Facilitation Of Reflex Research Articles

Effects of voluntary contraction on the soleus H-reflex of different amplitudes in healthy young adults and in the elderly.

A number of H-reflex studies used a moderate steady voluntary contraction in an attempt to keep the motoneuron pool excitability relatively constant. However, it is not clear whether the voluntary muscle activation itself represents a confounding factor for the elderly, as a few ongoing mechanisms of reflex modulation might be compromised. Further, it is well-known that the amount of either inhibition or facilitation from a given conditioning depends on the size of the test H-reflex. The present study aimed at evaluating the effects of voluntary contraction over a wide range of reflex amplitudes. A significant reflex facilitation during an isometric voluntary contraction of the soleus muscle (15% of the maximal voluntary isometric contraction-MVC) was found for both young adults and the elderly (p < 0.05), regardless of their test reflex amplitudes (considering the ascending limb of the H-reflex recruitment curve-RC). No significant difference was detected in the level of reflex facilitation between groups for all the amplitude parameters extracted from the RC. Simulations with a computational model of the motoneuron pool driven by stationary descending commands yielded qualitatively similar amount of reflex facilitation, as compared to human experiments. Both the experimental and modeling results suggest that possible age-related differences in spinal cord mechanisms do not significantly influence the reflex modulation during a moderate voluntary muscle activation. Therefore, a background voluntary contraction of the ankle extensors (e.g., similar to the one necessary to maintain upright stance) can be used in experiments designed to compare the RCs of both populations. Finally, in an attempt to elucidate the controversy around changes in the direct motor response (M-wave) during contraction, the maximum M-wave (Mmax) was compared between groups and conditions. It was found that the Mmax significantly increases (p < 0.05) during contraction and decreases (p < 0.05) with age arguably due to muscle fiber shortening and motoneuron loss, respectively.

Teaching Video NeuroImage: Reflex Facilitation in Lambert-Eaton Myasthenic Syndrome.

A 41-year-old woman presented with progressive fluctuating lower limb weakness, urinary incontinence, and dry eyes and mouth. Physical examination revealed proximal flaccid tetraparesis (Medical Research Council 4). The patellar reflex was absent, but with postexercise facilitation (video 1). Eyelid and eye movements were normal. Electroneuromyography revealed a presynaptic neuromuscular junction disorder (figure). Antibodies to anti-voltage-gated calcium channels were positive. Periodic cancer screening, including whole-body FDG-PET, was negative during 2 years of follow-up. These findings were consistent with nonparaneoplastic Lambert-Eaton myasthenic syndrome.1 The patient had a good response to IV immunoglobulin. The presence of ascending muscle weakness, autonomic dysfunction, and postexercise facilitation of reflexes should raise suspicion for the diagnosis.

Simultaneous Cervical and Lumbar Spinal Cord Stimulation Induces Facilitation of Both Spinal and Corticospinal Circuitry in Humans.

Coupling between cervical and lumbar spinal networks (cervico-lumbar coupling) is vital during human locomotion. Impaired cervico-lumbar coupling after neural injuries or diseases can be reengaged via simultaneous arm and leg cycling training. Sensorimotor circuitry including cervico-lumbar coupling may further be enhanced by non-invasive modulation of spinal circuity using transcutaneous spinal cord stimulation (tSCS). This project aimed to determine the effect of cervical, lumbar, or combined tSCS on spinal reflex (Hoffmann [H-]) and corticospinal (motor evoked potential [MEP]) excitability during a static or cycling cervico-lumbar coupling task. Fourteen neurologically intact study participants were seated in a recumbent leg cycling system. H-reflex and MEP amplitudes were assessed in the left flexor carpi radialis (FCR) muscle during two tasks (Static and Cycling) and four conditions: (1) No tSCS, (2) tSCS applied to the cervical enlargement (Cervical); (3) tSCS applied to the lumbar enlargement (Lumbar); (4) simultaneous cervical and lumbar tSCS (Combined). While cervical tSCS did not alter FCR H-reflex amplitude relative to No tSCS, lumbar tSCS significantly facilitated H-reflex amplitude by 11.1%, and combined cervical and lumbar tSCS significantly enhanced the facilitation to 19.6%. Neither cervical nor lumbar tSCS altered MEP amplitude alone (+4.9 and 1.8% relative to legs static, No tSCS); however, combined tSCS significantly increased MEP amplitude by 19.7% compared to No tSCS. Leg cycling alone significantly suppressed the FCR H-reflex relative to static, No tSCS by 13.6%, while facilitating MEP amplitude by 18.6%. When combined with leg cycling, tSCS was unable to alter excitability for any condition. This indicates that in neurologically intact individuals where interlimb coordination and corticospinal tract are intact, the effect of leg cycling on cervico-lumbar coupling and corticospinal drive was not impacted significantly with the tSCS intensity used. This study demonstrates, for the first time, that tonic activation of spinal cord networks through multiple sites of tSCS provides a facilitation of both spinal reflex and corticospinal pathways. It remains vital to determine if combined tSCS can influence interlimb coupling after neural injury or disease when cervico-lumbar connectivity is impaired.

