Proprioceptive Afferents Research Articles

Postnatal maturation of serotonergic modulation of spinal RORβ interneurons in the medial deep dorsal horn.

Proprioceptive input is essential for coordinated locomotion and this input must be properly gated to ensure smooth and effective movement. Presynaptic inhibition mediated by GABAergic interneurons provides regulation of sensory afferent feedback. Serotonin not only promotes locomotion, but also modulates feedback from sensory afferents, both directly and indirectly, potentially by acting on the GABAergic interneurons that mediate presynaptic inhibition. Developmental disruptions in presynaptic inhibition can produce deficits in sensorimotor processing. Importantly, both presynaptic inhibition of proprioceptive afferents and serotonergic innervation of the spinal cord become mature and functional after the first postnatal week. However, little is known about the serotonergic receptors involved in the modulation of interneurons mediating presynaptic inhibition and when developmentally their actions mature. Here, we used whole-cell patch clamp recordings in lumbar spinal slices from neonatal and juvenile mice to assess the intrinsic properties and serotonergic modulation of deep dorsal horn GABAergic RORβ interneurons previously shown to mediate presynaptic inhibition of proprioceptive afferents. RORβ interneurons from juvenile cords displayed more mature membrane properties. Further, serotonin increased the excitability of RORβ interneurons via actions at 5-HT 2A , 5-HT 2B/2C , and 5-HT 7 receptors in juvenile but not early neonatal spinal cords. Our findings indicate that deep dorsal horn RORβ interneurons undergo postnatal maturation in both their intrinsic excitability and ability to respond to serotonin, concurrent with the maturation of serotonergic innervation of the dorsal horn. This information can prompt future targeted studies testing relationships between impairments of serotonergic development, proprioceptive processing disorders, and presynaptic inhibition mediated by RORβ interneurons.

Maintained volitional activation of the muscle alters the cortical processing of proprioceptive afference from the ankle joint

Cortical proprioceptive processing of intermittent, passive movements can be assessed by extracting evoked and induced electroencephalographic (EEG) responses to somatosensory stimuli. Although the existent prior research on somatosensory stimulations, it remains unknown to what extent ongoing volitional muscle activation modulates the proprioceptive cortical processing of passive ankle-joint rotations.Twenty-five healthy volunteers (28.8 ± 7 yr, 14 males) underwent a total of 100 right ankle-joint passive rotations (4° dorsiflexions, 4 ± 0.25 s inter-stimulus interval, 30°/s peak angular velocity) evoked by a movement actuator during passive condition with relaxed ankle and active condition with a constant plantarflexion torque of 5 ± 2.5 Nm. Simultaneously, EEG, electromyographic (EMG) and kinematic signals were collected. Spatiotemporal features of evoked and induced EEG responses to the stimuli were extracted to estimate the modulation of the cortical proprioceptive processing between the active and passive conditions.Proprioceptive stimuli during the active condition elicited robustly ∼26 % larger evoked response and ∼38 % larger beta suppression amplitudes, but ∼42 % weaker beta rebound amplitude over the primary sensorimotor cortex than the passive condition, with no differences in terms of response latencies.These findings indicate that the active volitional motor task during naturalistic proprioceptive stimulation of the ankle joint enhances related cortical activation and reduces related cortical inhibition with respect to the passive condition. Possible factors explaining these results include mechanisms occurring at several levels of the proprioceptive processing from the peripheral muscle (i.e. mechanical, muscle spindle status, etc.) to the different central (i.e. spinal, sub-cortical and cortical) levels.

Using Electrical Muscle Stimulation to Enhance Electrophysiological Performance of Agonist-Antagonist Myoneural Interface.

