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Shinzaki, S.

Publications and source records attributed to Shinzaki, S..

2 recordsLinked to original sources

Muscle-specific reticulospinal contributions to limb-trunk coordination during standing arm curls in strength-trained and untrained individuals

Limb-trunk coordination plays an essential role in daily actions. The reticulospinal excitability of limb muscles has been suggested to be modulated by long-term motor experience, such as strength training. However, it remains unclear whether reticulospinal contributions in the limb and trunk muscles during limb-trunk coordinated movements are modulated by strength training. This study aimed to determine whether reticulospinal contributions to limb-trunk coordination differ between strength-trained and untrained individuals. Fifteen long-term ([≥]3 yrs) strength-trained and 15 untrained healthy men participated in this study. Participants performed a rapid bilateral arm-curl task while standing, using a load corresponding to 35% of their one-repetition maximum, in response to visual, visual-auditory (80 dB), or visual-startling (115 dB) stimuli. Electromyography (EMG) was recorded from the right biceps brachii (BB) and erector spinae (ES) muscles during the task. In the trained group, EMG onset of the ES was closer to that of the BB than in the untrained group, indicating tighter temporal coordination between the limb prime mover and trunk postural muscles in strength-trained individuals. In both groups, visual-startling stimuli shortened the EMG onset of both the BB and ES, suggesting reticulospinal contributions to both muscles. Notably, the reduction in EMG onset of the BB induced by the startling stimulus was smaller in the trained group than in the untrained group, whereas no difference between groups was observed for the ES. These findings suggest that long-term strength training may modify limb-trunk muscle coordination during standing arm curls and may be associated with muscle-specific adaptations in reticulospinal contributions.

neuroscience↗

Sympathetic Nervous System Overactivation Induces Colonic Eosinophil-Associated Microinflammation and Contributes to the Pathogenesis of Irritable Bowel Syndrome

ObjectiveMucosal microinflammation is a characteristic clinical manifestation of irritable bowel syndrome (IBS), and its symptoms are often triggered by psychological stress. In the present study, we aimed to investigate the impact of early life stress-associated dysfunction of the sympathetic nervous system (SNS) on mucosal immune changes in the gastrointestinal tract (GI) and its contribution to IBS pathogenesis. DesignWe utilised a traditional animal model of IBS with maternal separation (MS) and evaluated colorectal hypersensitivity, immune alterations, and SNS activity in adult rats with MS. We conducted a series of experiments to manipulate peripheral SNS activity pharmacologically and chemogenetically to explore the interaction between SNS activity and GI events. ResultsThe MS-induced IBS model exhibited visceral hypersensitivity and eosinophilic infiltration in the colonic mucosa, along with SNS overactivation. Degeneration of the SNS using 6-OHDA neurotoxin decreased eosinophil infiltration and visceral hypersensitivity in the MS model. Notably, specific chemogenetic activation of the peripheral SNS induced eosinophil infiltration in the intestinal mucosa through the noradrenergic signalling-mediated release of eotaxin-1 from mesenchymal cells. ConclusionThis study highlights the critical role of SNS overactivation in eotaxin-1-driven eosinophil infiltration in the colon, leading to the development of visceral hypersensitivity in IBS. The results provide important insights into the mechanistic links among increased sympathetic activity, mucosal microinflammation, and visceral hypersensitivity in individuals with IBS, suggesting potential therapeutic approaches. What is already known on this topicO_LIA subgroup of patients with irritable bowel syndrome (IBS) presents with microinflammation in the gastrointestinal tract (GI). C_LIO_LIEarly life stress is recognised as a major risk factor for the development of IBS in adulthood. C_LIO_LIOveractivation of the sympathetic nervous system (SNS) is frequently associated with IBS. C_LI What this study addsO_LIMaternal separation (MS) stress induces eosinophil-associated microinflammation in the colonic mucosa of adult rats. C_LIO_LIInhibition of SNS activity suppresses eosinophil infiltration and mitigates visceral hypersensitivity in the MS model. C_LIO_LINoradrenergic signalling within the peripheral sympathetic activation stimulates mesenchymal cells to release eotaxin-1, leading to substantial eosinophil-predominant immune alterations in the colon. C_LI How this study might affect research, practice, or policyO_LITreatment with fibroblast-derived eotaxin-1 and targeting eosinophil-associated microinflammation could be a potential strategy to alleviate visceral pain in patients with IBS. C_LIO_LIThe chemogenomic method specifically manipulates peripheral SNS and provides a valuable tool for future research. C_LI

neuroscience↗