BMC Neuroscience[JOURNAL]
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200 papers
Effects of different transcranial magnetic stimulation coil types on phosphene thresholds and their association with motor cortex excitability.
Fidancı H, Alaydın HC, Cöddü C … +2 more , Yakıcı İ, Arlıer Z
BMC Neurosci · 2025 Oct · PMID 41102626 · Full text
BACKGROUND: Phosphenes can be induced by applying transcranial magnetic stimulation (TMS) to the visual cortex. Since multiple factors influence phosphene perception, this study aimed to examine the effects of different...
BACKGROUND: Phosphenes can be induced by applying transcranial magnetic stimulation (TMS) to the visual cortex. Since multiple factors influence phosphene perception, this study aimed to examine the effects of different TMS coil types on phosphene thresholds (PTs). Additionally, the relationship between PT and motor cortex excitability was explored. METHODS: In Session 1, TMS was applied to the left visual cortex of 22 healthy individuals using a round coil and a figure-eight coil, and PT was recorded. Resting motor threshold (RMT), active motor threshold (AMT), and short-interval intracortical inhibition (SICI) were assessed by stimulating the left motor cortex. After 5–7 days, the visual cortex was stimulated again in Session 2 with the same healthy individuals. RESULTS: In Session 1, the mean PTs obtained with the round and figure-eight coils were 39.71 ± 9.67% (n = 17) and 53.93 ± 14.26% (n = 15), respectively (p = 0.001). In Session 2, the mean PTs were 37.83 ± 11.34% and 51.53 ± 14.03% (p = 0.001) for the round and figure-eight coils, respectively. The intraclass correlation coefficients for PTs across studies were 0.832 for the round coil and 0.591 for the figure-eight coil. No significant correlation was found between PT and AMT, RMT, or SICI. CONCLUSION: PTs were lower with the round coil than with the figure-eight coil. The reliability of PTs can be considered good for round coil and moderate for figure-eight coil. Additionally, the findings suggested that motor cortex and visual cortex excitability are different entities.
Dexmedetomidine pretreatment improves postsurgical delay in neurocognitive recovery in aged mice by inhibiting hippocampal microglial activation via activation of cholinergic anti-inflammatory pathways.
Zhang Q, Hao S, Wang G … +8 more , Liu C, Wang G, Zhang J, Zhao J, Li X, Li J, Wu J, Wang X
BMC Neurosci · 2025 Oct · PMID 41094378 · Full text
BACKGROUND: Perioperative use of dexmedetomidine (DEX) reduces the incidence of Delayed Neurocognitive Recovery (DNR) in elderly patients, though mechanisms remain unclear. This study investigated whether DEX improves DN...
BACKGROUND: Perioperative use of dexmedetomidine (DEX) reduces the incidence of Delayed Neurocognitive Recovery (DNR) in elderly patients, though mechanisms remain unclear. This study investigated whether DEX improves DNR by inhibiting microglial activation and explored the cholinergic anti-inflammatory pathway's role. METHODS: An exploratory laparotomy model was established in aged C57BL/6J mice, with preoperative treatment using DEX or DEX combined with α-bungarotoxin. Cognitive function was assessed through the novel object recognition (NOR) and Morris water maze (MWM) tests, while immunofluorescence was used to observe microglial morphology, and qPCR and ELISA were employed to detect inflammatory factor expression. RESULTS: DEX pretreatment significantly reduced the escape latency of aged mice on postoperative days 3-5 (50.50 ± 3.73 vs. 55.01 ± 4.01, P = 0.04; 36.36 ± 4.31 vs. 43.42 ± 5.64, P = 0.01; 27.00 ± 3.94 vs. 34.50 ± 5.54, P = 0.006), increased number of times crossing the previous platform location (2.50 ± 1.31 vs. 1.08 ± 0.90, P = 0.02), and percentage of dwell time in the target quadrant (37.87 ± 9.66 vs. 25.00 ± 4.48, P < 0.001). DEX pretreatment also reduced the expression of pro-inflammatory cytokines in the hippocampus (TNF-α, 604.10 ± 165.40 vs. 915.30 ± 97.64, P = 0.002; IL-6, 145.30 ± 12.11 vs. 176.50 ± 16.15, P = 0.002; IL-1β, 59.68 ± 4.29 vs. 68.73 ± 3.11, P = 0.001) of aged mice postoperatively, as well as in the spleen and serum. Additionally, DEX pretreatment reduces microglia count (96.60 ± 11.84 vs. 136.20 ± 32.62, P = 0.05), fluorescence (0.96 ± 0.06 vs. 1.10 ± 0.02, P < 0.001), morphology (7.20 ± 2.17 vs.12.80 ± 2.28, P = 0.002) in aged mice post-surgery. Pre-administration of α-bungarotoxin before DEX pretreatment partially reversed these effects. CONCLUSIONS: DEX pretreatment ameliorated DNR in aged mice is related to inhibition of microglial activation, which was at least partially attributed to activation of the cholinergic anti-inflammatory pathway.
