Neuroscience最新文献

{"title":"Antagonism of GABA-A receptor inhibits the effects of progesterone on nociceptive behaviors and electrophysiological alterations in a rat model of neuropathic pain","authors":"Morteza Jarrahi ,&nbsp;Hossein Ali Safakhah ,&nbsp;Payman Raise-Abdullahi ,&nbsp;Ali Rashidy-Pour","doi":"10.1016/j.neuroscience.2025.05.027","DOIUrl":"10.1016/j.neuroscience.2025.05.027","url":null,"abstract":"<div><div>Growing evidence highlights the neuroprotective potential of progesterone in mitigating various forms of nervous system injury. In previous research, we demonstrated that progesterone ameliorates both electrophysiological and behavioral deficits associated with chronic constriction injury (CCI) of the sciatic nerve in rats. However, the precise mechanisms underlying these effects remain poorly understood. This study aimed to elucidate the involvement of GABA-A receptors in mediating the therapeutic effects of progesterone on nociceptive behaviors, specifically thermal hyperalgesia and mechanical allodynia, as well as electrophysiological alterations in a rat model of CCI-induced neuropathic pain. Male rats received daily intraperitoneal injections of progesterone (6 mg/kg) starting on day 12 post-CCI and continuing through day 26. To evaluate the role of GABA-A receptors, the antagonist bicuculline (0.5 or 2 mg/kg, i.p.) was administered 30 min prior to progesterone in designated groups. Behavioral assessments were conducted on days 0, 12, 26, 28, and 35 post-CCI, followed by electrophysiological evaluations of the tibial and sural nerves. The results revealed that progesterone significantly attenuated both thermal hyperalgesia and mechanical allodynia and reversed CCI-induced electrophysiological impairments. Nevertheless, pretreatment with bicuculline blocked these beneficial effects at both behavioral and electrophysiological levels, suggesting that progesterone’s neuroprotective and analgesic properties are, at least in part, mediated through GABA-A receptor signaling pathways.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 154-160"},"PeriodicalIF":2.9,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144102302","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Perineuronal net degradation causes a delayed change in resting and sound evoked responses in the mouse auditory cortex","authors":"A. Hussain ,&nbsp;K.A. Razak","doi":"10.1016/j.neuroscience.2025.05.026","DOIUrl":"10.1016/j.neuroscience.2025.05.026","url":null,"abstract":"<div><div>Perineuronal nets (PNNs) are extracellular matrix assemblies that preferentially cover parvalbumin-expressing (PV+) interneurons in the neocortex. PV+ cells and PNNs are impaired in a variety of neurodevelopmental disorders including Fragile X Syndrome and schizophrenia. In both of these disorders, electroencephalograph (EEG) recordings show similar phenotypes, including elevated resting gamma band power and reduced temporal fidelity in the 40 Hz auditory steady state response (ASSR). Whether there is a causal link between PNN integrity and EEG abnormalities remains unclear. We tested this link by recording EEG responses in the auditory cortex (AC) in wildtype mice in which PNNs were enzymatically degraded (Chondroitinase ABC or ChABC). EEGs were recorded at two different time points (4- or 14-days post injection, cross-sectional design). In comparison to saline control, ChABC injected mice showed a ∼50 % reduction in PNN density after 4-days. However, there was no difference in resting EEG power spectral density, auditory event-related potential amplitudes or ASSR temporal fidelity between saline and ChABC mice. At the 14-day time point, there was a recovery of PNN density in the AC. Interestingly, EEG responses were abnormal at this time point, with elevated gamma band activity and reduced ASSR temporal fidelity. Thus, the electrophysiological consequences of PNN loss are not seen acutely, but over a delayed time course, suggesting abnormal plasticity after a circuit perturbation. Taken together, these data indicate acute shaping of auditory cortical responses is less dependent on PNNs, but long-term stability of responses following a circuit perturbation depends on the integrity of PNNs.