The agonist-antagonist myoneural interface (AMI), a surgical method to reinnervate physiologically-relevant proprioceptive feedback for control of limb prostheses, has demonstrated the ability to provide natural afferent sensations for limb amputees when actuating their prostheses. Following AMI surgery, one potential challenge is atrophy of the disused muscles, which would weaken the reinnervation efficacy of AMI. It is well known that electrical muscle stimulus (EMS) can reduce muscle atrophy. In this study, we conducted an animal investigation to explore whether the EMS can significantly improve the electrophysiological performance of AMI. AMI surgery was performed in 14 rats, in which the distal tendons of bilateral solei donors were connected and positioned on the surface of the left biceps femoris. Subsequently, the left tibial nerve and the common peroneus nerve were sutured onto the ends of the connected donor solei. Two stimulation electrodes were affixed onto the ends of the donor solei for EMS delivery. The AMI rats were randomly divided into two groups. One group received the EMS treatment (designated as EMS_on) regularly for eight weeks and another received no EMS (designated as EMS_off). Two physiological parameters, nerve conduction velocity (NCV) and motor unit number, were derived from the electrically evoked compound action potential (CAP) signals to assess the electrophysiological performance of AMI. Our experimental results demonstrated that the reinnervated muscles of the EMS_on group generated higher CAP signals in comparison to the EMS_off group. Both NCV and motor unit number were significantly elevated in the EMS_on group. Moreover, the EMS_on group displayed statistically higher CAP signals on the indirectly activated proprioceptive afferents than the EMS_off group. These findings suggested that EMS treatment would be promising in enhancing the electrophysiological performance and facilitating the reinnervation process of AMI.

Study of the electromyographic activity in patellofemoral pain syndrome accompanied by secondary myofascial pain syndrome specifically affecting the popliteus muscle following dry needling: a randomized clinical trial.

Myofascial pain syndrome in the popliteus muscle may change motor control in the affected and related muscles due to changes in proprioceptive and nociceptive afferents, which can exacerbate patellofemoral pain syndrome. The primary purpose of the current study was to explore the electromyographic activity of the local and proximal muscles of the knee joint in patellofemoral pain syndrome accompanied by secondary myofascial pain syndrome specifically affecting the popliteus muscle following dry needling. Myofascial pain syndrome in the popliteus muscle may change motor control in the affected and related muscles due to changes in proprioceptive and nociceptive afferents, which can exacerbate patellofemoral pain syndrome. The primary purpose of the current study was to explore the electromyographic activity of the local and proximal muscles of the knee joint in patellofemoral pain syndrome accompanied by secondary myofascial pain syndrome specifically affecting the popliteus muscle following dry needling. During step-up, the onset and offset latencies of the local and proximal muscles of the knee joint, except for the offset latency of the gluteus maximus muscle (p-value=0.162), significantly decreased in the intervention group compared to the control group (p-value<0.046). Additionally, there were no significant differences (p-value>0.116) between the groups in the amplitude ratio of the local and proximal muscles of the knee joint during both step-up and step-down. The present study revealed that dry needling of the popliteus muscle with secondary myofascial pain syndrome associated with patellofemoral pain syndrome constructively modified the local and proximal motor control of the knee joint during step-up.

A computational study of how an α- to γ-motoneurone collateral can mitigate velocity-dependent stretch reflexes during voluntary movement

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.

FUNDAMENTAL LIMITATIONS OF KILOHERTZ-FREQUENCY CARRIERS IN AFFERENT FIBER RECRUITMENT WITH TRANSCUTANEOUS SPINAL CORD STIMULATION.

The use of kilohertz-frequency (KHF) waveforms has rapidly gained momentum in transcutaneous spinal cord stimulation (tSCS) to restore motor function after paralysis. However, the mechanisms by which these fast-alternating currents depolarize efferent and afferent fibers remain unknown. Our study fills this research gap by providing a hypothesis-and evidence-based investigation using peripheral nerve stimulation, lumbar tSCS, and cervical tSCS in 25 unimpaired participants together with computational modeling. Peripheral nerve stimulation experiments and computational modeling showed that KHF waveforms negatively impact the processes required to elicit action potentials, thereby increasing response thresholds and biasing the recruitment towards efferent fibers. While these results translate to tSCS, we also demonstrate that lumbar tSCS results in the preferential recruitment of afferent fibers, while cervical tSCS favors recruitment of efferent fibers. Given the assumed importance of proprioceptive afferents in motor recovery, our work suggests that the use of KHF waveforms should be reconsidered to maximize neurorehabilitation outcomes, particularly for cervical tSCS. We posit that careful analysis of the mechanisms that mediate responses elicited by novel approaches in tSCS is crucial to understanding their potential to restore motor function after paralysis.

