately linked to the excitability levels at multiple sites, encompassing neurones within the corticospinal tract (CST), intracortical neurones within the primary motor cortex (M1), and the alpha motoneurone. The aim of this investigation was to examine the excitability of intracortical neurones, CST neurones, and the alpha motoneurone, and compare these between volleyball and basketball athletes with PT and matched asymptomatic controls. METHOD: Nineteen athletes with PT and 18 asymptomatic controls participated in this cross-sectional study. Transcranial magnetic stimulation was utilized to assess CST excitability, corticospinal inhibition (silent period, and short-interval cortical inhibition). Peripheral nerve stimulation was used to evaluate lumbar spine and alpha motoneurone excitability, including the evocation of lumbar-evoked potentials and maximal compound muscle action potential (MMAX ), and CSE with central activation ratio (CAR). Knee extension MVF was also assessed. RESULTS: Athletes with PT exhibited longer silent period duration and greater electrical stimulator output for MMAX , as well as lower MVF, compared to asymptomatic controls (p < 0.05). CONCLUSION: These findings indicate volleyball and basketball athletes with PT exhibit reduced excitability of the alpha motoneurone or the neuromuscular junction, which may be linked to lower MVF. Subtle alterations at specific sites may represent compensatory changes to excitability aiming to maintain efferent drive to the knee extensors.

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Serotonin modulates corticospinal excitability, motoneurone firing rates and contractile strength via 5-HT2 receptors. However, the effects of these receptors on cortical and motoneurone excitability during voluntary contractions have not been explored in humans. Therefore, the purpose of this study was to investigate how 5-HT2 antagonism affects corticospinal and motoneuronal excitability with and without descending drive to motoneurones. Twelve individuals (aged 24 ± 4 years) participated in a double-blind, placebo-controlled, crossover study, whereby the 5-HT2 antagonist cyproheptadine was administered. Transcranial magnetic stimulation (TMS) was delivered to the motor cortex to produce motor evoked potentials (MEPs), and electrical stimulation at the cervicomedullary junction was used to generate cervicomedullary motor evoked potentials (CMEPs) in the biceps brachii at rest and during a range of submaximal elbow flexions. Evoked potentials were also obtained after a conditioning TMS pulse to produce conditioned MEPs and CMEPs (100 ms inter-stimulus interval). 5-HT2 antagonism reduced maximal torque (p < 0.001), and compared to placebo, reduced unconditioned MEP amplitude at rest (p = 0.003), conditioned MEP amplitude at rest (p = 0.033) and conditioned MEP amplitude during contractions (p = 0.020). 5-HT2 antagonism also increased unconditioned CMEP amplitude during voluntary contractions (p = 0.041) but not at rest. Although 5-HT2 antagonism increased long-interval intracortical inhibition, net corticospinal excitability was unaffected during voluntary contractions. Given that spinal motoneurone excitability was only affected when descending drive to motoneurones was present, the current study indicates that excitatory drive is necessary for 5-HT2 receptors to regulate motoneurone excitability but not intracortical circuits.

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The primary motor cortex does not uniquely or directly produce alpha motoneurone (α-MN) drive to muscles during voluntary movement. Rather, α-MN drive emerges from the synthesis and competition among excitatory and inhibitory inputs from multiple descending tracts, spinal interneurons, sensory inputs, and proprioceptive afferents. One such fundamental input is velocity-dependent stretch reflexes in lengthening muscles, which should be inhibited to enable voluntary movement. It remains an open question, however, the extent to which unmodulated stretch reflexes disrupt voluntary movement, and whether and how they are inhibited in limbs with numerous multi-articular muscles. We used a computational model of a Rhesus Macaque arm to simulate movements with feedforward α-MN commands only, and with added velocity-dependent stretch reflex feedback. We found that velocity-dependent stretch reflex caused movement-specific, typically large and variable disruptions to arm movements. These disruptions were greatly reduced when modulating velocity-dependent stretch reflex feedback (i) as per the commonly proposed (but yet to be clarified) idealized alpha-gamma (α-γ) co-activation or (ii) an alternative α-MN collateral projection to homonymous γ-MNs. We conclude that such α-MN collaterals are a physiologically tenable, but previously unrecognized, propriospinal circuit in the mammalian fusimotor system. These collaterals could still collaborate with α-γ co-activation, and the few skeletofusimotor fibers (ß-MNs) in mammals, to create a flexible fusimotor ecosystem to enable voluntary movement. By locally and automatically regulating the highly nonlinear neuro-musculo-skeletal mechanics of the limb, these collaterals could be a critical low-level enabler of learning, adaptation, and performance via higher-level brainstem, cerebellar and cortical mechanisms.