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 252-263"},"PeriodicalIF":2.9,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144101117","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of a synthetic cannabinoid, 5F-MDMB-PICA, on metabolites and glutamatergic transporters in U87 cell line","authors":"Ibrahim N. Alsulaihim ,&nbsp;Mohammed Mufadhe Alanazi ,&nbsp;Khaled A. Alhosaini ,&nbsp;Syed Rizwan Ahamad ,&nbsp;Mohammad R. Khan ,&nbsp;Fahad S. Almezied ,&nbsp;Abdullah A. Aldossari ,&nbsp;Thamer H. Abekairi ,&nbsp;Mohammed A. Assiri ,&nbsp;Fawaz Alasmari","doi":"10.1016/j.neuroscience.2025.05.016","DOIUrl":"10.1016/j.neuroscience.2025.05.016","url":null,"abstract":"<div><div>Brian metabolic pathways have been impaired in animals exposed to drugs of abuse. The misuse of cannabinoids is associated with neuronal death and synaptic plasticity. Astrocytic glutamate transporters are therapeutic targets in several preclinical models of substance use disorders. Abused drugs could impair metabolic pathways in animal models, particularly those involving astrocytes, where glutamate transporters are critical regulators of neurotransmission. We here aimed to evaluate the metabolomic profile of a human glioblastoma cell line following exposure a synthetic cannabinoid, 5F-MDMB-PICA (5F-M-P), using an <em>in vitro</em> cell model (U87, glioblastoma astrocytic origin cell line). Additionally, we evaluated the effects of 5F-M-P on the expression of astrocytic glutamate transporters. After treatments, the cells were collected for metabolomic study using gas chromatography-mass spectrometry, and protein expression study using western blotting assay. 5F-M-P, especially at a concentration of 100 μM, altered the abundance of numerous metabolites. Enrichment analysis identified that specific signaling pathways were involved in the effects of 5F-M-P on metabolites, including the glutamate neurotransmission pathway. Additionally, 5F-M-P at 200 μM reduced the expression of glutamate transporter-1 and glutamate-aspartate co-transporter. Therefore, 5F-M-P exposure altered key metabolic pathways in astrocytes including glutamatergic pathways, an effect associated with reduced astrocytic glutamate transporter expression.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 190-199"},"PeriodicalIF":2.9,"publicationDate":"2025-05-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144102303","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Schaftoside restrains neuroinflammation and ameliorates cerebral ischemic injury associated with LncGm36 mediated COP1 upregulation","authors":"Ermei Lu ,&nbsp;Jie Chen ,&nbsp;Qiaoyun Wu ,&nbsp;Jiayu Wu ,&nbsp;Kecheng Zhou","doi":"10.1016/j.neuroscience.2025.05.023","DOIUrl":"10.1016/j.neuroscience.2025.05.023","url":null,"abstract":"<div><div>Schaftoside(SS), a bioactive compound derived from<!--> <!-->Herba Desmodii Styracifolii, has demonstrated anti-inflammatory properties in microglial cells; However, its role in ischemic brain injury in mice remains unclear. This study aimed to investigate the neuroprotective effects of schaftoside in a mouse model of middle cerebral artery occlusion (MCAO) and elucidate the underlying molecular mechanism. RNA sequencing revealed that schaftoside significantly upregulated the long noncoding RNA Gm32496 (LncGm36), which was prominently downregulated in the ischemic penumbra of MCAO mice. Administration of schaftoside reduced the infarct size, alleviated brain edema, and improved neurological outcomes in MCAO mice through LncGm36 upregulation. Mechanistically, schaftoside-induced LncGm36 expression was accompanied by elevated levels of COP1, a key regulator involved in neuroinflammation. RNA pull-down assays confirmed a direct interaction between LncGm36 and COP1. Silencing of either LncGm36 or COP1 attenuated schaftoside-mediated anti-inflammatory microglial polarization and neuroprotection. Collectively, these results indicate that schaftoside confers neuroprotection against ischemic brain injury by promoting an anti-inflammatory phenotypic shift of microglia through the LncGm36/COP1 pathway, suggesting its potential as a therapeutic agent for ischemic stroke.