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 multiarticular 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) coactivation or (ii) an alternative α-MN collateral projection to homonymous γ-MNs. We conclude that such α-MN collaterals are a physiologically tenable propriospinal circuit in the mammalian fusimotor system. These collaterals could still collaborate with α-γ coactivation, and the few skeletofusimotor fibers (β-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.

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 (β-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.

Purpose: Reduced proprioception affects fall risks in elderly people with lumbar spondylosis. The decrease in proprioception in the trunk or lower legs may contribute to a decline in postural stability. We aimed to investigate the association between proprioceptive postural stability and fall risks in elderly individuals with lumbar spondylosis.Materials and Methods: In this retrospective study, the centre-of-pressure displacement was determined in elderly individuals with lumbar spondylosis during upright stance while standing on a Wii Balance Board with their eyes closed (fall-risk group, n = 55; non-fall-risk group, n = 60). Vibratory stimulations at 30 Hz were applied to the lumbar multifidus and gastrocnemius to evaluate the relative contributions of proprioceptive signals used in postural control (relative proprioceptive weighting ratio).Results: Compared with the non-fall-risk group, the fall-risk group displayed a high relative proprioceptive weighting ratio (p = 0.024). Relative proprioceptive weighting ratio (odds ratio, 1.1; 95% confidence interval: 1.004-1.109) was independently associated with fall risks after adjusting for confounding factors. Among variables related to fall risk, the relative proprioceptive weighting ratio was a significant factor (p < 0.035).Conclusion: The fall-risk group of elderly individuals with lumbar spondylosis was dependent on the ankle strategy. The fall risk in elderly people with lumbar spondylosis could be due to over-dependence on the input from muscle spindles in the gastrocnemius.

Sensory loss is detrimental to sensorimotor control. Several studies have reported that loss and/or damage of primary (Ia) muscle spindle afferents significantly influence the stretch reflex responses of leg and foot muscles. However, a systematic experimental evaluation on how the impairment of Ia muscle spindle afferents affects the stretch reflex is difficult due to technical and ethical issues. In the present study, the aim was to use computer simulations of a multiscale neuromusculoskeletal model to investigate how changes in: i) the number of Ia afferents, ii) the synaptic conductance between Ia sensory fibers and spinal motor neurons (MNs), and iii) the conduction velocities (CVs) of Ia afferents, would influence the stretch reflex of a leg muscle (soleus). Simulation results showed that both anatomical and functional loss of Ia afferents exerted an influence on the amplitude of short-latency stretch reflex response (M1) and the late phase of medium-latency response (M2). Additionally, changes in CVs of Ia afferents mainly influenced the latency of M1 and the amplitude of M2. Our findings provide conceptual evidence that a combination of anatomical and functional loss, as well as changes in CVs of Ia afferents due to demyelination, can explain the stretch reflex responses observed in peripheral neuropathies.

Muscle spindles in the jaw-closing muscles, which are innervated by trigeminal mesencephalic neurons (MesV neurons), control the strength of occlusion and the position of the mandible. The mechanisms underlying cortical processing of proprioceptive information are critical to understanding how sensory information from the masticatory muscles regulates orofacial motor function. However, these mechanisms are mostly unknown. The present study aimed to identify the regions that process proprioception of the jaw-closing muscles using in vivo optical imaging with a voltage-sensitive dye in rats under urethane anesthesia. First, jaw opening that was produced by mechanically pulling down the mandible evoked an optical response, which reflects neural excitation, in two cortical regions: the most rostroventral part of the primary somatosensory cortex (S1) and the border between the ventral part of the secondary somatosensory cortex (S2) and the insular oral region (IOR). The kinetics of the optical signal, including the latency, amplitude, rise time, decay time and half duration, in the S1 region for the response with the largest amplitude were comparable to those in the region with the largest response in S2/IOR. Second, we visualized the regions responding to electrical stimulation of the masseter nerve, which activates both motor efferent fibers and somatosensory afferent fibers, including those that transmit nociceptive and proprioceptive information. Masseter nerve stimulation initially excited the rostral part of the S2/IOR region, and an adjacent region responded to jaw opening. The caudal part of the region showing the maximum response overlapped with the region responding to jaw opening, whereas the rostral part overlapped with the region responding to electrical stimulation of the maxillary and mandibular molar pulps. These findings suggest that proprioception of the masseter is processed in S1 and S2/IOR. Other sensory information, such as nociception, is processed in a region that is adjacent to these pulpal regions and is located in the rostral part of S2/IOR, which receives nociceptive inputs from the molar pulps. The spatial proximity of these regions may be associated with the mechanisms by which masseter muscle pain is incorrectly perceived as dental pain.

OBJECTIVE: The aims of this study were to determine whether the application of vibration on a postural lower limb muscle altered the sensorimotor control of its joint as measured by isometric force production parameters and to compare present findings with previous work conducted on trunk muscle.
METHODS: Twenty healthy adults were asked to reproduce submaximal isometric plantar flexion under 3 different conditions: no vibration and vibration frequencies of 30 and 80 Hz on the soleus muscle. Time to peak torque, variable error, as well as constant error and absolute error in peak torque were calculated and compared across conditions.
RESULTS: Under vibration, participants were significantly less accurate in the force reproduction task, as they mainly undershot the target torque. Applying an 80-Hz vibration resulted in a significantly higher negative constant error than lower-frequency vibration (30 Hz) or no-vibration condition. Decreases in isometric force production accuracy under vibration influence were also observed in a previous study conducted on trunk muscle. However, no difference in constant error was found between 30- and 80-Hz vibration conditions.
CONCLUSIONS: The results suggest that acute soleus muscle vibration interferes with plantar flexion torque generation by distorting proprioceptive information, leading to decreases in accuracy of a force reproduction task. Similar results in an isometric trunk extension force reproduction task were found with vibration applied on erector spinae muscle. However, high-frequency vibration applied on soleus muscle elicited higher force reproduction errors than low-frequency stimulation.