A Re-evaluation of Whether Non-monosynaptic Homonymous H Reflex Facilitation Tests Propriospinal Circuits.

The C3–C4 propriospinal system is an important pathway mediating movement in cats; it contributes to movements in primates (including humans), and may have a role in recovery after lesion. Validated clinical tests of this system would find many applications, therefore we sought to test whether non-monosynaptic homonymous facilitation of the forearm flexor H reflex is mediated solely via a C3–C4 propriospinal pathway. In one anesthetized macaque monkey, median nerve stimulation elicited an H reflex in the flexor carpi radialis (FCR). Median nerve conditioning stimuli at sub-threshold intensities facilitated the H reflex, for inter-stimulus intervals up to 30 ms. Successive spinal surgical hemisections were then made. C2 lesion left the homonymous facilitation intact, suggesting mediation by spinal, not supraspinal pathways. Facilitation also remained after a second lesion at C5, indicating a major role for segmental (C7–C8) rather than propriospinal (C3–C4) interneurons. In separate experiments in five healthy human subjects, a threshold tracking approach assessed changes in peripheral axon excitability after conditioning stimulation. This was found to be enhanced up to 20 ms after the conditioning stimulus, and could partly, although not completely, underlie the H reflex facilitation seen. We conclude that homonymous facilitation of the H reflex in FCR can be produced by segmental spinal mechanisms, as well as by a supranormal period of nerve excitability. Unfortunately, this straightforward test cannot therefore be used for selective assessment of propriospinal circuits.

Brain nitric oxide induces facilitation of the micturition reflex through brain glutamatergic receptors in rats.

Brain nitric oxide (NO) have been reported in regulation of the sympatho-adrenomedullary system, which can affect voiding and storage functions. Therefore, we investigated effects of intracerebroventricularly (icv) administered 3-(4-morpholinyl)sydnonimine, hydrochloride (SIN-1) (NO donor) on the micturition reflex, focusing on their dependence on the sympatho-adrenomedullary system and on brain N-methyl-D-aspartate (NMDA) and α-amino-3-hydroxy-5-methyl-4-isoxazole propionate (AMPA) receptors in urethane-anesthetized (0.8 g/kg, ip) male Wistar rats. Plasma noradrenaline and adrenaline were measured just before and 5 minutes after SIN-1 administration. Evaluation of urodynamic parameters was started 1 hour before SIN-1 administration or intracerebroventricular pretreatment with other drugs. SIN-1 (100 and 250 µg/animal) elevated plasma adrenaline and reduced intercontraction interval([ICI]values; 110.5% [SIN-1, 0 µg]and 54.9% [SIN-1, 250 µg]during 15 minutes after SIN-1 administration [P < .05;η2 = 0.59]) without affecting plasma noradrenaline or maximal voiding pressure. SIN-1 (250 µg/animal) reduced single-voided volume and bladder capacity without affecting post-voiding residual volume. The SIN-1 (250 µg/animal)-induced adrenaline elevation and ICI reduction were attenuated by 2-(4-carboxyphenyl)-4,4,5,5-tetramethylimidazoline-1-oxyl-3-oxide, sodium salt (carboxy-PTIO) (NO scavenger, icv) (ICI values; 44.7% [vehicle + SIN-1]and 77.5% [carboxy-PTIO + SIN-1]during 15 minutes after SIN-1 administration [P < .05;η2 = 0.51]). Acute bilateral adrenalectomyabolished SIN-1-induced adrenaline elevation, while showed no effect on the SIN-1-induced ICI reduction. The ICI reduction was attenuated by MK-801 (NMDA receptor antagonist, icv) (ICI values; 47.0% [vehicle + SIN-1]and 87.6% [MK-801 + SIN-1]during 15 minutes after SIN-1 administration [P < .05;η2 = 0.61]), but not by DNQX (AMPA receptor antagonist, icv). Brain NO is involved in facilitation of the rat micturition reflex through brain NMDA receptors, independently of the sympatho-adrenomedullary outflow modulation.