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The present study aimed to investigate whether a 2-wk arm cycling sprint interval training (SIT) program modulated corticospinal pathway excitability in healthy, neurologically intact participants. We employed a pre-post study design with two groups: 1) an experimental SIT group and 2) a nonexercising control group. Transcranial magnetic stimulation (TMS) of the motor cortex and transmastoid electrical stimulation (TMES) of corticospinal axons were used at baseline and post-training to provide indices of corticospinal and spinal excitability, respectively. Stimulus-response curves (SRCs) recorded from the biceps brachii were elicited for each stimulation type during two submaximal arm cycling conditions [25 watts (W) and 30% peak power output (PPO)]. All stimulations were delivered during the mid-elbow flexion phase of cycling. Compared with baseline, performance on the time-to-exhaustion (TTE) test at post-testing was improved for members of the SIT group but was not altered for controls, suggesting that SIT improved exercise performance. There were no changes in the area under the curve (AUC) for TMS-elicited SRCs for either group. However, the AUC for TMES-elicited cervicomedullary motor-evoked potential SRCs were significantly larger at post-testing in the SIT group only (25 W: P = 0.012, d = 0.870; 30% PPO: P = 0.016, d = 0.825). This data shows that overall corticospinal excitability is unchanged following SIT, whereas spinal excitability is enhanced. Although the precise mechanisms underlying these findings during arm cycling at post-SIT are unknown, it is suggested that the enhanced spinal excitability may represent a neural adaptation to training.NEW & NOTEWORTHY Two weeks of arm cycling sprint interval training (SIT) improves subsequent aerobic exercise performance and induces changes within the descending corticospinal pathway. Specifically, spinal excitability is enhanced following training, whereas overall corticospinal excitability does not change. These results suggest that the enhanced spinal excitability may represent a neural adaptation to training. Future work is required to discern the precise neurophysiological mechanisms underlying these observations.

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Serotonergic neuromodulation contributes to enhanced voluntary muscle activation. However, it is not known how the likely motoneurone receptor candidate (5-HT2 ) influences the firing rate and activation threshold of motor units (MUs) in humans. The purpose of this study was to determine whether 5-HT2 receptor activity contributes to human MU behaviour during voluntary ramped contractions of differing intensity. High-density surface EMG (HDsEMG) of the tibialis anterior was assessed during ramped isometric dorsiflexions at 10, 30, 50 and 70% of maximal voluntary contraction (MVC). MU characteristics were successfully extracted from HDsEMG of 11 young adults (four female) pre- and post-ingestion of 8 mg cyproheptadine or a placebo. Antagonism of 5-HT2 receptors caused a reduction in MU discharge rate during steady-state muscle activation that was independent of the level of contraction intensity [P < 0.001; estimated mean difference (∆) = 1.06 pulses/s], in addition to an increase in MU derecruitment threshold (P < 0.013, ∆ = 1.23% MVC), without a change in force during MVC (P = 0.652). A reduction in estimates of persistent inward current amplitude was observed at 10% MVC (P < 0.001, ∆ = 0.99 Hz) and 30% MVC (P = 0.003, ∆ = 0.75 Hz) that aligned with 5-HT changes in MU firing behaviour attributable to 5-HT2 antagonism. Overall, these findings indicate that 5-HT2 receptor activity has a role in regulating the discharge rate in populations of spinal motoneurones when performing voluntary contractions. This study provides evidence of a direct link between MU discharge properties, persistent inward current activity and 5-HT2 receptor activity in humans. KEY POINTS: Activation of 5-HT receptors on the soma and dendrites of motoneurones regulates their excitability. Previous work using chlorpromazine and cyproheptadine has demonstrated that the 5-HT2 receptor regulates motoneurone activity in humans with chronic spinal cord injury and non-injured control subjects. It is not known how the 5-HT2 receptor directly influences motor unit (MU) discharge and MU recruitment in larger populations of human motoneurones during voluntary contractions of differing intensity. Despite the absence of change in force during maximal voluntary dorsiflexions, 5-HT2 receptor antagonism caused a reduction in MU discharge rate during submaximal steady-state muscle contraction, in addition to an increase in MU derecruitment threshold, irrespective of the submaximal contraction intensity. Reductions in estimates of persistent inward currents after 5-HT2 receptor antagonism support the viewpoint that the 5-HT2 receptor plays a crucial role in regulating motor activity, whereby a persistent inward current-based mechanism is involved in regulating the excitability of human motoneurones.