Together with Hebbian plasticity, homeoplasticity presumably plays a significant, yet unclear, role in recovery postlesion. Here, we undertake a simulation study addressing the role of homeoplasticity and rehabilitation timing poststroke. We first hypothesize that homeoplasticity is essential for recovery and second that rehabilitation training delivered too early, before homeoplasticity has compensated for activity disturbances postlesion, is less effective for recovery than training delivered after a delay. We developed a neural network model of the sensory cortex driven by muscle spindle inputs arising from a six-muscle arm. All synapses underwent Hebbian plasticity, while homeoplasticity adjusted cell excitability to maintain a desired firing distribution. After initial training, the network was lesioned, leading to areas of hyper- and hypoactivity due to the loss of lateral synaptic connections. The network was then retrained through rehabilitative arm movements. We found that network recovery was unsuccessful in the absence of homeoplasticity, as measured by reestablishment of lesion-affected inputs. We also found that a delay preceding rehabilitation led to faster network recovery during the rehabilitation training than no delay. Our simulation results thus suggest that homeoplastic restoration of prelesion activity patterns is essential to functional network recovery via Hebbian plasticity.

When a muscle relaxes after a contraction, cross-bridges between actin and myosin in sarcomeres detach, but about 1% spontaneously form new, non-force-generating attachments. These bridges give muscle its thixotropic property. They remain in place for long periods if the muscle is left undisturbed and give the muscle a passive stiffness in response to a stretch. They are detached by stretch, but reform at the new length. If the muscle is then shortened, the presence of these bridges prevents muscle fibres from shortening and they fall slack. So, resting muscle can be in one of two states, where it presents in response to a stretch with a high stiffness, if no slack is present, or with a compliant response in the presence of slack. Intrafusal fibres of muscle spindles show thixotropic behaviour. For spindles, after a conditioning contraction, they are left stretch sensitive, with a high level of background discharge. Alternatively, if after the contraction the muscle is shortened, intrafusal fibres fall slack, leaving spindles with a low level of background activity and insensitivity to stretch. Muscle spindles are receptors involved in the senses of human limb position and movement. The technique of muscle conditioning can be used to help understand the contribution of muscle spindles to these senses and how the brain interprets signals arising in spindles. When, in a two-arm position-matching task, elbow muscles of the two arms are deliberately conditioned in opposite ways, the blindfolded subject makes large position errors of which they are unaware. The evidence suggests that the brain is concerned with the difference signal coming from the antagonists acting at the elbow and with the overall difference in signal from the two arms. Another way of measuring position sense is to use a single arm and indicate its perceived position with a pointer. Here, there is no access to a signal from the other limb, and position sense relies on referral to a central map of the body, the postural schema.

Processes underlying mechanotransduction and its regulation are poorly understood. Inhibitors of Ca2+-activated K+ channels cause a dramatic increase in afferent output from stretched muscle spindles. We used immunocytochemistry to test for the presence and location of small conductance Ca2+-activated K+ channels (SK1-3) in primary endings of muscle spindles and lanceolate endings of hair follicles in the rat. Tissue sections were double immunolabelled with antibodies to one of the SK channel isoforms and to either synaptophysin (SYN, as a marker of synaptic like vesicles (SLV), present in many mechanosensitive endings) or S100 (a Ca2+-binding protein present in glial cells). SK channel immunoreactivity was also compared to immunolabelling for the Na+ ion channel ASIC2, previously reported in both spindle primary and lanceolate endings. SK1 was not detected in sensory terminals of either muscle spindles or lanceolate endings. SK2 was found in the terminals of both muscle spindles and lanceolate endings, where it colocalised with the SLV marker SYN (spindles and lanceolates) and the satellite glial cell (SGC) marker S100 (lanceolates). SK3 was not detected in muscle spindles; by contrast it was present in hair follicle endings, expressed predominantly in SGCs but perhaps also in the SGC: terminal interface, as judged by colocalisation statistical analysis of SYN and S100 immunoreactivity. The possibility that all three isoforms might be expressed in pre-terminal axons, especially at heminodes, cannot be ruled out. Differential distribution of SK channels is likely to be important in their function of responding to changes in intracellular [Ca2+] thereby modulating mechanosensory transduction by regulating the excitability of the sensory terminals. In particular, the presence of SK2 throughout the sensory terminals of both kinds of mechanoreceptor indicates an important role for an outward Ca2+-activated K+ current in the formation of the receptor potential in both types of ending.

Although the occurrence of muscle spindles (MS) is quite high in most skeletal muscles of humans, few MS, or even absence, have been reported in digastric and mylohyoideus muscles. Even if this condition is generally accepted and quoted in many papers and books, observational studies are scarce and based on histological sections of a low number of specimens. The aim of the present study is to confirm previous data, assessing MS number in a sample of digastric and mylohyoideus muscles. We investigated 11 digastric and 6 mylohyoideus muscles from 13 donors. Muscle samples were embedded in paraffin wax, cross-sectioned in a rostrocaudal direction, and stained using haematoxylin-eosin. A mean of 5.1 ± 1.1 (range 3-7) MS was found in digastric muscles and mean of 0.5 ± 0.8 (range 0-2) in mylohyoideus muscles. A significant difference (P < 0.001) was found with the control sample, confirming the correctness of the histological procedure. Our results support general belief that the absolute number of spindles is sparse in digastric and mylohyoideus muscles. External forces, such as food resistance during chewing or gravity, do not counteract jaw-opening muscles. It is conceivable that this condition gives them a limited proprioceptive importance and a reduced need for having specific receptors as MS.