Modulation of soleus H-reflex excitability following cervical transspinal conditioning stimulation in humans

The aim of this study was to establish the effects of transcutaneous spinal cord (transspinal) stimulation over the cervical region on soleus H-reflex excitability in healthy subjects while at rest. Reflex effects were established at subthreshold and suprathreshold cervical transspinal conditioning stimulation intensities of the extensor carpi radialis transspinal evoked potential. Twenty soleus H-reflexes at 0.125 Hz were recorded randomly under control conditions and following transspinal conditioning stimulation at conditioning-test intervals that ranged from 0 to 55 ms and tested in increment of 5 ms steps and at 100 ms. Cervical transspinal stimulation at suprathreshold and not at subthreshold intensities produced short, medium, and long-latency soleus H-reflex facilitation. The observed facilitatory reflex effects are consistent with activation of excitatory components of long propriospinal neurons. We propose the use of cervical transspinal stimulation to potentiate excitatory neuronal interactions between arms and legs in neurological disorders.

Transspinal stimulation downregulates activity of flexor locomotor networks during walking in humans

The objective of this study was to establish the effects of transspinal stimulation on short-latency tibialis anterior (TA) flexion reflex during walking in healthy humans. Single pulse transspinal stimulation was delivered at a conditioning-test (C-T) interval either after (~20 ms) or simultaneously with the last pulse of the pulse train (0 ms) delivered to the medial arch of the right foot. Transspinal stimulation was delivered at sub- and supra-threshold intensities of the spinally-mediated TA transspinal evoked potential. Stimulation was delivered randomly at different phases of the step cycle, based on the foot switch threshold signal, which was divided into 16 equal bins. The TA flexion reflex facilitation under control conditions occurred at heel contact and then progressively from late stance phase reaching its peak at early and late swing phases. Transspinal stimulation at a negative and suprathreshold 0 ms C-T interval depressed flexion reflex excitability at all phases of the step cycle. The short-latency TA flexion reflex depression was possibly mediated through spinal inhibitory interneurons acting at both pre- and post- motoneuronal sites or by transspinal stimulation affecting directly the activity of the flexor half spinal center. These results reveal direct actions of transspinal stimulation on human spinal locomotor networks.

Effects of neuromuscular electrical stimulation and voluntary commands on the spinal reflex excitability of remote limb muscles

It is well known that contracting the upper limbs can affect spinal reflexes of the lower limb muscle, via intraneuronal networks within the central nervous system. However, it remains unknown whether neuromuscular electrical stimulation (NMES), which can generate muscle contractions without central commands from the cortex, can also play a role in such inter-limb facilitation. Therefore, the objective of this study was to compare the effects of unilateral upper limb contractions using NMES and voluntary unilateral upper limb contractions on the inter-limb spinal reflex facilitation in the lower limb muscles. Spinal reflex excitability was assessed using transcutaneous spinal cord stimulation (tSCS) to elicit responses bilaterally in multiple lower limb muscles, including ankle and thigh muscles. Five interventions were applied on the right wrist flexors for 70 s: (1) sensory-level NMES; (2) motor-level NMES; (3) voluntary contraction; (4) voluntary contraction and sensory-level NMES; (5) voluntary contraction and motor-level NMES. Results showed that spinal reflex excitability of ankle muscles was facilitated bilaterally during voluntary contraction of the upper limb unilaterally and that voluntary contraction with motor-level NMES had similar effects as just contracting voluntarily. Meanwhile, motor-level NMES facilitated contralateral thigh muscles, and sensory-level NMES had no effect. Overall, our results suggest that inter-limb facilitation effect of spinal reflex excitability in lower limb muscles depends, to a larger extent, on the presence of the central commands from the cortex during voluntary contractions. However, peripheral input generated by muscle contractions using NMES might have effects on the spinal reflex excitability of inter-limb muscles via spinal intraneuronal networks.