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There are observable decreases in muscle strength as a result of ageing that occur from the age of 40, which are thought to occur as a result of changes within the neuromuscular system. Strength-training in older adults is a suitable intervention that may counteract the age-related loss in force production. The neuromuscular adaptations (i.e., cortical, spinal and muscular) to strength-training in older adults are largely equivocal and a systematic review with meta-analysis will serve to clarify the present circumstances regarding the benefits of strength-training in older adults. 20 studies entered the meta-analysis and were analysed using a random-effects model. A best evidence synthesis that included 36 studies was performed for variables that had insufficient data for meta-analysis. One study entered both. There was strong evidence that strength-training increases maximal force production, rate of force development and muscle activation in older adults. There was limited evidence for strength-training to improve voluntary-activation, the volitional-wave and spinal excitability, but strong evidence for increased muscle mass. The findings suggest that strength-training performed between 2 and 12 weeks increases strength, rate of force development and muscle activation, which likely improves motoneurone excitability by increased motor unit recruitment and improved discharge rates.

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Nociceptive stimulation is predicted to uniformly inhibit motoneurone pools of painful muscles and those producing painful movements. Although reduced motoneurone discharge rate during pain provides some evidence, recent data show evidence of increased excitability of some motoneurones. These observations suggest non-uniform effects of nociception on motoneurone excitability. More direct measures are required, but this is difficult to assess as few measures enable in vivo evaluation of motoneurone excitability in humans. We investigated changes in motoneurone excitability during experimental pain using two methods in separate experiments: (i) estimation of the time-course of motoneurone afterhyperpolarization (AHP) from interval death rate analysis of interspike intervals of single motor unit discharge; and (ii) probability of early motoneurone discharge to a descending volley excited using transcranial magnetic stimulation (TMS). Tibialis anterior motor units were recorded with fine-wire electrodes before, during and after painful infusion of 5% hypertonic saline into the muscle. Activation of 17 units (16 participants) could be used for AHP analysis. Data show shortened (n = 11) and lengthened (n = 6) AHP time-course. Increased (n = 6) and decreased (n = 6) probability of early motoneurone discharge were observed in the TMS experiment. These convergent observations suggest non-uniform effects of nociceptive stimulation on motoneurone pools. This does not support the hypothesis that nociceptive input induces uniform inhibition of painful muscle. Instead, interpretation of results implies redistribution of activity between motor units, with possible benefit for unloading painful tissues. This finding supports an interpretation that differs from the generally accepted view in pain physiology regarding adaptation to motor function in pain.

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Background: We examined corticospinal and spinal excitability across multiple power outputs during arm cycling using a weak and strong stimulus intensity. Methods: We elicited motor evoked potentials (MEPs) and cervicomedullary motor evoked potentials (CMEPs) in the biceps brachii using magnetic stimulation over the motor cortex and electrical stimulation of corticospinal axons during arm cycling at six different power outputs (i.e., 25, 50, 100, 150, 200 and 250 W) and two stimulation intensities (i.e., weak vs. strong). Results: In general, biceps brachii MEP and CMEP amplitudes (normalized to maximal M-wave (Mmax)) followed a similar pattern of modulation with increases in cycling intensity at both stimulation strengths. Specifically, MEP and CMEP amplitudes increased up until ~150 W and ~100 W when the weak and strong stimulations were used, respectively. Further increases in cycling intensity revealed no changes on MEP or CMEP amplitudes for either stimulation strength. Conclusions: In general, MEPs and CMEPs changed in a similar manner, suggesting that increases and subsequent plateaus in overall excitability are likely mediated by spinal factors. Interestingly, however, MEP amplitudes were disproportionately larger than CMEP amplitudes as power output increased, despite being initially matched in amplitude, particularly with strong stimulation. This suggests that supraspinal excitability is enhanced to a larger degree than spinal excitability as the power output of arm cycling increases.