A NEW POSTURAL MOTOR RESPONSE TO SPINAL CORD STIMULATION: POST-STIMULATION REBOUND EXTENSION.

Spinal cord stimulation (SCS) has emerged as a therapeutic tool for improving motor function following spinal cord injury. While many studies focus on restoring locomotion, little attention is paid to enabling standing which is a prerequisite of walking. In this study, we fully characterize a new type of response to SCS, a long extension activated post-stimulation (LEAP). LEAP is primarily directed to ankle extensors and hence has great clinical potential to assist postural movements. To characterize this new response, we used the decerebrate cat model to avoid the suppressive effects of anesthesia, and combined EMG and force measurement in the hindlimb with intracellular recordings in the lumbar spinal cord. Stimulation was delivered as five-second trains via bipolar electrodes placed on the cord surface, and multiple combinations of stimulation locations (L4 to S2), amplitudes (50-600 uA), and frequencies (10-40 Hz) were tested. While the optimum stimulation location and frequency differed slightly among animals, the stimulation amplitude was key for controlling LEAP duration and amplitude. To study the mechanism of LEAP, we performed in vivo intracellular recordings of motoneurons. In 70% of motoneurons, LEAP increased at hyperpolarized membrane potentials indicating a synaptic origin. Furthermore, spinal interneurons exhibited changes in firing during LEAP, confirming the circuit origin of this behavior. Finally, to identify the type of afferents involved in generating LEAP, we used shorter stimulation pulses (more selective for proprioceptive afferents), as well as peripheral stimulation of the sural nerve (cutaneous afferents). The data indicates that LEAP primarily relies on proprioceptive afferents and has major differences from pain or withdrawal reflexes mediated by cutaneous afferents. Our study has thus identified and characterized a novel postural motor response to SCS which has the potential to expand the applications of SCS for patients with motor disorders.

An alpha- to gamma-motoneurone collateral can mitigate velocity-dependent stretch reflexes during voluntary movement: A computational study.

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.

Effectiveness of Sub-occipital Release In Cervicogenic Vertigo

Background: Cervicogenic vertigo is defined as a sensation of rotation, resulting from an alteration of the neck proprioceptive afferents of the upper cervical spine. Sub-occipital Release, a type of Myofascial Release (MFR) is a form of manual therapy technique which can be used for the treatment of cervicogenic vertigo. Purpose: The purpose of this study is to minimize the use of equipment and patient positioning, thus making it easy for providers to treat by using the suboccipital myofascial release technique and find the effects of this technique on cervicogenic vertigo. Objective: To determine whether sub-occipital myofascial release technique in upper cervical region is more effective than the use of conventional exercises in improvement of the symptoms of cervicogenic vertigo. Setting: Otolaryngology(ENT) and orthopaedic clinics of Pune city. Method: We carried out a prospective, randomized controlled, in 60 subjects with cervicogenic vertigo who were assigned randomly to an Exercise group (N = 17) and Sub-occipital Release group (N = 17). Subjects received treatment three times a week, for 2 weeks. By the end of session, pre‑ and post‑comparison was done for the signs and symptoms of cervicogenic vertigo. Participants: Age group 20-40 years were taken for the study. Patients with other types or causes of vertigo, acute cervical fractures or atlanto-axial joint instability were excluded from the study. Outcome measure: The primary outcome measure of this study was to find the intensity of the signs and symptoms of cervicogenic vertigo by using a Dizziness Handicap Inventory-NDI Questionnaire[6] . Results: Statistical significance was found between and within the groups with respect to the signs and symptoms of cervicogenic vertigo. The results showed a statistically significant difference (P&lt;0.05) between the pre-treatment and post-treatment values for both the groups. Also, a significant improvement of signs and symptoms of cervicogenic vertigo was found in the sub-occipital group as compared to the exercise group. Conclusion: This study concluded that sub-occipital release technique is significantly effective for the treatment of cervicogenic vertigo.