Long-term neprilysin gene transfer is associated with reduced levels of intracellular Abeta and behavioral improvement in APP transgenic mice.
Spencer B, Marr RA, Rockenstein E … +7 more , Crews L, Adame A, Potkar R, Patrick C, Gage FH, Verma IM, Masliah E
BMC Neurosci · 2025 Oct · PMID 41073908 · Full text
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Characterisation of the expression of P2X7 receptor, cancer stem cell markers and immunological mediators in human high-grade gliomas.
Kan LK, Drill M, Muscat A … +12 more , Sanfilippo P, Sequeira RP, Jayakrishnan PC, Vo A, Wong NC, Todaro M, McLean C, Drummond KJ, Hunn M, Williams DA, O'Brien TJ, Monif M
BMC Neurosci · 2025 Oct · PMID 41034696 · Full text
INTRODUCTION: Glioblastoma is the most aggressive primary brain cancer. It is considered an 'immunologically cold' tumour where immune infiltrates are polarised to drive immunosuppression-and therefore tumour proliferati...
INTRODUCTION: Glioblastoma is the most aggressive primary brain cancer. It is considered an 'immunologically cold' tumour where immune infiltrates are polarised to drive immunosuppression-and therefore tumour proliferation. An important driver of neuroinflammation in glioma is the purinergic P2X7 receptor (P2X7R). While much of the complex glioma microenvironment has been characterised, studies expounding the associations between various cytokines/chemokines, immune cell markers, P2X7R expression and glioma stemness are lacking. Here we aimed to characterise the mRNA expression profiles of various tumour markers, and common 'pro-' and 'anti-tumour' inflammatory mediators, and correlate this to P2X7R expression in human high-grade glioma samples compared to 'healthy' non-tumour post-mortem brain. METHODS: High grade gliomas were collected from 34 patients undergoing routine tumour resection surgery and compared to 12 'healthy' post-mortem controls. High throughput qPCR was performed on extracted RNA converted to cDNA to examine a custom-made panel of 38 tumour and immune related genes. RESULTS: Markers of innate immunity including CD68, S100A9, HLADR, NLPR3, interleukin (IL) 1β, IL-6, TNFα and NF-κB were significantly increased in human derived glioblastoma samples compared to healthy control brain. P2X7R was also upregulated in the glioma microenvironment and its expression was linked to the expression of VEGFB, MMP9, PCNA, IL-4 and IL-8. The level of expression of P2X7R was not associated with overall survival in high grade gliomas. DISCUSSION: Collectively, this study confirms the significant overexpression of P2X7R in human high-grade gliomas as well as highlights the presence of a multidirectional neuroinflammatory milieu in which both tumour-promoting and tumour-suppressive genes are overexpressed.
Publisher Correction: Mir-199a-3p aggravates neuroinflammation in an Alzheimer's disease transgenic mouse model by promoting M1-polarization microglia.
Wang C, Bu X, Cao M … +7 more , Lian Y, Ling H, You M, Yi J, Gao X, Wu D, Li Y
BMC Neurosci · 2025 Sep · PMID 40954500 · Full text
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Investigating topological alterations in procedural memory network across neuropsychiatric disorders using rs-fMRI and graph theory.
Mohammadkhanloo M, Sharini H, Yousefpour M … +1 more , Pooyan M
BMC Neurosci · 2025 Sep · PMID 40898026 · Full text
BACKGROUND: Cognitive network dysfunction represents a core pathophysiological feature across major neuropsychiatric disorders, including Attention Deficit Hyperactivity Disorder (ADHD), bipolar disorder (BD), and schizo...
