Motoneuron Firing Research Articles

Role of the motor cortex in the generation of classically conditioned eyelid and vibrissae responses

The eyelid motor system has been used for years as an experimental model for studying the neuronal mechanisms underlying motor and cognitive learning, mainly with classical conditioning procedures. Nonetheless, it is not known yet which brain structures, or neuronal mechanisms, are responsible for the acquisition, storage, and expression of these motor responses. Here, we studied the temporal correlation between unitary activities of identified eyelid and vibrissae motor cortex neurons and the electromyographic activity of the orbicularis oculi and vibrissae muscles and magnetically recorded eyelid positions during classical conditioning of eyelid and vibrissae responses, using both delay and trace conditioning paradigms in behaving mice. We also studied the involvement of motor cortex neurons in reflexively evoked eyelid responses and the kinematics and oscillatory properties of eyelid movements evoked by motor cortex microstimulation. Results show the involvement of the motor cortex in the performance of conditioned responses elicited during the classical conditioning task. However, a timing correlation analysis showed that both electromyographic activities preceded the firing of motor cortex neurons, which must therefore be related more with the reinforcement and/or proper performance of the conditioned responses than with their acquisition and storage.

Model-Based Analysis of Muscle Strength and EMG-Force Relation with respect to Different Patterns of Motor Unit Loss

This study presents a model-based sensitivity analysis of the strength of voluntary muscle contraction with respect to different patterns of motor unit loss. A motor unit pool model was implemented including simulation of a motor neuron pool, muscle force, and surface electromyogram (EMG) signals. Three different patterns of motor unit loss were simulated, including (1) motor unit loss restricted to the largest ones, (2) motor unit loss restricted to the smallest ones, and (3) motor unit loss without size restriction. The model outputs including muscle force amplitude, variability, and the resultant EMG-force relation were quantified under two different motor neuron firing strategies. It was found that motor unit loss restricted to the largest ones had the most dominant impact on muscle strength and significantly changed the EMG-force relation, while loss restricted to the smallest motor units had a pronounced effect on force variability. These findings provide valuable insight toward our understanding of the neurophysiological mechanisms underlying experimental observations of muscle strength, force control, and EMG-force relation in both normal and pathological conditions.

From Motor-Output to Connectivity: An In-Depth Study of in-vitro Rhythmic Patterns in the Cockroach Periplaneta americana.

The cockroach is an established model in the study of locomotion control. While previous work has offered important insights into the interplay among brain commands, thoracic central pattern generators, and the sensory feedback that shapes their motor output, there remains a need for a detailed description of the central pattern generators' motor output and their underlying connectivity scheme. To this end, we monitored pilocarpine-induced activity of levator and depressor motoneurons in two types of novel in-vitro cockroach preparations: isolated thoracic ganglia and a whole-chain preparation comprising the thoracic ganglia and the subesophageal ganglion. Our data analyses focused on the motoneuron firing patterns and the coordination among motoneuron types in the network. The burstiness and rhythmicity of the motoneurons were monitored, and phase relations, coherence, coupling strength, and frequency-dependent variability were analyzed. These parameters were all measured and compared among network units both within each preparation and among the preparations. Here, we report differences among the isolated ganglia, including asymmetries in phase and coupling strength, which indicate that they are wired to serve different functions. We also describe the intrinsic default gait and a frequency-dependent coordination. The depressor motoneurons showed mostly similar characteristics throughout the network regardless of interganglia connectivity; whereas the characteristics of the levator motoneurons activity were mostly ganglion-dependent, and influenced by the presence of interganglia connectivity. Asymmetries were also found between the anterior and posterior homolog parts of the thoracic network, as well as between ascending and descending connections. Our analyses further discover a frequency-dependent inversion of the interganglia coordination from alternations between ipsilateral homolog oscillators to simultaneous activity. We present a detailed scheme of the network couplings, formulate coupling rules, and review a previously suggested model of connectivity in light of our new findings. Our data support the notion that the inter-hemiganglia coordination derives from the levator networks and their coupling with local depressor interneurons. Our findings also support a dominant role of the metathoracic ganglion and its ascending output in governing the anterior ganglia motor output during locomotion in the behaving animal.

