Jacob R Sorensen, Daniel B Hoffman, Christiana J Raymond-Pope, Thomas J Lillquist, Amanda M Russell, Benjamin T Corona, Sarah M Greising
{"title":"Inhibition of ErbB2 mitigates secondary denervation after traumatic muscle injury.","authors":"Jacob R Sorensen, Daniel B Hoffman, Christiana J Raymond-Pope, Thomas J Lillquist, Amanda M Russell, Benjamin T Corona, Sarah M Greising","doi":"10.1113/JP287435","DOIUrl":"10.1113/JP287435","url":null,"abstract":"<p><p>Secondary denervation has recently been described as part of the sequela of volumetric muscle loss (VML) injury, occurring along with a significantly elevated neurotrophic response, specifically neuregulin-1 (NRG1). This may contribute to chronic functional impairments associated with the injury, representing an overlooked treatment target. Thus, though paradoxical, the goal of this study was to pharmacologically reduce neurotrophic signalling after VML using a monoclonal antibody (Herceptin) that inhibits ErbB2 receptors. We also assessed whether ErbB2 inhibition combined with a myogenic treatment (i.e. minced muscle graft) would have a synergistically beneficial effect on function. Adult male Lewis rats underwent surgical induction of tibialis anterior muscle VML injury and were randomized into one of four groups: VML untreated, VML Herceptin, VML muscle graft and VML muscle graft + Herceptin, with comparisons to the contralateral (uninjured) control muscle. Rats receiving Herceptin were administered the drug (8 mg/kg i.p.) at the time of surgery and thrice per week for the duration of the study (48 days). Terminally individual NMJs were quantitatively evaluated, and maximal in vivo torque was tested. ErbB2 inhibition fully restored the normal rates of NMJ innervation and morphology after VML injury, and improved innervation of de novo myofibres after a muscle-graft treatment. However ErbB2 inhibition did not improve skeletal muscle function alone or in combination with a muscle-graft treatment. We conclude that ErbB2 inhibition is a promising therapeutic option for treating VML injury, yet more work is needed to optimize the translation of improved NMJ characteristics to recover function. KEY POINTS: In cases of complex traumatic musculoskeletal injury, such as volumetric muscle loss (VML), the endogenous ability of skeletal muscle to regenerate and recover function is lost. Innervation, or the connection of a motor axon to each individual myofibre, is a necessary component of myofibre survival and contractile function, which is disrupted after VML. Paradoxically a monocolonal antibody inhibitor of neurotrophic signalling (receptor tyrosine kinase ErbB2; Herceptin) has been shown to improve regeneration in rodent models of nerve injury. Here we show that pharmaceutical ErbB2 inhibition following a rat model of VML improves muscle innervation; however it did not correspondingly recover muscle function. Although ErbB2 inhibition alone is an ineffective treatment for VML injury, its ability to improve innervation is noteworthy and should be considered as an adjunctive or combinatorial therapy option.</p>","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143544397","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Federico Picciau, Valdemar Brimnes Ingemann Johansen, Christoffer Merrild
{"title":"More strain, more brain: the impact of exercise intensity on neurogenesis","authors":"Federico Picciau, Valdemar Brimnes Ingemann Johansen, Christoffer Merrild","doi":"10.1113/JP288408","DOIUrl":"10.1113/JP288408","url":null,"abstract":"","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":"603 6","pages":"1357-1359"},"PeriodicalIF":4.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143544425","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Vanessa Chiappini, Maria Fernanda Veloz Castillo, Francesco Biancardi, Ferdinando Di Cunto, Pierre J Magistretti, Alessandro Vercelli, Marco Agus, Corrado Calì