BACKGROUND: Cognitive network dysfunction represents a core pathophysiological feature across major neuropsychiatric disorders, including Attention Deficit Hyperactivity Disorder (ADHD), bipolar disorder (BD), and schizophrenia (SZ). The procedural memory network (PMN), involving cortico-striatal-cerebellar circuits, is vital for skill learning and automatic cognition. However, its topological changes and link to cognitive impairments have not been studied across major neuropsychiatric disorders. METHODS: This study analyzed resting-state functional MRI (rs-fMRI) data from 40 individuals with ADHD, 49 with BD, 50 with SZ, and 50 healthy controls (HCs). PMN was defined using 34 regions of interest (ROIs) from Harvard-Oxford Atlas, with graph theory measures calculated for all regions. Significant network disruptions emerged, showing altered local efficiency (LE), average path length (APL), and degree (P < 0.05) across groups. RESULTS: Key findings show that in ADHD, increased APL in left cerebellar lobule VII indicates disrupted information flow and emotional processing, while decreased connectivity in the right claustrum may impair integration and working memory. In BD, reduced LE in right cerebellar lobule II is linked to attention and motor control deficits; increased APL in lobules I and VIII suggests disrupted network communication and emotional processing; and decreased connectivity in the right subthalamic nucleus and lobule VIII may contribute to mood swings and attention problems. In SZ, decreased LE in right putamen and left cerebellar lobule VIII relates to working memory and emotional processing deficits; reduced APL in right caudate and cerebellar lobule II implies more effort for regional communication; and increased connectivity in the caudate and right cerebellar lobules I and II likely reflects compensatory or pathological hyperactivity. Comparisons indicate SZ shows increased connectivity in the claustrum and cerebellar lobule I, unlike ADHD which shows decreases in these areas; SZ has lower network efficiency but higher caudate connectivity than BD, which has more cerebellar and subthalamic disruptions; and BD shows decreased connectivity in the claustrum and subthalamic nucleus compared to ADHD, which has more cerebellar and attention network changes. CONCLUSION: These findings suggest that the PMN, particularly its segregation and integration properties, plays a key role in explaining cognitive deficits in ADHD, BD, and SZ. CLINICAL TRIAL NUMBER: Not applicable.
SRT1720 ameliorates LPS-induced depressive-like behaviors in mice and activates Parkin-mediated mitophagy.
Sun L, Li C, Shi J … +4 more , Zeng W, Wu L, Wan S, Wang Y
BMC Neurosci · 2025 Aug · PMID 40885954 · Full text
BACKGROUND: Emerging evidence suggests a connection between mitophagy-a key mitochondrial quality control mechanism-and depression. Furthermore, sirtuin 1 (SIRT1), a NAD⁺-dependent deacetylase, has been implicated in the...
BACKGROUND: Emerging evidence suggests a connection between mitophagy-a key mitochondrial quality control mechanism-and depression. Furthermore, sirtuin 1 (SIRT1), a NAD⁺-dependent deacetylase, has been implicated in the pathophysiology of depression, though its precise role remains elusive. This study aimed to investigate how SIRT1 modulates depressive-like behaviors in mice and to determine whether mitophagy mediates this process. METHODS: Male BALB/c mice were administered lipopolysaccharide (LPS) to mimic depressive-like behaviors. The treatment group received a pre-administration of SRT1720 (50 mg/kg, i.p.), a specific SIRT1 activator. Depressive-like behaviors were assessed by sucrose preference test (SPT) and forced swimming test (FST). Additionally, hippocampal neuronal and mitochondrial ultrastructure was detected via transmission electron microscopy (TEM), and mitophagy-related protein expression was examined by western blotting. RESULTS: Results demonstrated that activation of SIRT1 significantly mitigated LPS-induced depressive-like behaviors in mice. Moreover, it was observed that SIRT1 activation protected against LPS-induced neuronal and mitochondrial damage in the hippocampus. TEM analysis revealed a marked increase in hippocampal autophagosomes following SIRT1 activation, accompanied by significantly elevated expression of LC3II and Parkin, suggesting enhanced mitophagy. In vitro experiment using HT-22 cells provided additional evidence that SIRT1 activation ameliorated LPS-induced mitochondrial dysfunction and promoted mitophagy via Parkin-mediated pathway. CONCLUSIONS: These findings suggested that activation of SIRT1 could alleviate depressive-like behaviors in mice following LPS challenge, potentially through a Parkin-dependent mitophagy mechanism.