Pholcodine-induced Stevens-Johnson syndrome in a patient with COVID-19

Reaction time is accelerated if a loud (startling) sound accompanies the cue—the “StartReact” effect. Animal studies revealed a reticulospinal substrate for the startle reflex; StartReact may similarly involve the reticulospinal...

In-silico development and assessment of a Kalman filter motor decoder for prosthetic hand control

Up to 50% of amputees abandon their prostheses, partly due to rapid degradation of the control systems, which require frequent recalibration. The goal of this study was to develop a Kalman filter-based approach to decoding motoneuron activity to identify movement kinematics and thereby provide stable, long-term, accurate, real-time decoding. The Kalman filter-based decoder was examined via biologically varied datasets generated from a high-fidelity computational model of the spinal motoneuron pool. The estimated movement kinematics controlled a simulated MuJoCo prosthetic hand. This clear-box approach showed successful estimation of hand movements under eight varied physiological conditions with no retraining. The mean correlation coefficient of 0.98 and mean normalized root mean square error of 0.06 over these eight datasets provide proof of concept that this decoder would improve long-term integrity of performance while performing new, untrained movements. Additionally, the decoder operated in real-time (~0.3 ms). Further results include robust performance of the Kalman filter when re-trained to more severe post-amputation limitations in the type and number of motoneurons remaining. An additional analysis shows that the decoder achieves better accuracy when using the firing of individual motoneurons as input, compared to using aggregate pool firing. Moreover, the decoder demonstrated robustness to noise affecting both the trained decoder parameters and the decoded motoneuron activity. These results demonstrate the utility of a proof of concept Kalman filter decoder that can support prosthetics’ control systems to maintain accurate and stable real-time movement performance.

Gap junction-mediated glycinergic inhibition ensures precise temporal patterning in vocal behavior.

Precise neuronal firing is especially important for behaviors highly dependent on the correct sequencing and timing of muscle activity patterns, such as acoustic signaling. Acoustic signaling is an important communication modality for vertebrates, including many teleost fishes. Toadfishes are well known to exhibit high temporal fidelity in synchronous motoneuron firing within a hindbrain network directly determining the temporal structure of natural calls. Here, we investigated how these motoneurons maintain synchronous activation. We show that pronounced temporal precision in population-level motoneuronal firing depends on gap junction-mediated, glycinergic inhibition that generates a period of reduced probability of motoneuron activation. Super-resolution microscopy confirms glycinergic release sites formed by a subset of adjacent premotoneurons contacting motoneuron somata and dendrites. In aggregate, the evidence supports the hypothesis that gap junction-mediated, glycinergic inhibition provides a timing mechanism for achieving synchrony and temporal precision in the millisecond range for rapid modulation of acoustic waveforms.

Computing Temporal Sequences Associated With Dynamic Patterns on the C. elegans Connectome.

Understanding how the structural connectivity and spatial geometry of a network constrains the dynamics it is able to support is an active and open area of research. We simulated the plausible dynamics resulting from the known C. elegans connectome using a recent model and theoretical analysis that computes the dynamics of neurobiological networks by focusing on how local interactions among connected neurons give rise to the global dynamics in an emergent way. We studied the dynamics which resulted from stimulating a chemosensory neuron (ASEL) in a known feeding circuit, both in isolation and embedded in the full connectome. We show that contralateral motorneuron activations in ventral (VB) and dorsal (DB) classes of motorneurons emerged from the simulations, which are qualitatively similar to rhythmic motorneuron firing pattern associated with locomotion of the worm. One interpretation of these results is that there is an inherent—and we propose—purposeful structural wiring to the C. elegans connectome that has evolved to serve specific behavioral functions. To study network signaling pathways responsible for the dynamics we developed an analytic framework that constructs Temporal Sequences (TSeq), time-ordered walks of signals on graphs. We found that only 5% of TSeq are preserved between the isolated feeding network relative to its embedded counterpart. The remaining 95% of signaling pathways computed in the isolated network are not present in the embedded network. This suggests a cautionary note for computational studies of isolated neurobiological circuits and networks.