A case of proximal muscle weakness and areflexia with post exercise facilitation of deep tendon reflexes

Lambert-Eaton syndrome (LES) is a rare presynaptic neuromuscular junction disorder which is characterised by proximal limb muscle weakness, decreased deep tendon reflexes and various autonomic symptoms. A 60 year old gentleman presented with complaints of progressive proximal muscle weakness of both upper limbs and lower limbs since 6 months. He had significant weight loss and anorexia. He gave history of dryness of mouth, difficulty in swallowing and erectile dysfunction since past six months. On examination there was symmetrical, proximal more than distal, lower limb more than upper limb weakness. No wasting or fasciculation was noted. Gait was waddling. All deep tendon reflexes were absent. However, the reflexes showed a post exercise facilitation (after 10 s of tonic contraction) especially the knee jerk (video available). High frequency RNS performed showed an incremental response. Chest X ray showed a non-homogenous opacity in right middle zone. CECT thorax showed a heterogeneously enhancing lesion in right hilum involving mediastinum. A guided biopsy from lesion showed features of small cell neuroendocrine carcinoma. Anti-VGCC antibody was tested and it was positive confirming diagnosis of LES. Patient was transferred to oncology department and initiated on chemotherapy. I have obtained patient and Institutional Review Board approval. In conclusion, post exercise facilitation of deep tendon reflexes can be considered as the telltale sign of LES. LES is considered a harbinger of malignancy, especially small cell lung cancer (SCLC). A diagnosis of LES may lead to the timely detection of SCLC, significantly improving patient prognosis and survival.

Influence of kinesthetic motor imagery and effector specificity on the long-latency stretch response.

The long-latency "reflexive" response (LLR) following an upper limb mechanical perturbation is generated by neural circuitry shared with voluntary control. This feedback response supports many task-dependent behaviors and permits the expression of goal-directed corrections at latencies shorter than voluntary reaction time. An extensive body of literature has demonstrated that the LLR shows flexibility akin to voluntary control, but it has not yet been tested whether instruction-dependent LLR changes can also occur in the absence of an overt voluntary response. The present study used kinesthetic motor imagery (experiment 1) and instructed participants to execute movement with the unperturbed contralateral limb (experiment 2) to explore the relationship between the overt production of a voluntary response and LLR facilitation. Activity in stretched right wrist flexors were compared with standard "do not-intervene" and "compensate" conditions. Our findings revealed that on ~40% of imagery and ~50% of contralateral trials, a response occurred during the voluntary epoch in the stretched right wrist flexors. On these "leaked" trials, the early portion of the LLR (R2) was facilitated and displayed a similar increase to compensate trials. The latter half of the LLR (R3) showed further modulation, mirroring the patterns of voluntary epoch activity. By contrast, the LLR on "non-leaked" imagery and contralateral trials did not modulate. We suggest that even though a hastened voluntary response cannot account for all instruction-dependent LLR modulation, the overt execution of a response during the voluntary epoch in the same muscle(s) as the LLR is a prerequisite for instruction-dependent facilitation of this feedback response.NEW & NOTEWORTHY Using motor imagery and contralateral responses, we provide novel evidence that facilitation of the long-latency reflex (LLR) requires the execution of a response during the voluntary epoch. A high proportion of overt response "leaks" were found where the mentally simulated or mirrored response appeared in stretched muscle. The first half of the LLR was categorically sensitive to the appearance of leaks, whereas the latter half displayed characteristics closely resembling activity in the ensuing voluntary period.

Central angiotensin II type 1 receptor as a therapeutic target against frequent urination.