Test-retest reliability of corticokinematic coherence in young children with cerebral palsy: An observational longitudinal study

ObjectivesTo assess the test-retest reliability of the corticokinematic coherence (CKC), an electrophysiological marker of proprioception, in children with cerebral palsy (CP). MethodsElectroencephalography (EEG) signals from 15 children with unilateral or bilateral CP aged 23 to 53 months were recorded in two sessions 3 months apart using 128-channel EEG caps. During each session, children's fingers were moved at 2 Hz by an experimenter, in separate recordings for the more-affected (MA) and less-affected (LA) hands. The CKC was computed at the electrode and source levels, at movement frequency F0 (2 Hz) and its first harmonic F1 (4 Hz). A two-way mixed-effects model intraclass-correlation coefficient (ICC) was computed for the maximum CKC strength across electrodes at F0 and F1 obtained during the two sessions. ResultsICC of the CKC strength acquired from LA and MA hands pooled together were respectively 0.51 (95% CI: 0.30–0.68) at F0 and 0.96 (95% CI: 0.93–0.98) at F1. The mean distances separating the CKC peaks in the source space at the two evaluation times were in the order of a centimeter. ConclusionCKC is a robust electrophysiologic marker to study the longitudinal changes in cortical processing of proprioceptive afferences in young children with CP.

Skin and not dorsal root stimulation reduces hypertonus in thoracic motor complete spinal cord injury: a single case report.

On demand and localized treatment for excessive muscle tone after spinal cord injury (SCI) is currently not available. Here, we examine the reduction in leg hypertonus in a person with mid-thoracic, motor complete SCI using a commercial transcutaneous electrical stimulator (TES) applied at 50 or 150 Hz to the lower back and the possible mechanisms producing this bilateral reduction in leg tone. Hypertonus of knee extensors without and during TES, with both cathode (T11-L2) and anode (L3-L5) placed over the spinal column (midline, MID) or 10 cm to the left of midline (lateral, LAT) to only active underlying skin and muscle afferents, was simultaneously measured in both legs with the pendulum test. Spinal reflexes mediated by proprioceptive (H-reflex) and cutaneomuscular reflex (CMR) afferents were examined in the right leg opposite to the applied LAT TES. Hypertonus disappeared in both legs but only during thoracolumbar TES, and even during LAT TES. The marked reduction in tone was reflected in the greater distance both lower legs first dropped to after being released from a fully extended position, increasing by 172.8% and 94.2% during MID and LAT TES, respectively, compared with without TES. Both MID and LAT (left) TES increased H-reflexes but decreased the first burst, and lengthened the onset of subsequent bursts, in the cutaneomuscular reflex of the right leg. Thoracolumbar TES is a promising method to decrease leg hypertonus in chronic, motor complete SCI without activating spinal cord structures and may work by facilitating proprioceptive inputs that activate excitatory interneurons with bilateral projections that in turn recruit recurrent inhibitory neurons.NEW & NOTEWORTHY We present proof of concept that surface stimulation of the lower back can reduce severe leg hypertonus in a participant with motor complete, thoracic spinal cord injury (SCI) but only during the applied stimulation. We propose that activation of skin and muscle afferents from thoracolumbar transcutaneous electrical stimulation (TES) may recruit excitatory spinal interneurons with bilateral projections that in turn recruit recurrent inhibitory networks to provide on demand suppression of ongoing involuntary motoneuron activity.