Early Hypoexcitability in a Subgroup of Spinal Motoneurons in Superoxide Dismutase 1 Transgenic Mice, a Model of Amyotrophic Lateral Sclerosis

In amyotrophic lateral sclerosis (ALS), large motoneurons degenerate first, causing muscle weakness. Transgenic mouse models with a mutation in the gene encoding the enzyme superoxide dismutase 1 (SOD1) revealed that motoneurons innervating the fast-fatigable muscular fibres disconnect very early. The cause of this peripheric disconnection has not yet been established. Early pathological signs were described in motoneurons during the postnatal period of SOD1 transgenic mice. Here, we investigated whether the early changes of electrical and morphological properties previously reported in the SOD1G85R strain also occur in the SOD1G93A-low expressor line with particular attention to the different subsets of motoneurons defined by their discharge firing pattern (transient, sustained, or delayed-onset firing). Intracellular staining and recording were performed in lumbar motoneurons from entire brainstem-spinal cord preparations of SOD1G93A-low transgenic mice and their WT littermates during the second postnatal week. Our results show that SOD1G93A-low motoneurons exhibit a dendritic overbranching similar to that described previously in the SOD1G85R strain at the same age. Further we found an hypoexcitability in the delayed-onset firing SOD1G93A-low motoneurons (lower gain and higher voltage threshold). We conclude that dendritic overbranching and early hypoexcitability are common features of both low expressor SOD1 mutants (G85R and G93A-low). In the high-expressor SOD1G93A line, we found hyperexcitability in the sustained firing motoneurons at the same period, suggesting a delay in compensatory mechanisms. Overall, our results suggest that the hypoexcitability indicate an early dysfunction of the delayed-onset motoneurons and could account as early pathological signs of the disease.

Concurrent Prediction of Finger Forces Based on Source Separation and Classification of Neuron Discharge Information.

A reliable neural-machine interface is essential for humans to intuitively interact with advanced robotic hands in an unconstrained environment. Existing neural decoding approaches utilize either discrete hand gesture-based pattern recognition or continuous force decoding with one finger at a time. We developed a neural decoding technique that allowed continuous and concurrent prediction of forces of different fingers based on spinal motoneuron firing information. High-density skin-surface electromyogram (HD-EMG) signals of finger extensor muscle were recorded, while human participants produced isometric flexion forces in a dexterous manner (i.e. produced varying forces using either a single finger or multiple fingers concurrently). Motoneuron firing information was extracted from the EMG signals using a blind source separation technique, and each identified neuron was further classified to be associated with a given finger. The forces of individual fingers were then predicted concurrently by utilizing the corresponding motoneuron pool firing frequency of individual fingers. Compared with conventional approaches, our technique led to better prediction performances, i.e. a higher correlation ([Formula: see text] versus [Formula: see text]), a lower prediction error ([Formula: see text]% MVC versus [Formula: see text]% MVC), and a higher accuracy in finger state (rest/active) prediction ([Formula: see text]% versus [Formula: see text]%). Our decoding method demonstrated the possibility of classifying motoneurons for different fingers, which significantly alleviated the cross-talk issue of EMG recordings from neighboring hand muscles, and allowed the decoding of finger forces individually and concurrently. The outcomes offered a robust neural-machine interface that could allow users to intuitively control robotic hands in a dexterous manner.

Development of γ-aminobutyric acid-, glycine-, and glutamate-immunopositive boutons on the rat genioglossal motoneurons.