{"title":"Ultrastructure of astrocytes using volume electron microscopy: A scoping review.","authors":"Vanessa Chiappini, Maria Fernanda Veloz Castillo, Francesco Biancardi, Ferdinando Di Cunto, Pierre J Magistretti, Alessandro Vercelli, Marco Agus, Corrado Calì","doi":"10.1113/JP287455","DOIUrl":"https://doi.org/10.1113/JP287455","url":null,"abstract":"<p><p>The morphological features of astrocytes are crucial for brain homeostasis, synaptic activity and structural support, yet remain poorly quantified. As a result of the nanometre-sized cross-section of neuropil astrocytic processes, electron microscopy (EM) is the only technique availabe to date capable of revealing their finest morphologies. Volume EM (vEM) techniques, such as serial block-face or focused ion beam scanning EM, enable high-resolution imaging of large fields and allow more extensive 3-D model analyses, revealing new astrocytic morphological features. This scoping review aims to summarize the state of the art of astrocyte ultrastructural analysis. This review included 45 of 439 non-duplicated articles from a Pubmed search, categorizing studies by research focus, animal models, brain region, vEM techniques and segmentation methods. By answering classical questions such as volume, surface area, branching complexity and synaptic ensheathment reported in the literature, this work is a valuable resource for scientists working on structural biology or computational neuroscience.</p>","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-03-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143544381","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Andrew G. Horn, Zachary J. White, Stephanie E. Hall, Kristina H. Morrison, Kiana M. Schulze, Judy Muller-Delp, David C. Poole, Brad J. Behnke
{"title":"Ageing impairs endothelium-dependent vasodilatation and alters redox signalling in diaphragm arterioles from male and female Fischer-344 rats","authors":"Andrew G. Horn, Zachary J. White, Stephanie E. Hall, Kristina H. Morrison, Kiana M. Schulze, Judy Muller-Delp, David C. Poole, Brad J. Behnke","doi":"10.1113/JP287451","DOIUrl":"10.1113/JP287451","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 \u0000 <div>Diaphragm hyperaemia and regional blood flow distribution are impaired with ageing, potentially consequent to altered vascular structure and/or diminished vasomotor function. Evidence from locomotory skeletal muscle suggests that age-related diaphragm vasomotor dysfunction may be related to a blunted endothelium-mediated vasodilatation, decreased nitric oxide (NO) bioavailability and/or augmented reactive oxygen species (ROS) generation. We hypothesized that, in the medial costal diaphragm with old age, there would be fewer feed arteries (FAs) and impaired vasomotor function, via endothelium-specific mechanisms, in first-order (1A) arterioles. In young (Y) and old (O) Fischer-344 rats, the number of medial costal diaphragm FAs was quantified. 1A arterioles (117–220 µm) were isolated, cannulated and pressurized via hydrostatic reservoirs. Thereafter endothelium-dependent (via ACh) vasodilatory responses were assessed. In a separate set of arterioles, ACh-mediated dilatation was assessed before and after treatment with the superoxide dismutase mimetic Tempol (100 µ<span>m</span>) and Tempol plus the hydrogen peroxide (H<sub>2</sub>O<sub>2</sub>) scavenger catalase (100 U/ml). The average number of medial costal FAs was lower in the rat diaphragm with old age (<i>p</i> = 0.001). Endothelium- and nitric oxide synthase (NOS)-dependent vasodilatation was 21% lower in medial costal 1A arterioles from O rats (<i>p</i> < 0.001). Tempol decreased ACh-mediated vasodilatation of medial costal 1A arterioles from Y and O rats but did not eliminate age-related differences. Tempol plus catalase further decreased ACh-mediated vasodilatation in O but not Y vessels. In the medial costal diaphragm vasculature, ageing is associated with (1) arterial rarefaction, (2) impaired endothelium-dependent vasodilatation via NOS- and ROS-dependent mechanisms and (3) increased reliance on ROS-mediated vasodilatation.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </div>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Key points</h3>\u0000 \u0000 <div>\u0000 <ul>\u0000 \u0000 <li>Old age blunts the hyperaemic response and alters regional blood flow distribution in the diaphragm. The effect of ageing on vascular structure and function in respiratory skeletal muscle is unknown.</li>\u0000 \u0000 <li>In young and old Fischer-344 rats of both sexes, we quantified the number of feed arteries (FAs) and assessed the vasoreactivity of first-order (1A) arterioles in the medial costal diaphragm.</li>\u0000 \u0000 <li>The number of medial costal diaphragm FAs was lower in old rats. In 1A arterioles endothelium-dependent vasodilatation was blunted, and r","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":"603 6","pages":"1439-1459"},"PeriodicalIF":4.7,"publicationDate":"2025-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143538026","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Georgia S. Clarke, Hui Li, Elaheh Heshmati, Lisa M. Nicholas, Kathryn L. Gatford, Amanda J. Page