МЕТОДИКА КОНТРОЛЬНОГО ТЕСТИРОВАНИЯ ПРИ ИССЛЕДОВАНИИ ВЛИЯНИЯ «СУХОЙ» ИММЕРСИИ НА ПАРАМЕТРЫ ВЫПОЛНЕНИЯ ЗРИТЕЛЬНО-МОТОРНОЙ ЗАДАЧИ

Effects of reduced support, tactile and proprioceptive afferentation on mapping and manual operating the joystick were evaluated with participation of 14 female subjects. The idea was to compare performance of a 15 minute motor-ocular task in the conditions of dry immersion and lying supine on a couch. The subjects were to direct the pointer from the screen center to one of 8 randomly emerging targets. Pointer coordinates and emergence scenarios were registered; time to reach the target and geometry of pointer trajectories were calculated. Comparison was made by 4 characteristics: latent time of reaction, time of implementing the reaction, relative trajectory length, and averaged precision of trajectory to a target and the sum of trajectories. It was found that despite some individual differences, for all participants these 4 characteristics, equally of moving to a specific target or the sum of targets, were essentially similar. The results attest to the applicability of testing supine subject's manual tracking of the pointer to a target as a baseline data collection in dry immersion experiments aimed to define whether support-deprivation impacts effectiveness of manual moving the pointer to target.

PHYSICAL THERAPY AND NEUROREHABILITATION OF PATIENTS WITH CEREBROVASCULAR STROKE

Cerebral stroke represents an acute disturbance of circulation in the brain, which occurs with local and general brain symptoms. Main etiological factors are: arteriosclerosis, increased blood pressure, arterial hypotension, heart diseases, malformations of brain blood vessels, etc. Stroke is the most common neurological disease and the leading cause of mortality in the world, right after cardiovascular and malignant diseases. Cerebrovascular stroke is a focal neurological deficit caused by intracerebral hemorrhage. It is a condition that occurs due to a change in blood circulation in the brain and a very low supply of oxygen and nutrients to parts of the brain, which results in their damage and disruption of the functions that depend on them. There are two types of cerebrovascular stroke: ischemic - thrombosis and thromboembolism (85%) and hemorrhagic – intracerebral and subarachnoid bleeding (15%). The clinical picture can develop gradually or, the patient can suddenly fall into a coma. Absence of movements of the affected limbs predominates, always opposite to the side of the impact with an outburst of the facial nerve of the central type. Hemiplegia is a loss of the voluntary movements of one half of the body, caused by damage to the opposite brain hemisphere. The musculature is atonic, tendon reflexes are reduced or lost. The aim of the research is to determine the effectiveness of physical therapy and neurorehabilitation in patients with cerebrovascular brain stroke. Treatment of stroke: In the acute stage, physical therapy is aimed at preventing complications of the loco-motor apparatus (contractures, muscle and tendon retraction, heterotropic ossifications), the respiratory system (hypostatic pneumonia) and the skin (decubitus). This is achieved through treatment with position (frequent change of the position of the body in bed), passive exercises performed according to strictly defined rules, breathing exercises, exercises for healthy limbs and great care of the skin. The trophic changes of the skin are treated with ultraviolet radiation in suberythemic doses or with D’Arsonval currents. The research was conducted at the University of Southeast Europe - (Stul University) at the Faculty of Health Sciences in the Department of Physical Therapy and Rehabilitation, over a period of 6 months, from the beginning of From the beginning of May - to the end of October 2023. The research included 27 stroke patients, of which 11 patients had a left-sided stroke, and the remaining 14 patients had a right-sided stroke. According to the gender structure, 12 patients are male and the remaining 15 patients are female. After completing the six-month treatment with physical therapy, kinesitherapy and the methods of Vojta and Carl and Bertha Bobat, the results show great progress in almost all parameters. A decrease in tonic primitive reflexes, neck and labyrinthine tonic reflexes, reduction of extensor hypertonia, improvement of motor-reflex activity, proprioceptive afference, coordination, reduction of neck tone, foot reflex, stimulation of the grip reflex and improvement of the position of the neck, limbs and body. The presented results shows significant improvement in both groups of participants. Physical therapy and rehabilitation combined with kinesitherapy have an exceptional positive effect in: prevention of pathological primitive reflexes;creation and automation of normal active movements;saving irregular positions of the limbs and the whole body;establishment of balance and correct pattern of movement; fight against spasticity, secondary contractures and deformities; improvement of coordination and awareness of the body in relation to the environment.