Detailed information about the development of excitatory and inhibitory synapses on the genioglossal (GG) motoneuron may help to understand the mechanism of fine control of GG motoneuron firing and the coordinated tongue movement during postnatal development. For this, we investigated the development of γ-aminobutyric acid (GABA)-immunopositive (GABA +), glycine + (Gly +), and glutamate + (Glut +) axon terminals (boutons) on the somata of rat GG motoneurons at a postnatal day 2 (P2), P6 and P18 by retrograde labeling of GG motoneurons with horseradish peroxidase, electron microscopic postembedding immunogold staining with GABA, Gly, and Glut antisera, and quantitative analysis. The number of boutons per GG motoneuron somata and the mean length of bouton apposition, measures of bouton size and synaptic covering percentage, were significantly increased from P2/P6 to P18. The number and fraction of GABA + only boutons of all boutons decreased significantly, whereas those of Gly + only boutons increased significantly from P2/P6 to P18, suggesting developmental switch from GABAergic to glycinergic synaptic transmission. The fraction of mixed GABA +/Gly + boutons of all boutons was the highest among inhibitory bouton types throughout the postnatal development. The fractions of excitatory and inhibitory boutons of all boutons remained unchanged during postnatal development. These findings reveal a distinct developmental pattern of inhibitory synapses on the GG motoneurons different from that on spinal or trigeminal motoneurons, which may have an important role in the regulation of the precise and coordinated movements of the tongue during the maturation of the oral motor system.

Evidence of two modes of spiking evoked in human firing motoneurones by Ia afferent electrical stimulation.

Neurone firing behaviour is a result of complex interaction between synaptic inputs and cellular intrinsic properties. Intriguing firing behaviour, delayed spiking, was shown in some neurones, in particular, in cat neocortical neurones and rat pyramidal hippocampal neurones. In contrast, the similar spiking mode was not reported for animal spinal motoneurones. In the present study, an attempt was made to look for possible evidence of delayed spiking in human motoneurones firing within the low-frequency, sub-primary range, characteristic for voluntary muscle contractions and postural tasks. Forty-seven firing motor units (MUs) were analyzed in ten experiments on three muscles (the flexor carpi ulnaris, the tibialis anterior, and the abductor pollicis brevis) in four healthy humans. Single MUs were activated by gentle voluntary muscle contractions. MU peri-stimulus time histograms, durations of inter-spike intervals, and motoneurone excitability changes within a target interspike interval were analyzed. It was found that during testing the firing motoneurone excitability by small, transient excitatory Ia afferent volley, depending firstly on volley timing within a target interspike interval and excitatory volley strength, the same motoneurone displayed either the direct short-latency response (the H-reflex) or the delayed response (with prolonged and variable latency). Thus, the findings, for the first time, provide evidence for a possibility of two modes of spiking in firing motoneurones. Methods of the estimation of delayed responses and their possible functional significance are discussed. It is emphasized that, for understanding of this issue, the integration of data from studies on experimental animals and humans is desirable.

Development of a human neuromuscular tissue-on-a-chip model on a 24-well-plate-format compartmentalized microfluidic device.

Engineered three-dimensional models of neuromuscular tissues are promising for use in mimicking their disorder states in vitro. Although several models have been developed, it is still challenging to mimic the physically separated structures of motor neurons (MNs) and skeletal muscle (SkM) fibers in the motor units in vivo. In this study, we aimed to develop microdevices for precisely compartmentalized coculturing of MNs and engineered SkM tissues. The developed microdevices, which fit a well of 24 well plates, had a chamber for MNs and chamber for SkM tissues. The two chambers were connected by microtunnels for axons, permissive to axons but not to cell bodies. Human iPSC (hiPSC)-derived MN spheroids in one chamber elongated their axons into microtunnels, which reached the tissue-engineered human SkM in the SkM chamber, and formed functional neuromuscular junctions with the muscle fibers. The cocultured SkM tissues with MNs on the device contracted spontaneously in response to spontaneous firing of MNs. The addition of a neurotransmitter, glutamate, into the MN chamber induced contraction of the cocultured SkM tissues. Selective addition of tetrodotoxin or vecuronium bromide into either chamber induced SkM tissue relaxation, which could be explained by the inhibitory mechanisms. We also demonstrated the application of chemical or mechanical stimuli to the middle of the axons of cocultured tissues on the device. Thus, compartmentalized neuromuscular tissue models fabricated on the device could be used for phenotypic screening to evaluate the cellular type specific efficacy of drug candidates and would be a useful tool in fundamental research and drug development for neuromuscular disorders.