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"579 ","pages":"Pages 93-104"},"PeriodicalIF":2.9,"publicationDate":"2025-05-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144094421","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The genetic risk factors, molecular pathways, microRNAs, and the gut microbiome in Alzheimer’s disease","authors":"Aathira N.S ,&nbsp;Amanpreet Kaur ,&nbsp;Arun Kumar ,&nbsp;Ghulam Mehdi Dar ,&nbsp;Nimisha ,&nbsp;Abhay Kumar Sharma ,&nbsp;Pinki Bera ,&nbsp;Bhawna Mahajan ,&nbsp;Atri Chatterjee ,&nbsp;Sundeep Singh Saluja","doi":"10.1016/j.neuroscience.2025.05.021","DOIUrl":"10.1016/j.neuroscience.2025.05.021","url":null,"abstract":"<div><div>Alzheimer’s disease (AD) is the most prevalent form of dementia worldwide. It is a multifaceted condition resulting from interplay of genetic mutations (e.g., <em>APP, PSEN1, PSEN2</em>) that account for less than 5% of cases, several genetic risk variants such as <em>APOE4, TREM2, CD33, CLU, SORL1,</em> and <em>CR1</em> contribute to disease susceptibility and epigenetic factors, which may mediate the influence of environmental and lifestyle factors over time. Other critical contributors such as aging, protein misfolding and aggregation (amyloid-β and tau), molecular and transcriptomic dysregulation affecting neuronal function, and modifiable lifestyle factors like diet, physical activity, and environmental exposures presents challenges in accurate diagnosis and management. Research has predominantly focused on the diverse molecular pathways in the pathogenesis of AD, with particular attention given to the amyloidogenic pathways, tau pathology, calcium signalling, endolysosomal pathways, and others, whether they are directly or indirectly involved. Apart from these known molecular pathways, miRNAs are gaining attention as important regulators, which have been implicated in moderating the expression of mRNA targets involved in various processes associated with the clearance of pathogenic β-amyloid proteins. A mounting body of research suggests the possible role of gut microbiota in AD which regulates inflammation, neurotransmitters, and the blood–brain barrier. Gut dysbiosis can trigger neuroinflammation and amyloid-beta aggregation, making microbiome composition a potential early AD biomarker. This review aims to explore briefly the diverse risk encompassing genetic polymorphisms, altered molecular pathways implicated in AD pathogenesis, miRNA regulatory mechanisms, and the potential impact of gut microbiota on AD risk.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 217-227"},"PeriodicalIF":2.9,"publicationDate":"2025-05-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079272","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A novel predictive model constructed based on the combination of SIX3OS1, miR-511-3p and RBP4 for stroke-prost cognitive impairment","authors":"Te Wang ,&nbsp;Rui Wang ,&nbsp;Junsheng Zeng ,&nbsp;Wei Zhao ,&nbsp;Yan Liu ,&nbsp;Hui Xiao","doi":"10.1016/j.neuroscience.2025.05.020","DOIUrl":"10.1016/j.neuroscience.2025.05.020","url":null,"abstract":"<div><h3>Background</h3><div>The incidence of stroke is increasing year by year. Post-stroke cognitive impairment (PSCI) is one of the most serious complications of stroke, which lacks effective early prediction tools.</div></div><div><h3>Methods</h3><div>A total of 147 S patients and 80 healthy individuals were enrolled, with corresponding clinical data and serum samples collected. The expression of SIX3OS1, miR-511-3p and retinol binding protein 4 (RBP4) were detected by reverse transcription-quantitative PCR (RT-qPCR). These data were then used to build a logistic regression model, and receiver operating characteristic (ROC) curves were drawn to evaluate the clinical value of SIX3OS1, miR-511-3p and RBP4.</div></div><div><h3>Results</h3><div>Our study found that SIX3OS1, miR-511-3p and RBP4 abnormally expressed in stroke and the area under the curve (AUC) of the combined detection of these was 0.965. Additionally, ROC curve showed that the AUC of SIX3OS1, miR-511-3p and RBP4 combined was 0.955 for the prediction of PSCI. Based on SIX3OS1 (X1), miR-511-3p (X2) and RBP4 (X3), we developed multivariate logistic regression predictive model, <em>p</em> = 1/ [1 + e (7.190–5.400X1 + 11.109X2–3.585X3)].</div></div><div><h3>Conclusion</h3><div>Serum SIX3OS1, miR-511-3p and RBP4 are candidate diagnostic biomarker in stroke and PSCI patients, which achieve good diagnostic performance when used in combination with other factors, and may have the potential to be novel therapeutic targets for PSCI.