{"title":"Pregnancy and a high-fat, high-sugar diet each attenuate mechanosensitivity of murine gastric vagal afferents, with no additive effects","authors":"Georgia S. Clarke, Hui Li, Elaheh Heshmati, Lisa M. Nicholas, Kathryn L. Gatford, Amanda J. Page","doi":"10.1113/JP286115","DOIUrl":"10.1113/JP286115","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 \u0000 <div>Gastric vagal afferents (GVAs) sense food-related mechanical stimuli and signal to the CNS to initiate meal termination. Pregnancy and diet-induced obesity are independently associated with dampened GVA mechanosensitivity and increased food intake. Whether a high-fat, high-sugar diet (HFHSD) impacts pregnancy-related adaptations in GVA signalling is unknown and was investigated in this study. Three-week-old female Glu Venus-expressing mice, on a C57BL/6 background, were fed standard laboratory diet (SLD) or HFHSD for 12 weeks, and then half of each group were mated to generate late pregnant (Day 17.5; P-SLD <i>N</i> = 12, P-HFHSD <i>N</i> = 14) or non-pregnant (NP-SLD <i>N</i> = 12, NP-HFHSD <i>N</i> = 16) groups. Body weight and food intake were monitored in Promethion metabolic cages from before mating until Day 17.5 of pregnancy or equivalent ages in non-pregnant mice, prior to tissue collection at 07.00 h for <i>in vitro</i> single fibre GVA recording and gene expression analysis. Pregnant mice gained more weight than non-pregnant mice but weight gain was unaffected by diet. By mid-pregnancy, light-phase food intake (kJ and g) was higher in pregnant than in non-pregnant mice (each <i>P</i> < 0.001) due to larger meals (kJ and g, each <i>P < </i>0.001), irrespective of diet. Pregnancy and HFHSD-feeding reduced tension-sensitive GVA mechanosensitivity (each <i>P</i> < 0.01), but pregnancy did not further downregulate GVA stretch responses within HFHSD mice (<i>P</i> = 0.652). Nodose ganglia growth hormone receptor mRNA abundance was upregulated in pregnancy, possibly contributing to lower GVA mechanosensitivity during pregnancy in SLD mice. Larger light-phase meals in pregnant compared to non-pregnant HFHSD mice may therefore reflect the downregulation of other satiety pathways.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </div>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Key points</h3>\u0000 \u0000 <div>\u0000 <ul>\u0000 \u0000 <li>Gastric vagal afferents (GVAs) regulate food intake by sensing the arrival and quantity of food and communicating this information to the brain.</li>\u0000 \u0000 <li>In standard laboratory diet (SLD) mice, gastric tension-sensitive vagal afferent mechanosensitivity was attenuated in pregnant compared to non-pregnant mice, which is concurrent with increases in total food intake and meal size.</li>\u0000 \u0000 <li>Nodose ganglia growth hormone receptor mRNA abundance was increased in pregnancy, possibly accounting for attenuated GVA mechanosensitivity in pregnant SLD mice.</li>\u0000 ","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":"603 6","pages":"1461-1481"},"PeriodicalIF":4.7,"publicationDate":"2025-03-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1113/JP286115","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143538031","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The gut microbiota: an amazing technicolour dream coat or the emperor's new clothes?","authors":"Ken D O'Halloran","doi":"10.1113/JP288465","DOIUrl":"https://doi.org/10.1113/JP288465","url":null,"abstract":"","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143532083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Katiuscia Martinello, Addolorata Mascia, Sara Casciato, Giancarlo Di Gennaro, Vincenzo Esposito, Michele Zoli, Cecilia Gotti, Sergio Fucile