Volitional muscle activation intensifies neuronal processing of proprioceptive afference in the primary sensorimotor cortex: an EEG study.

Proprioception refers to the ability to perceive the position and movement of body segments in space. The cortical aspects of the proprioceptive afference from the body can be investigated using corticokinematic coherence (CKC). CKC accurately quantifies the degree of coupling between cortical activity and limb kinematics, especially if precise proprioceptive stimulation of evoked movements is used. However, there is no evidence on how volitional muscle activation during proprioceptive stimulation affects CKC strength. Twenty-five healthy volunteers (28.8 ± 7 yr, 11 females) participated in the experiment, which included electroencephalographic (EEG), electromyographic (EMG), and kinematic recordings. Ankle-joint rotations (2-Hz) were elicited through a movement actuator in two conditions: passive condition with relaxed ankle and active condition with constant 5-Nm plantar flexion exerted during the stimulation. In total, 6 min of data were recorded per condition. CKC strength was defined as the maximum coherence value among all the EEG channels at the 2-Hz movement frequency for each condition separately. Both conditions resulted in significant CKC peaking at the Cz electrode over the foot area of the primary sensorimotor (SM1) cortex. Stronger CKC was found for the active (0.13 ± 0.14) than the passive (0.03 ± 0.04) condition (P < 0.01). The results indicated that volitional activation of the muscles intensifies the neuronal proprioceptive processing in the SM1 cortex. This finding could be explained both by peripheral sensitization of the ankle joint proprioceptors and central modulation of the neuronal proprioceptive processing at the spinal and cortical levels.NEW & NOTEWORTHY The current study is the first to investigate the effect of volitional muscle activation on CKC-based assessment of cortical proprioception of the ankle joint. Results show that the motor efference intensifies the neuronal processing of proprioceptive afference of the ankle joint. This is a significant finding as it may extend the use of CKC method during active tasks to further evaluate the motor efference-proprioceptive afference relationship and the related adaptations to exercise, rehabilitation, and disease.

Cortical processing of ankle joint proprioceptive afference during active and passive conditions: an EEG study

Cortical processing of ankle joint proprioceptive afference during active and passive conditions: an EEG study

Descending interneurons of the stick insect connecting brain neuropiles with the prothoracic ganglion.

Stick insects respond to visual or tactile stimuli with whole-body turning or directed reach-to-grasp movements. Such sensory-induced turning and reaching behaviour requires interneurons to convey information from sensory neuropils of the head ganglia to motor neuropils of the thoracic ganglia. To date, descending interneurons are largely unknown in stick insects. In particular, it is unclear whether the special role of the front legs in sensory-induced turning and reaching has a neuroanatomical correlate in terms of descending interneuron numbers. Here, we describe the population of descending interneurons with somata in the brain or gnathal ganglion in the stick insect Carausius morosus, providing a first map of soma cluster counts and locations. By comparison of interneuron populations with projections to the pro- and mesothoracic ganglia, we then estimate the fraction of descending interneurons that terminate in the prothoracic ganglion. With regard to short-latency, touch-mediated reach-to-grasp movements, we also locate likely sites of synaptic interactions between antennal proprioceptive afferents to the deutocerebrum and gnathal ganglion with descending or ascending interneuron fibres. To this end, we combine fluorescent dye stainings of thoracic connectives with stainings of antennal hair field sensilla. Backfills of neck connectives revealed up to 410 descending interneuron somata (brain: 205 in 19 clusters; gnathal ganglion: 205). In comparison, backfills of the prothorax-mesothorax connectives stained only up to 173 somata (brain: 83 in 16 clusters; gnathal ganglion: 90), suggesting that up to 60% of all descending interneurons may terminate in the prothoracic ganglion (estimated upper bound). Double stainings of connectives and antennal hair field sensilla revealed that ascending or descending fibres arborise in close proximity of afferent terminals in the deutocerebrum and in the middle part of the gnathal ganglia. We conclude that two cephalothoracic pathways may convey cues about antennal movement and pointing direction to thoracic motor centres via two synapses only.