The goal of this study was to test whether central corticotropin-releasing factor (CRF) was involved in angiotensin II (Ang II) and Ang II type 1 (AT1) receptor-mediated facilitation of micturition reflex and to investigate whether peripherally administered telmisartan, AT1 receptor antagonist, suppresses the central Ang II-induced facilitation of micturition reflex in rats. Urethane anesthetized male Wistar rats were placed under continuous cystometry before and after intracerebroventricular administration of each drug. Rats were intracerebroventricularly administered telmisartan (AT1 receptor antagonist), CP154526 (CRF1 receptor antagonist), or K41498 (CRF2 receptor antagonist) 30 minutes before intracerebroventricular administration of Ang II. Some male Wistar rats were perorally pretreated with either vehicle, AT1 receptor antagonist telmisartan or valsartan, once daily for 8 days, then measured blood pressure. Thereafter, Ang II was intracerebroventricularly administered for continuous cystometry. Intracerebroventricularly administered telmisartan or CP154526 dose-dependently suppressed the central Ang II-induced intercontraction interval (ICI) reduction. In contrast, intracerebroventricularly administered K41498 did not affect the central Ang II-induced response compared to vehicle pretreatment. Peripherally administered telmisartan but not valsartan suppressed the central Ang II-induced ICI reduction in rats compared to vehicle administration without altering blood pressure. Central Ang II induced facilitation of the micturition reflex through AT1 and CRF1 receptors. Peripherally administered telmisartan suppressed central Ang II-induced facilitation of micturition reflex.

O-13 Control over supraorbital nerve stimulation overrules the facilitation of blink reflex in defensive peripersonal space

Background The blink reflex (BR) to electrical supraorbital nerve stimulation (SON-S) is a protective reflex. Knowledge about imminent SON-S via acoustic prepulse, verbal forewarning, or self-delivery of stimulation, causes R2 suppression. The BR following median nerve stimulation increases when elicited in the defensive peripersonal space of the face (DPPS-F). Here we studied modulation of BR to SON-S by self-stimulation or visual control over hetero-stimulation in or outside the DPPS-F. Methods Twenty-three subjects participated in two sets of BR recordings following SON-S (E1, n = 10; E2, n = 17). Conditions either involved hetero-stimulation by the experimenter (E1A, E1C, E2A, E2B) or self-stimulation by subjects (E1B, E2C, E2D), with the stimulator probe in (E1B, E1C, E2B, E2D) or outside (E1A, E2A, E2C) their DPPS-F, and with subjects being aware (E1B, E2B, E2C, E2D) or unaware (E1A, E1C, E2A) about imminent stimulation. Results Compared to baseline (standard BR, E1A, E2A), R2 was facilitated with the probe held in the DPPS-F, but being unaware of stimulus triggering (E1C). Visual control of imminent stimulation (seeing the experimenter’s finger triggering the probe: E2B) and self-triggering (E1B, E2C, E2D) facilitated R1 and inhibited R2. With self-triggering, there was no difference between the probe in (E2C) or outside (E2D) the DPPS-F. Conclusion BR-R2 is facilitated in a threatening situation (probe in DPPS-F) without control (hetero-stimulation unseen by subject). R1 is facilitated and R2 inhibited when subjects have visual control or full initiative over stimulation, irrespective of seeing the probe in the DPPS-F or not.

Dysregulation of mechanosensory circuits coordinating the actions of antagonist motor pools following peripheral nerve injury and muscle reinnervation

Movement disorders observed following peripheral nerve injury and muscle reinnervation suggest discoordination in the activation of antagonist muscles. Although underlying mechanisms remain undecided, dysfunction in spinal reflex circuits is a reasonable candidate. Based on the well known role of reflex inhibition between agonist and antagonist muscles in normal animals, we hypothesized its reduction following muscle reinnervation, similar to that associated with other disorders exhibiting antagonist discoordination, e.g. spinal cord injury and dystonia. Experiments performed on acutely-decerebrated rats examined interactions of mechanosensory reflexes between ipsilateral muscles acting as mechanical antagonists at the ankle joint: ankle extensor, gastrocnemii (G) muscles (agonists) and ankle flexor, tibialis anterior (TA) muscle (antagonist). The force of agonist stretch reflex contraction was measured for its suppression or facilitation by concurrent conditioning stretch of the antagonist muscle. Data were compared between two groups of adult rats, an antagonist reinnervation group with TA muscle reinnervated and a control group with TA normally innervated. Results revealed a three-fold increase in reflex suppression in the antagonist reinnervation group, contrary to our predicted decrease. Reflex facilitation also increased, not only in strength, seven-fold, but also in its frequency of stochastic occurrence across stimulus trials. These observations suggest dysregulation in specific spinal reflex circuits as novel candidate origins of modified antagonist muscle coordination following peripheral nerve injury and muscle reinnervation.