{"title":"α4β2* nicotinic acetylcholine receptors drive human temporal glutamate/GABA balance toward inhibition","authors":"Katiuscia Martinello, Addolorata Mascia, Sara Casciato, Giancarlo Di Gennaro, Vincenzo Esposito, Michele Zoli, Cecilia Gotti, Sergio Fucile","doi":"10.1113/JP285689","DOIUrl":"10.1113/JP285689","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 \u0000 <div>Heteromeric nicotinic acetylcholine nAChRs (nAChRs) containing the α4 and β2 subunits (α4β2<sup>*</sup> nAChRs) modulate neurotransmitter release in several regions of the brain. In temporal lobe epilepsy, inhibitory GABAergic neurotransmission is altered, whereas no evidence of nicotinic dysfunction has been reported. Here, we investigated, in human epileptic cortical tissues, the ability of α4β2<sup>*</sup> nAChRs to modulate synaptic transmission. An increased expression of α4 and β2 subunits was observed in the temporal cortex of epileptic patients. We then recorded excitatory and inhibitory postsynaptic currents from layer 5 pyramidal neurons in the cortex of temporal lobe epilepsy patients, before and during selective modulation of α4β2<sup>*</sup> nAChRs by desformylflustrabromine (a selective α4β2<sup>*</sup> positive allosteric modulator). We observed a decrease in both frequency and amplitude of spontaneous excitatory postsynaptic currents, along with an increase in spontaneous inhibitory postsynaptic current frequency. Both these effects were blocked by dihydro-β-erythroidine, a selective α4* antagonist. α4β2<sup>*</sup> activation enhanced the excitability of interneurons (but not of layer 5 pyramidal neurons) by lowering the action potential threshold. Moreover, upon block of action potential propagation by TTX, α4β2<sup>*</sup> activation did not alter miniature inhibitory postsynaptic currents recorded from pyramidal neurons, at the same time as reducing the release at glutamatergic synapses by a GABA<sub>B</sub>-dependent process.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </div>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Key points</h3>\u0000 \u0000 <div>\u0000 <ul>\u0000 \u0000 <li>Heteromeric nicotinic acetylcholine receptors containing the α4 and β2 subunits (α4β2<sup>*</sup> nAChRs) increase GABA release in several regions of the brain.</li>\u0000 \u0000 <li>We observe an increase of α4β2<sup>*</sup> nAChRs expression in the temporal cortex of patients with temporal lobe epilepsy (TLE, the most represented human focal epilepsy).</li>\u0000 \u0000 <li>When selectively activated with the positive allosteric modulator desformylflustrabromine (dFBr), α4β2<sup>*</sup> nAChRs increase the frequency of GABA release and decrease the glutamate release onto pyramidal neurons in the layer 5 of human TLE cortex.</li>\u0000 \u0000 <li>The increase of GABA release is related to an α4β2<sup>*</sup>-mediated enhanced excitability of cortical interneurons; instead, the decrease of glutamate releas","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":"603 6","pages":"1645-1662"},"PeriodicalIF":4.7,"publicationDate":"2025-03-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1113/JP285689","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143532015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Koyal Garg, Julia Brockhouse, Christopher M McAndrew, Alex J Reiter, Johnny G Owens, Ryan J Mueller, Gerard Pena, Amelia Ridolfo, David L Johnson
{"title":"Regenerative rehabilitation: Navigating the gap between preclinical promises and clinical realities for treating trauma-induced volumetric muscle loss.","authors":"Koyal Garg, Julia Brockhouse, Christopher M McAndrew, Alex J Reiter, Johnny G Owens, Ryan J Mueller, Gerard Pena, Amelia Ridolfo, David L Johnson","doi":"10.1113/JP286551","DOIUrl":"https://doi.org/10.1113/JP286551","url":null,"abstract":"<p><p>Regenerative rehabilitation is an emerging interdisciplinary field that combines regenerative medicine principles with rehabilitation science to improve recovery in musculoskeletal trauma cases such as volumetric muscle loss (VML). This article reviews preclinical and clinical studies, aiming to bridge the gap between these domains, summarize recent advancements and identify areas for further exploration. The review delves into preclinical studies, which explore the potential of regenerative approaches, including cellular