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"579 ","pages":"Pages 47-53"},"PeriodicalIF":2.9,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Evidence of a hormetic-like cytoprotective effect by erythropoietin in the SH-SY5Y cell model of oxygen-glucose deprivation","authors":"Alejandra Guadalupe Marín-López,&nbsp;Rafael de Jesús Macias-Velez,&nbsp;José Jaime Jarero-Basulto,&nbsp;Martha Catalina Rivera-Cervantes","doi":"10.1016/j.neuroscience.2025.05.018","DOIUrl":"10.1016/j.neuroscience.2025.05.018","url":null,"abstract":"<div><div>Erythropoietin is recognized as a neuroprotective agent for the brain and it has been suggested that may have a biphasic hormetic-like response, with low to intermediate doses providing greater cytoprotective benefits, whereas high doses have been associated with undesirable side effects related to its systemic application; however, it is unknown whether this occurs in brain and what mechanisms could be implicated. This study investigated the potential hormetic effects of recombinant human erythropoietin (rhEPO) on SH-SY5Y cells subjected to oxygen and glucose deprivation (OGD) and reoxygenation (reox) injury. We developed an <em>in vitro</em> protocol to investigate the rhEPO's hormetic effect under conditions similar to ischemic stroke. Cell vitality assays were conducted, and the gene and protein expression of EPO, erythropoietin receptor (EPOR), β-common receptor (βcR), and Bcl-xL were analyzed. We found that all evaluated doses of rhEPO exhibited a cytoprotective effect on cells treated during the 24 h reox period. Notably, the intermediate 50 IU/mL dose showed significantly higher cell vitality than the high 100 IU/mL dose (p &lt; 0.05), suggesting a potential hormetic-like effect. Interestingly, both EPO and EPOR mRNA levels increased after OGD, followed by an increase in EPOR protein levels after the reox period. However, no changes were observed in EPOR or Bcl-xL mRNA expression after 4 and 8 h of rhEPO treatment during reox. Finally, βcR mRNA expression was not detected in any group. While further research is needed, these results suggest that rhEPO treatment may exert a hormetic-like effect and offer cytoprotection against ischemic stroke-like injury.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 114-122"},"PeriodicalIF":2.9,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144068248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"YOLOv11-Based quantification and temporal analysis of repetitive behaviors in deer mice","authors":"Farhan Augustine ,&nbsp;Shawn M. Doss ,&nbsp;Ryan M. Lee ,&nbsp;Harvey S. Singer","doi":"10.1016/j.neuroscience.2025.05.017","DOIUrl":"10.1016/j.neuroscience.2025.05.017","url":null,"abstract":"<div><div>Detailed temporal dynamics of deer mouse (<em>Peromyscus maniculatus bairdii</em>) behavior remain poorly characterized. This study presents an integrated automated system combining YOLOv11 deep learning for direct behavior classification, post-processing for bout reconstruction, and a comprehensive temporal analysis suite tailored for deer mice. YOLOv11 performs frame-by-frame classification of key whole-body behaviors (e.g., Exploration, Grooming, Rearing types) using bounding boxes, bypassing initial kinematic feature engineering. This methodology facilitates objective, high-throughput quantification of behavior frequency, duration, and complex temporal organization, including transition patterns and sequential structure revealed through analyses like transition probabilities, behavior sequence mining, and lead-follower behavior relationships. In addition to describing a new methodology, this study provides initial baseline temporal data for deer mice, a powerful suite of analyses for future <em>Peromyscus</em> studies evaluating natural variation and experimental manipulations, or for use in other movement disorder models. In conclusion, the described YOLOv11-based system provides an efficient, reliable, and accessible methodology for both detailing behavioral activity and enhancing investigations of temporal dynamics in deer mice and other animal models.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 343-356"},"PeriodicalIF":2.9,"publicationDate":"2025-05-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144079273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Investigating potential molecular mechanisms of antiepileptic drug-induced depression through network toxicology and molecular docking","authors":"Xunan Ji ,&nbsp;Bingtao Jiang ,&nbsp;Ying Chang ,&nbsp;Zuqing Lu ,&nbsp;Yuanjiang Zhou ,&nbsp;Lili Wang ,&nbsp;Yanchen Liu ,&nbsp;Xiong Zhang ,&nbsp;Faping Yi ,&nbsp;Mingyuan Tian ,&nbsp;Jian Zhou","doi":"10.1016/j.neuroscience.2025.05.015","DOIUrl":"10.1016/j.neuroscience.2025.05.015","url":null,"abstract":"<div><div>Antiepileptic drugs (AEDs) are essential for epilepsy