MP11-13 CENTRALLY ADMINISTERED BOMBESIN INDUCES FREQUENT URINATION VIA BRAIN CORTICOTROPIN-RELEASING FACTOR RECEPTOR TYPE 1 IN RATS

INTRODUCTION AND OBJECTIVES:Psychological stress exacerbates bladder dysfunction such as overactive bladder (OAB) and bladder pain syndrome/interstitial cystitis (BPS/IC). We previously reported that bombesin (BB), a stress-related neuropeptide, centrally induces facilitation of the rat micturition reflex. Brain BB is reported to activate hypothalamo-pituitary-adrenal axis and sympathetic nerves, as representative responses to stressful conditions, via brain corticotropin-releasing factor (CRF), another stress-related neuropeptide. Therefore, we examined whether brain CRF is involved in the BB-induced frequent urination in rats.METHODS:(1) In urethane anesthetized (0.8 g/kg, ip) male Sprague-Dawley (SD) rats (300-400 g), a catheter was inserted into the bladder to perform cystometry (CMG, 12 ml/h saline infusion). Astressin (a non-selective CRF receptor antagonist, 1 or 3 nmol/rat) was intracerebroventricularly (icv) pretreated 60 min before BB administration (0.03 nmol/rat, icv). CMG was started 60 min b...

Abstract #88: Cortical Contributions to Neuroplasticity after Repetitive Transspinal Stimulation in Healthy Humans

Introduction: Non-invasive repetitive brain and/or spinal stimulation have shown to be an effective neuromodulatory method that can promote neuroplasticity. For example, repetitive pulsed transspinal stimulation decreases the afferent-mediated motor evoked potential (MEP) facilitation, increases the subthreshold transcranial magnetic stimulation (TMS) mediated flexor reflex facilitation, and increases corticospinal excitability of arm and leg muscles in spinal intact and after spinal cord injury subjects (Knikou et al., 2015; Murray and Knikou, 2017).

Management of Overactive Bladder Symptoms After Radical Prostatectomy.

Post-prostatectomy overactive bladder (OAB) is a common and challenging condition to manage. The aim of the present report was to review the recent evidences regarding OAB symptoms that develop in men after prostatectomy and how to manage them. The prevalence of OAB after radical prostatectomy may range from 15.2 to 37.8%. Recent studies have highlighted the role of the urethrogenic mechanism (facilitation of the urethrovesical reflex due to stress urinary incontinence (SUI)) in the genesis of post-prostatectomy OAB in a significant proportion of patients. Several other pathophysiological factors such as iatrogenic decentralization of the bladder, defunctionalized bladder due to severe SUI, detrusor underactivity, or bladder outlet obstruction might be involved. The evaluation should aim to identify the underlying mechanism to tailor the treatment, which could range from SUI surgery, to fixing a urethral stricture, improving bladder emptying or using the conventional spectrum of OAB therapies. There is a paucity of data for OAB therapies specific to post-prostatectomy patients, with the exception of solifenacin, tolterodine, and botulinum toxin. There is currently no data on how preoperative management or surgical technique may prevent post-prostatectomy OAB.

Age-related reversal of spinal excitability during anticipatory postural control

IntroductionAn internal perturbation of standing balance activates muscles critical for maintaining balance and is preceded by anticipatory postural adjustments (APAs). In healthy younger adults, a measure of spinal excitability in the form of the Hoffmann (H) reflex becomes depressed during APAs but how aging affects the reflex control of APAs is unknown.MethodsWe compared H reflex excitability profiles in the right soleus muscle, indirectly indicating APA, between younger (n = 11, age 19–24 years), middle-aged (n = 10, age 37–56 years), and older healthy adults (n = 11, age 63–78 years). Subjects rapidly raised the right-dominant arm in response to an auditory cue. The H reflex was evoked 120 ms, 100 ms, 80 ms, 60 ms, 40 ms, 20 ms, and 0 ms before as well as 20 ms after the onset of the right anterior deltoid muscle activation. For data processing, each trial was controlled for the corresponding background EMG activity before normalizing the standing data to the data in sitting in the 8 time bins.ResultsAll subjects showed a silent period in the soleus background electromyographic activity, suggesting the presence of APA. We found that the stereotypical H reflex depression associated with APAs in younger adults was reduced in middle-aged adults and reversed to facilitation in older adults. The depression occurred in 10 out of 11 younger adults, whereas all 11 older adults exhibited facilitation.ConclusionBecause APAs are organized at the supraspinal level, we speculate a supraspinal origin of the age-related reflex facilitation during APAs.