and acellular scaffolds, to augment exercise-based rehabilitation. These studies demonstrate that regenerative rehabilitation can aid in functional recovery post-VML through various mechanisms such as modulation of fibrosis, angiogenesis, myogenesis and innervation. However, the approach in clinical studies differs significantly, involving diverse exercise therapy regimens both before and after surgical interventions. To date, only acellular extracellular matrix scaffolds have been combined with physical therapy in VML-injured patients, resulting in modest improvements in functional recovery. The field of regenerative rehabilitation is nascent but has seen noteworthy progress, with ample room for improvement. This article also highlights the need for closer collaboration between researchers in the fields of tissue engineering, orthopaedic surgery and physical therapy to improve recovery outcomes following traumatic muscle injuries.</p>","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":" ","pages":""},"PeriodicalIF":4.7,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143525210","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"The interplay between Hebbian and homeostatic plasticity in the adult visual cortex","authors":"Antoine Prosper, Thomas Blanchard, Claudia Lunghi","doi":"10.1113/JP287665","DOIUrl":"10.1113/JP287665","url":null,"abstract":"<div>\u0000 \u0000 <section>\u0000 \u0000 \u0000 <div>Homeostatic and Hebbian plasticity co-operate during the critical period, refining neuronal circuits; however, the interaction between these two forms of plasticity is still unclear, especially in adulthood. Here, we directly investigate this issue in adult humans using two consolidated paradigms to elicit each form of plasticity in the visual cortex: the long-term potentiation-like change of the visual evoked potential (VEP) induced by high-frequency stimulation (HFS) and the shift of ocular dominance induced by short-term monocular deprivation (MD). We tested homeostatic and Hebbian plasticity independently, then explored how they interacted by inducing them simultaneously in a group of adult healthy volunteers. We successfully induced both forms of plasticity: 60 min of MD induced a reliable change in ocular dominance and HFS reliably modulated the amplitude of the P1 component of the VEP. Importantly, we found that, across participants, homeostatic and Hebbian plasticity were negatively correlated, indicating related neural mechanisms, potentially linked to intracortical excitation/inhibition balance. On the other hand, we did not find an interaction when the two forms of plasticity were induced simultaneously. Our results indicate a largely preserved plastic potential in the visual cortex of the adult brain, for both short-term homeostatic and Hebbian plasticity. Crucially, we show for the first time a direct relationship between these two forms of plasticity in the adult human visual cortex, which could inform future research and treatment protocols for neurological diseases.\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </div>\u0000 </section>\u0000 \u0000 <section>\u0000 \u0000 <h3> Key points</h3>\u0000 \u0000 <div>\u0000 <ul>\u0000 \u0000 <li>Homeostatic and Hebbian plasticity co-operate during the critical period to refine neuronal circuits in the visual cortex.</li>\u0000 \u0000 <li>The interaction between these two forms of plasticity is still unknown, especially after the closure of the critical periods and in humans.</li>\u0000 \u0000 <li>We directly investigate the interplay between Hebbian and homeostatic visual plasticity in adult humans using non-invasive paradigms.</li>\u0000 \u0000 <li>We found a negative correlation between these forms of plasticity showing for the first time a direct relationship between Hebbian and homeostatic plasticity.</li>\u0000 \u0000 <li>Our results could inform future research and treatment protocols for neurological diseases.</li>\u0000 ","PeriodicalId":50088,"journal":{"name":"Journal of Physiology-London","volume":"603 6","pages":"1521-1540"},"PeriodicalIF":4.7,"publicationDate":"2025-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1113/JP287665","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143527990","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}