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BACKGROUND: The recovery of neurophysiological parameters at various time intervals following fatiguing exercise has been investigated previously. However, the repetition of neuromuscular assessments during the recovery period may have interfered with the true corticomotor excitability responses. In this experiment, fatiguing contractions were combined with a single post-fatigue assessment at varying time points. Ten participants undertook 5 bouts of 60-s maximal voluntary contractions (MVC) of the elbow flexors, separated by 20 min. Before and after each 60-s fatiguing exercise (FAT), participants performed a series of 6-s contractions at 100, 75 and 50% of their MVC during which transcranial magnetic, transmastoid electrical and brachial plexus electrical stimuli were used to elicit motor evoked potentials (MEP), cervicomedullary motor evoked potentials (CMEP) and compound muscle action potentials (Mmax) in the biceps brachii muscle, respectively. Post-FAT measurements were randomly performed 0, 15, 30, 60, or 120 s after each FAT. RESULTS: MVC force declined to 65.1 ± 13.1% of baseline following FAT and then recovered to 82.7 ± 10.2% after 60 s. The MEP·Mmax-1 ratio recorded at MVC increased to 151.1 ± 45.8% and then returned to baseline within 60 s. The supraspinal excitability (MEP·CMEP-1) measured at MVC increased to 198.2 ± 47.2% and fully recovered after 30 s. The duration of post-MEP silent period recorded at MVC elongated by 23.4 ± 10.6% during FAT (all P < 0.05) but fully recovered after 15 s. CONCLUSIONS: The current study represents the first accurate description of the time course and pattern of recovery for supraspinal and spinal excitability and inhibition following a short maximal fatiguing exercise in upper limb.

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KEY POINTS: Animal preparations have revealed that moderate synaptic release of serotonin (5-HT) onto motoneurones enhances motor activity via activation of 5-HT2 receptors, whereas intense release of 5-HT causes spillover of 5-HT to extrasynaptic 5-HT1A receptors on the axon initial segment to reduce motoneurone activity. We explored if increasing extracellular concentrations of endogenously released 5-HT (via the selective serotonin reuptake inhibitor paroxetine) influences the ability to perform unfatigued and fatigued maximal voluntary contractions in humans. Following the ingestion of paroxetine, voluntary muscle activation and torque generation increased during brief unfatigued maximal contractions. In contrast, the ability to generate maximal torque with increased 5-HT availability was compromised under fatigued conditions, which was consistent with paroxetine-induced reductions in motoneurone excitability and voluntary muscle activation. This is the first in vivo human study to provide evidence that 5-HT released onto the motoneurones could play a role in central fatigue. ABSTRACT: Brief stimulation of the raphe-spinal pathway in the turtle spinal cord releases serotonin (5-HT) onto motoneurones to enhance excitability. However, intense release of 5-HT via prolonged stimulation results in 5-HT spillover to the motoneurone axon initial segment to activate inhibitory 5-HT1A receptors, thus providing a potential spinal mechanism for exercise-induced central fatigue. We examined how increased extracellular concentrations of 5-HT affect the ability to perform brief, as well as sustained, maximal voluntary contractions (MVCs) in humans. Paroxetine was used to enhance 5-HT concentrations by reuptake inhibition, and three studies were performed. Study 1 (n = 14) revealed that 5-HT reuptake inhibition caused an ∼4% increase in elbow flexion MVC. However, when maximal contractions were sustained, time-to-task failure was reduced and self-perceived fatigue was higher with enhanced availability of 5-HT. Study 2 (n = 11) used twitch interpolation to reveal that 5-HT-based changes in motor performance had a neural basis. Enhanced 5-HT availability increased voluntary activation for the unfatigued biceps brachii and decreased voluntary activation of the biceps brachii by 2-5% following repeated maximal elbow flexions. The final study (n = 8) investigated whether altered motoneurone excitability may contribute to 5-HT changes in voluntary activation. F-waves of the abductor digiti minimi (ADM) were unaffected by paroxetine for unfatigued muscle and marginally affected following a brief 2-s MVC. However, F-wave area and persistence were significantly decreased following a prolonged 60-s MVC of the ADM. Overall, high serotonergic drive provides a spinal mechanism by which higher concentrations of 5-HT may contribute to central fatigue.