Distinct neural circuits processing pleasant and unpleasant sounds: an fMRI-based approach.
Aldhafeeri FM
BMC Neurosci · 2025 Aug · PMID 40859135 · Full text
BACKGROUND: Investigating how the human brain processes the emotional valance of sounds is critical for understanding sensory, emotional, and motor integration at the neurobiological level. The current study utilized fun...
BACKGROUND: Investigating how the human brain processes the emotional valance of sounds is critical for understanding sensory, emotional, and motor integration at the neurobiological level. The current study utilized functional magnetic resonance imaging (fMRI) to investigate the differential brain activation patterns elicited by pleasant, unpleasant, and neutral sounds from the International Affective Digital Sounds (IADS-2) collection. Thirty healthy volunteers listened to these sounds under fMRI, followed by post-scan ratings of valence (pleasant versus unpleasant) and arousal (calm versus exciting). RESULTS: Average ratings did not differ from IADS-2 norms. Pleasant sounds significantly activated brain regions implicated in reward and positive affect, including the mPFC, ventral anterior cingulate cortex, and inferior frontal gyrus, compared to neutral sounds. Alternatively, unpleasant sounds elicited stronger and more widespread activation, particularly in the amygdala, nucleus accumbens, insula, and cerebellum, regions associated with negative affect and aversive learning. CONCLUSION: These results demonstrate the pivotal contributions of the amygdala in identifying unpleasant stimuli and of the mPFC in assessing pleasant auditory inputs, expand our current understanding of affective regulation at the neural circuit level, and provide a foundation for the development of sound-based interventions to treat auditory-emotional disorders such as misophonia and anxiety. CLINICAL TRIAL NUMBER: Not applicable.
Comparative study of F-labeled PET radiopharmaceuticals in an Alzheimer's disease mouse model.
Park BN, Kim SM, An YS
BMC Neurosci · 2025 Aug · PMID 40877783 · Full text
BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is the leading cause of dementia, characterized by memory loss, cognitive decline, and significant social and economic burdens. Despit...
BACKGROUND: Alzheimer's disease (AD) is a progressive neurodegenerative disorder that is the leading cause of dementia, characterized by memory loss, cognitive decline, and significant social and economic burdens. Despite extensive research into amyloid positron emission tomography (PET) radiopharmaceuticals, the effectiveness of various F-labeled tracers for imaging amyloid plaques in AD mouse models remains uncertain. This study aimed to evaluate the performance of three radiopharmaceuticals-F-florbetaben (FBB), F-flutemetamol (FMM), and F-florapronol (FPN)-in differentiating amyloid deposition in AD and control mice. RESULTS: F-FMM and F-FBB demonstrated significantly higher standardized uptake value ratios (SUVRs) in AD mice than in controls. For F-FBB, the mean SUVR in AD mice was 1.06, significantly higher than the 0.81 in controls (p < 0.001). Similarly, F-FMM showed a mean SUVR of 0.97 in AD mice compared to 0.94 in controls (p = 0.024). In contrast, F-FPN did not show significant SUVR differences between AD and control groups (p = 0.071). Comparative analysis revealed that F-FBB exhibited a significantly greater SUVR difference between AD and control groups compared to F-FMM (p < 0.001). CONCLUSIONS: F-FBB emerged as the most effective radiopharmaceutical for imaging amyloid deposition in AD mouse models, providing superior differentiation between AD and control groups. These findings support the optimization of amyloid PET tracers for preclinical studies, facilitating advancements in Alzheimer's research. CLINICAL TRIAL NUMBER: Not applicable.
Threat context impairs cognitive control of neutral words processing in social anxiety individuals: evidence from ERP and theta oscillations.
Zhao H, Si F, Meng H … +4 more , Yang H, Sun D, Peng L, Cao J
BMC Neurosci · 2025 Aug · PMID 40877774 · Full text
BACKGROUND: Social anxiety (SA) is characterized by cognitive control impairments, particularly in the processing of threat, yet how threat-laden environments modulate cognitive control over neutral stimuli remains uncle...