Imbalanced Subthreshold Currents Following Sepsis and Chemotherapy: A Shared Mechanism Offering a New Therapeutic Target?

Both sepsis and treatment of cancer with chemotherapy are known to cause neurologic dysfunction. The primary defects seen in both groups of patients are neuropathy and encephalopathy; the underlying mechanisms are poorly understood. Analysis of preclinical models of these disparate conditions reveal similar defects in ion channel function contributing to peripheral neuropathy. The defects in ion channel function extend to the central nervous system where lower motoneurons are affected. In motoneurons the defect involves ion channels responsible for subthreshold currents that convert steady depolarization into repetitive firing. The inability to correctly translate depolarization into steady, repetitive firing has profound effects on motor function, and could be an important contributor to weakness and fatigue experienced by both groups of patients. The possibility that disruption of function, either instead of, or in addition to neurodegeneration, may underlie weakness and fatigue leads to a novel approach to therapy. Activation of serotonin (5HT) receptors in a rat model of sepsis restores the normal balance of subthreshold currents and normal motoneuron firing. If an imbalance of subthreshold currents also occurs in other central nervous system neurons, it could contribute to encephalopathy. We hypothesize that pharmacologically restoring the proper balance of subthreshold currents might provide effective therapy for both neuropathy and encephalopathy in patients recovering from sepsis or treatment with chemotherapy.

Amyotrophic lateral sclerosis weakens spinal recurrent inhibition and post-activation depression

ObjectivesAmyotrophic lateral sclerosis (ALS) disrupts motoneurons that control movement and some vital functions, however, exact details of the neuronal circuits involved in ALS have yet to be fully endorsed. To contribute to our understanding of the responsible neuronal circuits, we aimed to investigate the spinal recurrent inhibition (RI) and post-activation depression (P-AD) in ALS patients. MethodsIn two groups of ALS patients, i.e. lumbar-affected (clinical signs in leg muscles) and nonlumbar-affected (clinical signs in arms or bulbar region but not in the legs), RI and P-AD on the soleus muscle were investigated using single motor units and amplitude changes of H-reflex in surface electromyography, respectively. The data were compared with healthy subjects. ResultsCompared to controls, P-AD of H-reflex was reduced severely in lumbar-affected patients and reduced to a certain degree in nonlumbar-affected patients. Similarly, a significant reduction in the duration of RI on firing motoneurons was found in lumbar-affected patients (11.5 ± 2.6 ms) but not in nonlumbar-affected patients (29.7 ± 12.4 ms, P < 0.0001) compared to controls (30.8 ± 7.2 ms, P < 0.0001). ConclusionThe current study revealed that spinal inhibitory circuits are impaired in ALS. SignificanceThese findings may provide insight for proposing new therapeutic approaches and following disease progression in humans.

Allopregnanolone Enhances GABAergic Inhibition in Spinal Motor Networks.

The neurosteroid allopregnanolone (ALLO) causes unconsciousness by allosteric modulation of γ-aminobutyric acid type A (GABAA) receptors, but its actions on the spinal motor networks are unknown. We are therefore testing the hypothesis that ALLO attenuates the action potential firing of spinal interneurons and motoneurons predominantly via enhancing tonic, but not synaptic GABAergic inhibition. We used video microscopy to assess motoneuron-evoked muscle activity in organotypic slice cultures prepared from the spinal cord and muscle tissue. Furthermore, we monitored GABAA receptor-mediated currents by performing whole-cell voltage-clamp recordings. We found that ALLO (100 nM) reduced the action potential firing of spinal interneurons by 27% and that of α-motoneurons by 33%. The inhibitory effects of the combination of propofol (1 µM) and ALLO on motoneuron-induced muscle contractions were additive. Moreover, ALLO evoked a tonic, GABAA receptor-mediated current (amplitude: 41 pA), without increasing phasic GABAergic transmission. Since we previously showed that at a clinically relevant concentration of 1 µM propofol enhanced phasic, but not tonic GABAergic inhibition, we conclude that ALLO and propofol target distinct subpopulations of GABAA receptors. These findings provide first evidence that the combined application of ALLO and propofol may help to reduce intraoperative movements and undesired side effects that are frequently observed under total intravenous anesthesia.