Locomotor-related propriospinal V3 neurons produce primary afferent depolarization and modulate sensory transmission to motoneurons.

When a muscle is stretched, sensory feedback not only causes reflexes but also leads to a depolarization of sensory afferents throughout the spinal cord (primary afferent depolarization, PAD), readying the whole limb for further disturbances. This sensory-evoked PAD is thought to be mediated by a trisynaptic circuit, where sensory input activates first-order excitatory neurons that activate GABAergic neurons that in turn activate GABAA receptors on afferents to cause PAD, though the identity of these first-order neurons is unclear. Here, we show that these first-order neurons include propriospinal V3 neurons, as they receive extensive sensory input and in turn innervate GABAergic neurons that cause PAD, because optogenetic activation or inhibition of V3 neurons in mice mimics or inhibits sensory-evoked PAD, respectively. Furthermore, persistent inward sodium currents intrinsic to V3 neurons prolong their activity, explaining the prolonged duration of PAD. Also, local optogenetic activation of V3 neurons at one segment causes PAD in other segments, due to the long propriospinal tracts of these neurons, helping to explain the radiating nature of PAD. This in turn facilitates monosynaptic reflex transmission to motoneurons across the spinal cord. In addition, V3 neurons directly innervate proprioceptive afferents (including Ia), causing a glutamate receptor-mediated PAD (glutamate PAD). Finally, increasing the spinal cord excitability with either GABAA receptor blockers or chronic spinal cord injury causes an increase in the glutamate PAD. Overall, we show the V3 neuron has a prominent role in modulating sensory transmission, in addition to its previously described role in locomotion.NEW & NOTEWORTHY Locomotor-related propriospinal neurons depolarize sensory axons throughout the spinal cord by either direct glutamatergic axoaxonic contacts or indirect innervation of GABAergic neurons that themselves form axoaxonic contacts on sensory axons. This depolarization (PAD) increases sensory transmission to motoneurons throughout the spinal cord, readying the sensorimotor system for external disturbances. The glutamate-mediated PAD is particularly adaptable, increasing with either an acute block of GABA receptors or chronic spinal cord injury, suggesting a role in motor recovery.

Head Orientation Modulates Vestibular Cerebellar Evoked Potentials (VsCEPs) and Reflexes Produced by Impulsive Mastoid and Midline Skull Stimulation

The cerebellum plays a critical role in the modulation of vestibular reflexes, dependent on input from proprioceptive afferents. The mechanism of this cerebellar control is not well understood. In a sample of 11 healthy human subjects, we investigated the effects of head orientation on ocular, cervical, postural and cerebellar short latency potentials evoked by impulsive stimuli applied at both mastoids and midline skull sites. Subjects were instructed to lean backwards with the head positioned straight ahead or held rotated in different degrees of yaw towards the right and left sides. Impulsive mastoid stimulation, a potent method of utricular stimulation, produced localised vestibular cerebellar evoked potentials (VsCEPs: P12-N17) which were strongly modulated by head orientation. The response was larger on the side opposite to the direction of head rotation and with stimulation on the side of rotation. In contrast, ocular VEMPs (oVEMPs: n10-p16) were present but showed little change with head posture, while cervical VEMPs (cVEMPs: p15-n23) were larger with the head held rotated away from the side of the recording. Postural effects with lateral vestibular stimulation were strongly modulated by head rotation, with more powerful effects occurring bilaterally with stimulation on the side of rotation. The duration of the postural EMG changes was similar to the post-excitation inhibition of the electrocerebellogram (ECeG), consistent with cerebellar participation. We conclude that head rotation selectively affects evoked vestibular reflexes towards different targets, consistent with their physiological roles. Changes in VsCEPs may contribute to the modulation of postural reflexes by the cerebellum.

