bioRxiv Science⌕ Search

bioRxiv · 10.1101/2022.09.14.507870

Tactile stimulation restores inhibited stretch reflex attributable to attenuation of Ia afferents during surprise landing

Abstract

PurposeArthrogenic muscle inhibition(AMI) is induced by pathological knee conditions. The present study aimed to investigate the effect of tactile stimulation on reflex changes induced by simulated AMI during unpredictable landing performances. MethodsTwenty participants performed six unilateral landing tasks: 15cm normal landing (15NL), 30cm normal landing(30NL), surprise landing(SL), 30cm normal landing following vibration (30NLV), surprise landing following vibration(SLV), and surprise landing following vibration with Kinesiology-tape(SLK). For the surprise landing tasks, the solid landing platform(15cm) was removed and replaced by a false plate platform. Since the false plate dislodged easily under load, participants unpredictably fell through the plate to the actual landing surface 15cm below. After completing 15NL, 30NL, SL, vibration stimulation was applied to participants knees to induce neurological changes similar to AMI. After vibration stimulation, participants performed 30NLV, SLV and SLK in a random order. EMG in the post-landing short latency(31-60 ms) and medium latency(61-90 ms) periods were examined. EMG signals from the vastus lateralis(VL), vastus medialis(VM), and lateral hamstrings(LH) were recorded and compared between tasks. ResultsEMG of all muscles were significantly enhanced in the medium latency period. Enhanced EMG were suppressed by vibration stimulation in the VL, but the suppressed EMG were restored after cutaneous stimulation(p<0.01). ConclusionOur findings suggest that AMI could alter motor control patterns during unpredictable landing, and that tactile stimulation could restore the altered motor control to a normal state. The use of tactile stimulation may help maintain normal motor control patterns in injured individuals.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Konishi, Y., Yoshii, R., Takeshita, D.. 2022-09-17. Tactile stimulation restores inhibited stretch reflex attributable to attenuation of Ia afferents during surprise landing. https://doi.org/10.1101/2022.09.14.507870

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related preprints

Selective activation of estrogen receptors modulates electrical activity and insulin secretion in human EndoC-βH1 cells

Estrogen receptors (ERs), ER and ER{beta} have important roles in the physiology of the endocrine pancreas in animal models, but the effects of ER activation on insulin-secreting human cells are still poorly understood. Here, we investigated the role of ER and ER{beta} as modulators of electrical activity and insulin secretion in the insulin-secreting human cell line EndoC-{beta}H1. Immunocytochemical analysis revealed a widespread cellular distribution of ER, while ER{beta} was predominantly localized outside the nucleus. We observed that both estradiol (E2) and the ER{beta} agonist diarylpropionitrile (DPN) led to a decrease in insulin secretion in the absence of stimulatory glucose concentrations, without affecting insulin content. Patch-clamp experiments revealed that a 48-hour treatment with either the ER agonist PPT or DPN resulted in depolarization of the resting membrane potential, increased action potential firing frequency, and altered the action potential waveform in EndoC-{beta}H1 cells. PPT increased voltage-dependent Ca2+ channel currents, while DPN reduced K+ and Na+ currents. These results suggest that activation of ER and ER{beta} modulates beta-cell electrical activity through distinct pathways involving ion channels. The effects of E2, PPT, and DPN were not caused by altered expression levels of ion channel genes after 48 hours of treatment. This suggests that these receptors act extranuclearly without affecting gene expression. Together, our findings demonstrate that selective activation of ER and ER{beta} modulates beta-cell excitability through distinct electrophysiological mechanisms and that E2 and DPN reduce basal insulin secretion in human EndoC-{beta}H1 cells. These results support ER and ER{beta} as potential targets for modulating human pancreatic beta-cell function.

physiology↗

Body weight modifies the efficacy of lifespan-extending interventions in ad libitum-fed mice

Geroprotective interventions are often assessed by extension of lifespan in ad libitum-fed mice. Increased lifespan could therefore reflect rescue of adverse phenotypes of unhealthy controls. We analysed body weight and survival for 33,780 mice in the Interventions Testing Program (ITP) to test whether treatment effects varied with body weight. In males, each added standard deviation of attained adult weight made treatment 6% more favourable (HR 0.94), more apparent for interventions that lowered body weight (HR 0.90). Median lifespan increase rose from 6.2% in mice in the lightest quartile to 20.2% in the heaviest pre-dosing weight quartile among those experiments, mainly because control survival declined more steeply with weight than that of the intervention group. The effect of body weight was consistent across 13 of 14 compounds and reflected weight attained during adulthood rather than in early life. Weight-dependence of intervention effects was weak in ITP females, possibly because median survival of controls exceeded that of every sampled non-ITP female control group. Amelioration of weight-associated risk is therefore implicated as a major contributor to lifespan increases relative to heavy, short-lived controls. The geroprotective effects of these interventions may thus be less apparent in metabolically healthier mice or humans.

physiology↗

Single-nucleus analysis reveals renal STAT1/CEBPB signaling as a modifiable relay of proinflammatory FGF23 effects in diabetic kidney disease

Background Circulating fibroblast growth factor 23 (FGF23) rises dramatically in chronic kidney disease, particularly in diabetic kidney disease (DKD). At high concentrations, and with declining Klotho, FGF23 has been linked to renal inflammation. The cell types and transcriptional programs mediating these off-target actions remain undefined. We asked whether the diseased kidney responds to FGF23 differently from the healthy kidney, and whether any disease-specific response could be targeted. Methods Male and female DBA/2J mice received streptozotocin or vehicle to induce DKD. On day 56, mice received a single dose intravenous injection of FGF23 (0.3 g) or vehicle, with tissue collected 1 h later for single-nucleus RNA sequencing, differential expression and regulon (inferred transcription factor activity) analysis. Candidate pathways were tested in precision-cut kidney slices using the CEBPB inhibitor ST-101. Results Streptozotocin-treated male mice developed early DKD with a 6-fold increase in urinary albumin/creatinine ratio and 50% higher blood urea nitrogen with preserved glomerular filtration rate. All major renal cell types were annotated. Canonical FGF23 signaling was intact in disease, with segment-specific target induction conserved in both conditions (e.g. Cyp24a1 in PT-S1 and DCT1). Superimposed on this were disease-restricted responses, including Wsb1 in DCT1 and Pdk4 in PT-S2, PST, DCT1 and DCT2. Regulon analysis revealed DKD-specific induction of CEBPB regulon activity by FGF23 across all analyzed tubular segments, and of STAT1 in several segments. Pre-treatment with a CEBPB inhibitor suppressed CEBPB activity, downstream NF-KB and pro-inflammatory gene sets, and immune-like cell abundance in diseased slices. Conclusion In the diabetic kidney, FGF23 engages a STAT1-CEBPB-NF-{kappa}B axis absent from healthy kidney and extending beyond its canonical Klotho-dependent target segments, identifying CEBPB as a potential treatment target for FGF23's pathological inflammatory actions.

physiology↗