management but frequently induce adverse effects including depression. This study employs network toxicology and molecular docking to investigate molecular mechanisms underlying AED-induced depression. After identifying eight AEDs (Topiramate, Zonisamide, Phenobarbital, Primidone, Levetiracetam, Gabapentin, Tiagabine, and Perampanel) potentially associated with depression via a literature review, further analysis integrating drug and disease target databases revealed 25 targets relevant to AED-induced depression. Gene ontology analysis conducted with DAVID, indicated that biological processes including synaptic transmission and plasticity, glutamate receptor signaling, and calcium ion regulation are critical to this phenomenon. KEGG pathway analysis demonstrated that AEDs primarily affect neuroactive ligand-receptor interactions, which are essential for synaptic transmission and plasticity, and disrupt calcium, cAMP, MAPK, and oxytocin signaling pathways. These pathways are vital for the proper functioning of the central nervous system, as neurotransmitter interactions activate crucial signaling pathways. The drug-target interaction network analysis identified 12 candidate targets that directly interact with the eight AEDs, and GeneMANIA network expansion provided deeper insights into their functional associations. Molecular docking results revealed the interactions between AEDs and their respective direct targets, with Zonisamide exhibiting significant potential to induce depression through strong binding to multiple targets. In vitro experiments demonstrated that Zonisamide treatment elevated the expression and activity of MAOA protein in the prefrontal cortex of mice, which may influence monoaminergic neurotransmission through MAO pathway regulation, potentially leading to depression. Collectively, this integrated approach elucidates the mechanisms underlying AED-induced depression, thereby establishing a foundation for future therapeutic strategies.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 25-36"},"PeriodicalIF":2.9,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143942133","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of contact with a dog on prefrontal brain activation in patients in a minimally conscious state: A controlled crossover trial","authors":"Rahel Marti ,&nbsp;Milena Petignat ,&nbsp;Valentine L. Marcar ,&nbsp;Jan Hattendorf ,&nbsp;Martin Wolf ,&nbsp;Margret Hund-Georgiadis ,&nbsp;Karin Hediger","doi":"10.1016/j.neuroscience.2025.05.014","DOIUrl":"10.1016/j.neuroscience.2025.05.014","url":null,"abstract":"<div><div>The first studies have indicated that animal-assisted therapy benefits patients in a minimally conscious state (MCS), but the evidence is scarce. It is thus crucial to understand how these patients react to animal contact. This study aimed to measure the prefrontal brain activation in MCS patients during contact with a dog compared with a plush animal using functional near-infrared spectroscopy (fNIRS). We conducted a controlled crossover trial with 22 MCS patients, who each participated in six sessions. Patients interacted with a dog in three sessions and with a plush animal in three control sessions. Each session consisted of five 2-minute phases with a neutral phase at the start and the end. The contact intensity with the dog or the plush animal increased from the second to the fourth phase. The fNIRS parameters did not differ between the conditions. The mean heart rate was significantly higher in the dog condition than in the control. In both conditions, prefrontal brain activation, mean heart rate, and one heart rate variability parameter increased with the increased intensity of contact with the dog and plush animal. The results show that MCS patients react with the same prefrontal brain activation during contact with a dog and a plush animal but have increased heart rate in contact with the dog, indicating physiological arousal. These findings suggest that the incorporation of animals into MCS therapy has the potential to stimulate patients, thereby facilitating greater participation. However, more research is needed to understand the effects of animals on brain activation.</div></div>","PeriodicalId":19142,"journal":{"name":"Neuroscience","volume":"577 ","pages":"Pages 175-189"},"PeriodicalIF":2.9,"publicationDate":"2025-05-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143971996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}