Spinal motoneuron firing properties mature from rostral to caudal during postnatal development of the mouse.

Key points Many mammals are born with immature motor systems that develop through a critical period of postnatal development.In rodents, postnatal maturation of movement occurs from rostral to caudal, correlating with maturation of descending supraspinal and local spinal circuits.We asked whether development of fundamental electrophysiological properties of spinal motoneurons follows the same rostro‐caudal sequence.We show that in both regions, repetitive firing parameters increase and excitability decreases with development; however, these characteristics mature earlier in cervical motoneurons.We suggest that in addition to autonomous mechanisms, motoneuron development depends on activity resulting from their circuit milieu. Altricial mammals are born with immature nervous systems comprised of circuits that do not yet have the neuronal properties and connectivity required to produce future behaviours. During the critical period of postnatal development, neuronal properties are tuned to participate in functional circuits. In rodents, cervical motoneurons are born prior to lumbar motoneurons, and spinal cord development follows a sequential rostro‐caudal pattern. Here we asked whether birth order is reflected in the postnatal development of electrophysiological properties. We show that motoneurons of both regions have similar properties at birth and follow the same developmental profile, with maximal firing increasing and excitability decreasing into the third postnatal week. However, these maturative processes occur in cervical motoneurons prior to lumbar motoneurons, correlating with the maturation of premotor descending and local spinal systems. These results suggest that motoneuron properties do not mature by cell autonomous mechanisms alone, but also depend on developing premotor circuits.

Multiplexed chemogenetics in astrocytes and motoneurons restore blood-spinal cord barrier in ALS.

Blood-spinal cord barrier (BSCB) disruption is thought to contribute to motoneuron (MN) loss in amyotrophic lateral sclerosis (ALS). It is currently unclear whether impairment of the BSCB is the cause or consequence of MN dysfunction and whether its restoration may be directly beneficial. We revealed that SOD1 G93A , FUS ΔNLS , TDP43 G298S , and Tbk1 +/- ALS mouse models commonly shared alterations in the BSCB, unrelated to motoneuron loss. We exploit PSAM/PSEM chemogenetics in SOD1 G93A mice to demonstrate that the BSCB is rescued by increased MN firing, whereas inactivation worsens it. Moreover, we use DREADD chemogenetics, alone or in multiplexed form, to show that activation of Gi signaling in astrocytes restores BSCB integrity, independently of MN firing, with no effect on MN disease markers and dissociating them from BSCB disruption. We show that astrocytic levels of the BSCB stabilizers Wnt7a and Wnt5a are decreased in SOD1 G93A mice and strongly enhanced by Gi signaling, although further decreased by MN inactivation. Thus, we demonstrate that BSCB impairment follows MN dysfunction in ALS pathogenesis but can be reversed by Gi-induced expression of astrocytic Wnt5a/7a.

External Resistance Is Imperative for Training-Induced Efferent Neural Drive Enhancement in Older Adults.