Changes in synaptic inputs to dI3 INs and MNs after complete transection in adult mice.

Spinal cord injury (SCI) is a debilitating condition that disrupts the communication between the brain and the spinal cord. Several studies have sought to determine how to revive dormant spinal circuits caudal to the lesion to restore movements in paralyzed patients. So far, recovery levels in human patients have been modest at best. In contrast, animal models of SCI exhibit more recovery of lost function. Previous work from our lab has identified dI3 interneurons as a spinal neuron population central to the recovery of locomotor function in spinalized mice. We seek to determine the changes in the circuitry of dI3 interneurons and motoneurons following SCI in adult mice. After a complete transection of the spinal cord at T9-T11 level in transgenic Isl1:YFP mice and subsequent treadmill training at various time points of recovery following surgery, we examined changes in three key circuits involving dI3 interneurons and motoneurons: (1) Sensory inputs from proprioceptive and cutaneous afferents, (2) Presynaptic inhibition of sensory inputs, and (3) Central excitatory glutamatergic synapses from spinal neurons onto dI3 INs and motoneurons. Furthermore, we examined the possible role of treadmill training on changes in synaptic connectivity to dI3 interneurons and motoneurons. Our data suggests that VGLUT1+ inputs to dI3 interneurons decrease transiently or only at later stages after injury, whereas levels of VGLUT1+ remain the same for motoneurons after injury. Levels of VGLUT2+ inputs to dI3 INs and MNs may show transient increases but fall below levels seen in sham-operated mice after a period of time. Levels of presynaptic inhibition to VGLUT1+ inputs to dI3 INs and MNs can rise shortly after SCI, but those increases do not persist. However, levels of presynaptic inhibition to VGLUT1+ inputs never fell below levels observed in sham-operated mice. For some synaptic inputs studied, levels were higher in spinal cord-injured animals that received treadmill training, but these increases were observed only at some time points. These results suggest remodeling of spinal circuits involving spinal interneurons that have previously been implicated in the recovery of locomotor function after spinal cord injury in mice.

DISTRIBUTION OF PARVALBUMIN-EXPRESSING NEURONAL POPULATIONS IN THE CAT CERVICAL AND LUMBAR SPINAL CORD GRAY MATTER

Parvalbumin is a classical marker of interneuronal populations in the central nervous system. Analyzing the cervical and lumbar spinal cord segments of cats (Felis catus), both individual cells and entire populations of neurons expressing parvalbumin were identified in most of the gray matter laminae. These populations have strict laminar and nuclear localization. Numerous neuronal clusters are located in the medial part of lamina V–VI and in laminae VII of cervical and lumbar enlargements. We believe that the first one located in segments C4–C8 and L4–L7 may participate in the modulatory mechanisms of locomotor activity via the convergence of cutaneous and proprioceptive afferentation from the limbs. Neuronal populations in lamina VII consist of Ia interneurons and Renshaw interneurons that participate in the motoneuron inhibition. Less numerous populations of parvalbumin-immunopositive cells found in laminae III possibly participated in the regulation of cutaneous sensitivity. Another population located in lamina VIII possibly forms commissural and propriospinal connections and participates in modulating the activity of motoneurons. Immunopositive interneurons also revealed in the precerebellar nuclei: central cervical nucleus and Clarke’s nucleus; unlike the general population of these nuclei, neurons revealed are interneurons. Scarce immunopositive cells are found in lamina I of L6–L7 segments, as well as in laminae II, IV, and X of all segments investigated.