Neurons in a Subregion of the Medial Parabrachial Nucleus (mPBN) Attenuate the Gain of the Hering‐Breuer (H‐B) Reflex

This study provides new evidence showing that a subregion of the mPBN, which plays a key role in the control of breathing frequency (1), also attenuates the H‐B expiratory facilitatory reflex. Experiments were performed in decerebrate, vagotomized dogs during isocapnic hyperoxia. Phase durations TI and TE were obtained from the phrenic neurogram(PNG). A small concentric bipolar electrode was used to microstimulate the mPBN subregion. Lung inflations and/or weak electrical stimulation of a desheathed cervical vagus nerve were used to activate the slowly adapting pulmonary stretch receptors (PSRs) to produce the H‐B reflex. Pulse‐train PSR stimulation at various frequencies (Fs) were delivered during the E‐phase of test cycles separated by several non‐stimulated control cycles. During every other PSR test cycle, pulse‐train stimulation of the pontine subregion at a predetermined frequency was concurrently delivered to determine its effect on the PSR‐induced increase in TE (e.g., fig A). The effect of the pontine stimulus in the absence of the PSR input was also measured. Plots of TE vs. PSR step Fs have the shape of an increasing exponential function. The effect of the pontine input was a proportional reduction in TE at each of the PSR step Fs, and was shown as an attenuated curve in the TE‐Fs plots (fig B). The relationship between the reduction in the H‐B reflex and the pontine stimulus frequency was linear over the range of 0 to 20 Hz, with a maximum attenuation of the H‐B reflex to ~20% of control (no pontine stimulus) produced by pontine stimulus frequencies in the 20–40 Hz range. These findings suggest that as inputs from the pontine subregion increase breathing frequency, this region concurrently attenuates the H‐B expiratory facilitatory reflex. This mechanism counteracts the PSR‐induced increase in TE, which reduces breathing frequency.Support or Funding InformationSupported by VA grant 2 I01BX000721‐07This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Convergent Spinal Circuits Facilitating Human Wrist Flexors.

Noninvasive assessment of spinal circuitry in humans is limited, especially for Ib pathways in the upper limb. We developed a protocol in which we evoke the H-reflex in flexor carpi radialis (FCR) by median nerve stimulation and condition it with electrical stimulation above motor threshold over the extensor carpi radialis (ECR) muscle belly. Eighteen healthy adults (8 male, 10 female) took part in the study. There was a clear reflex facilitation at a 30 ms interstimulus interval (ISI) and suppression at a 70 ms ISI, which was highly consistent across subjects. We investigated the following two hypotheses of the possible source of the facilitation: (1) ECR Ib afferents from Golgi tendon organs, activated by the twitch following ECR stimulation; and (2) FCR afferents, from spindles and/or Golgi tendon organs, activated by the wrist extension movement that follows ECR stimulation. Several human and monkey experiments indicated a role for both of these sets of afferents. Our results provide evidence for a spinal circuit in which flexor motoneurons receive convergent excitatory input from flexor afferents as well as from extensor Ib afferents; this circuit can be straightforwardly assessed noninvasively in humans.SIGNIFICANCE STATEMENT Here we described a novel spinal circuit, which is easy to assess noninvasively in humans. Understanding this circuit in more detail could be beneficial for the design of clinical tests in neurological conditions.

Influence of motor imagery on spinal reflex excitability of multiple muscles

The effects of motor imagery on spinal reflexes such as the H-reflex are unclear. One reason for this is that the muscles that can be used to record spinal reflexes are limited to traditional evoking methods Recently, transcutaneous spinal cord stimulation has been used for inducing spinal reflexes from multiple muscles and we aimed to examine the effect of motor imagery on spinal reflexes from multiple muscles. Spinal reflexes evoked by transcutaneous spinal cord stimulation were recorded from six muscles from lower limbs during motor imagery of right wrist extension and ankle plantarflexion with maximum isometric contraction. During both imaginary tasks, facilitation of spinal reflexes was detected in the ankle ipsilateral plantarflexor and dorsiflexor muscles, but not in thigh, toe or contralateral lower limb muscles. These results suggest that motor imagery of isometric contraction facilitates spinal reflex excitability in muscles of the ipsilateral lower leg and the facilitation does not correspond to the imaginary involved muscles.