Strength training performed with heavy loads and maximal intended velocity is documented to enhance efferent neural drive to maximally contracting musculature in older adults. However, it remains unclear whether the neural plasticity following training result from motor skill learning or if external resistance is a prerequisite. To investigate this, we assessed electrically evoked potentials (H-reflex and V-waves normalized to maximal M-wave) and voluntary activation (VA) in 36 older adults (73 ± 4 years) randomized to 3 weeks of plantar flexion strength training, with (maximal strength training [MST]) or without (unloaded ballistic training [UBT]) heavy external loading (90% of one repetition maximum), or a control group. Both training groups aimed to execute the concentric phase of movement as fast and forcefully as possible. The MST group improved maximal voluntary contraction (MVC) and rate of force development (RFD) by 18% ± 13% (p = .001; Hedges g = 0.66) and 35% ± 17% (p < .001; g = 0.94), respectively, and this was different (MVC: p = .013; RFD: p = .001) from the UBT group which exhibited a 7% ± 8% (p = .033; g = 0.32) increase in MVC and a tendency to increase RFD (p = .119; g = 0.22). Concomitant improvements in efferent neural drive (Vmax/Msup ratio: 0.14 ± 0.08 to 0.24 ± 0.20; p = .010) and a tendency towards increased VA (79% ± 9% to 84% ± 5%; p = .098), were only apparent after MST. No changes were observed in Hmax/Mmax ratio for the groups. In conclusion, external loading during exercise training appears to be a prerequisite for efferent neural drive enhancement in older adults. Thus, strength training with heavy loads should be recommended to counteract the typically observed age-related decline in motoneuron firing frequency and recruitment.

External Resistance Is Imperative For Training-induced Efferent Neural Drive Enhancement In Older Individuals

Strength training performed with heavy loads and maximal intended velocity is documented to enhance efferent neural drive in older individuals. However, it remains unclear whether the neural plasticity following training result from motor skill learning or if external resistance is a prerequisite. PURPOSE: To investigate the importance of external resistance on neural plasticity in older individuals. METHODS: Electrically evoked potentials (H-reflex and V-waves normalized to maximal M-wave) and voluntary activation (VA) were assessed in 36 older individuals (73±4 years). Participants were randomized to 3 weeks of plantar flexion strength training, with (maximal strength training; MST) or without (unloaded ballistic training; UBT) heavy external loading (90% of one repetition maximum), or a control group. Both training groups aimed to execute the concentric phase of movement as fast and forcefully as possible. RESULTS: The MST group improved maximal voluntary contraction (MVC) and rate of force development (RFD) by 18±13% (p<0.01) and 35±17% (p<0.01), respectively, and this was different (p<0.01) from the UBT group which exhibited a 7±8% (p<0.05) increase in MVC (p<0.05) and a tendency of an increase in RFD (p=0.12). Concomitant improvements in efferent neural drive, evident as a 79±80% increase in V/M-ratio (p<0.01) and a tendency towards increased VA (p=0.11), were only apparent after MST. No changes were observed in H/M-ratio for any of the groups. CONCLUSION: External loading following exercise training appears to be a prerequisite for efferent neural drive enhancement in older individuals, and advocates that heavy resistance training should be recommended to counteract the typically observed age-related decline in motoneuron firing frequency and recruitment.

Neuromuscular Password-Based User Authentication

In this article, we propose a novel neuromuscular password-based user authentication method. The method consists of two parts: surface electromyogram (sEMG) based finger muscle isometric contraction password (FMICP) and neuromuscular biometrics. FMICP can be entered through isometric contraction of different finger muscles in a prescribed order without actual finger movement, which makes it difficult for observers to obtain the password. In our study, the isometric contraction patterns of different finger muscles were recognized through high-density sEMG signals acquired from the right dorsal hand. Moreover, both time-frequency-space domain features at macroscopic level (interference-pattern EMG) and motor neuron firing rate features at microscopic level (via decomposition) were extracted to represent neuromuscular biometrics, serving as a second defense. The FMICP and macro-micro neuromuscular biometrics together form a neuromuscular password. The proposed neuromuscular password achieved an equal error rate (EER) of 0.0128 when impostors entered a wrong FMICP. Even when impostors entered the correct FMICP, the neuromuscular biometrics, as the second defense, inhibited impostors with an EER of 0.1496. To the best of our knowledge, this is the first study to use individually unique neuromuscular information during unobservable muscle isometric contractions for user authentication, with training and testing data acquired on different days.