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There are hardly any published data on the characteristics of muscle nerve sympathetic discharges occurring in parallel with the somatic motoneurone discharges in the same nerves. Here, we take advantage of the naturally occurring respiratory activity in recordings of efferent discharges from branches of the intercostal and abdominal nerves in anesthetized cats to make this comparison. The occurrence of efferent spikes with amplitudes below that for alpha motoneurones were analyzed for cardiac modulation, using cross-correlation between the times of the R-wave of the ECG and the efferent spikes. The modulation was observed in nearly all recordings, and for all categories of nerves. It was strongest for the smallest amplitude spikes or spike-like waveforms, which were deduced to comprise postsynaptic sympathetic discharges. New observations were: (1) that the cardiac modulation of these discharges was modest compared to most previous reports for muscle nerves; (2) that the amplitudes of the sympathetic discharges compared to those of the somatic spikes were strongly positively correlated to nerve diameter, such that, for the larger nerves, their amplitudes overlapped considerably with those of gamma motoneurone spikes. This could be explained by random summation of high rates of unit sympathetic spikes. We suggest that under some experimental circumstances this overlap could lead to considerable ambiguity in the identity of the discharges in efferent neurograms.

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Motoneurons demonstrate adaptations in their physiological properties to alterations in chronic activity levels. The most consistent change that appears to result from endurance-type exercise training is the reduced excitatory current required to initiate and maintain rhythmic firing. While the precise mechanisms through which these neurons adapt to activity are currently unknown, evidence exists that adaptation may involve alterations in the expression of genes that code for membrane receptors, which can influence the responses of neurons to transmitters during activation. The influence of these adaptations may also extend to the resting condition, where ambient levels of neuroactive substances may influence ion conductances at rest, and thus result in the activation or inhibition of specific ion conductances that underlie the measurements of increased excitability that have been reported for motoneurons in the anesthetised state. We have applied motoneuron excitability and muscle unit contractile changes with endurance training to a mathematical computerized model of motor unit recruitment (Heckman and Binder 1991; J. Neurophysiol. 65(4):952-967). The results from the modelling exercise demonstrate increased task efficiency at relative levels of effort during a submaximal contraction. The physiological impact that nerve and muscle adaptations have on the neuromuscular system during standardized tasks seem to fit with reported changes in motor unit behaviour in trained human subjects.

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Perineuronal nets (PNNs) are extracellular matrix structures surrounding neuronal sub-populations throughout the central nervous system, regulating plasticity. Enzymatically removing PNNs successfully enhances plasticity and thus functional recovery, particularly in spinal cord injury models. While PNNs within various brain regions are well studied, much of the composition and associated populations in the spinal cord is yet unknown. We aim to investigate the populations of PNN neurones involved in this functional motor recovery. Immunohistochemistry for choline acetyltransferase (labelling motoneurones), PNNs using Wisteria floribunda agglutinin (WFA) and chondroitin sulphate proteoglycans (CSPGs), including aggrecan, was performed to characterise the molecular heterogeneity of PNNs in rat spinal motoneurones (Mns). CSPG-positive PNNs surrounded ~70-80% of Mns. Using WFA, only ~60% of the CSPG-positive PNNs co-localised with WFA in the spinal Mns, while ~15-30% of Mns showed CSPG-positive but WFA-negative PNNs. Selective labelling revealed that aggrecan encircled ~90% of alpha Mns. The results indicate that (1) aggrecan labels spinal PNNs better than WFA, and (2) there are differences in PNN composition and their associated neuronal populations between the spinal cord and cortex. Insights into the role of PNNs and their molecular heterogeneity in the spinal motor pools could aid in designing targeted strategies to enhance functional recovery post-injury.

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In quadrupeds, special circuity located within the spinal cord, referred to as central pattern generators (CPGs), is capable of producing complex patterns of activity such as locomotion in the absence of descending input. During these motor outputs, the electrical properties of spinal motoneurones are modulated such that the motoneurone is more easily activated. Indirect evidence suggests that like quadrupeds, humans also have spinally located CPGs capable of producing locomotor outputs, albeit descending input is considered to be of greater importance. Whether motoneurone properties are reconfigured in a similar manner to those of quadrupeds is unclear. The purpose of this review is to summarize our current state of knowledge regarding the modulation of motoneurone excitability during CPG-mediated motor outputs using animal models. This will be followed by more recent work initially aimed at understanding changes in motoneurone excitability during CPG-mediated motor outputs in humans, which quickly expanded to also include supraspinal excitability.

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