BACKGROUND: Social anxiety (SA) is characterized by cognitive control impairments, particularly in the processing of threat, yet how threat-laden environments modulate cognitive control over neutral stimuli remains unclear. This study examined whether threat context impairs the processing of neutral words in individuals with high social anxiety (HSA) through electrophysiological and oscillatory dynamics. METHODS: A total of 151 participants (HSA vs. low social anxiety, LSA) completed a Stroop task in two conditions: (1) threat context (neutral words intermixed with social threat words), and (2) neutral-only (neutral words only). Behavioral responses (RTs), ERP (N2, N450, SP), and frontal-midline theta oscillations were analyzed. RESULTS: Threat context significantly prolonged RTs in HSA compared to LSA individuals. ERP data revealed that LSA individuals exhibited larger N450 and reduced SP under threat than under neutral-only conditions, indicating efficient conflict resolution. However, LSA individuals showed blunted N450 but amplified SP, suggesting prolonged attentional engagement with neutral stimuli in threat contexts. Time-frequency analyses further demonstrated that LSA participants increased frontal theta power in the threat context, whereas HSA individuals displayed suppressed theta activity, reflecting impaired top-down cognitive control. Threat contexts contaminate the processing of neutral stimuli in HSA individuals, marked by attenuated conflict detection (N450), increased attention engagement (SP), and deficient theta-mediated control. CONCLUSION: These findings indicate that threat context impairs cognitive control of neutral word processing in HSA individuals when threat is possible, bridging cognitive and clinical models of attentional dysregulation. CLINICAL TRIAL NUMBER: Not applicable.
Altered theta oscillations in basolateral amygdala and ventral hippocampus related to social defeat.
Wang X, Liu Y, He F … +8 more , Guo D, Liu A, Bai W, Yang H, Xu X, Zheng X, Xu X, Liu T
BMC Neurosci · 2025 Aug · PMID 40866806 · Full text
BACKGROUND: Depression is a prevalent mental disorder, and prolonged exposure to social defeat is a major contributing factor in the onset of depression. Repeated social defeat stress (RSDS) is a commonly used animal mod...
BACKGROUND: Depression is a prevalent mental disorder, and prolonged exposure to social defeat is a major contributing factor in the onset of depression. Repeated social defeat stress (RSDS) is a commonly used animal model for depression, significantly impacting on the pathogenesis of depression-related to social disorders. The basolateral amygdala (BLA) and the ventral hippocampus (vHPC) are critical brain regions involved in RSDS-induced social behavioral disorders, but the specific neural oscillations occurring in these regions following social defeat remain unclear. METHODS: Using simultaneous multi-electrode recordings, we captured local field potentials (LFPs) from BLA and vHPC while the stressed mice underwent a social interaction test. Power spectral analysis and Amplitude transform entropy were respectively applied to assess social defeat-induced alterations in neural oscillatory activity and directional inter-regional communication. RESULTS: Our study demonstrated that repeated social defeat induces social avoidance and depression-like behaviors. Notably, the power spectral analysis within the BLA and vHPC revealed statistically differences in the theta band (4-12 Hz) between control and RSDS groups, particularly during the With CD1 phase in the 0-3 s stage, when mice entered the social interaction zone, compared to the - 3 -0 s stage prior to enter the zone. Moreover, machine learning analysis successfully classified control and RSDS groups based on neural oscillatory activity in the BLA and vHPC. Finally, ketamine treatment was found to reduce social avoidance and depressive-like behaviors, as well as enhance theta oscillation in the BLA and vHPC. CONCLUSION: These results suggest that social defeat alters theta oscillations in the BLA and vHPC, highlighting potential therapeutic avenues for addressing depression-related social dysfunction.
Hybrid molecule SA-10 and its PLGA nanosuspension protect human and rodent retinal ganglion cells against neuronal injury.
Pham JH, Zhang W, Le KT … +13 more , Kodati B, Amankwa CE, DebNath B, Johnson GA, Bui TT, Gitter RY, Gutierrez JP, Hatfield BR, Satyal R, Sinnott ER, Krishnamoorthy RR, Acharya S, Stankowska DL
BMC Neurosci · 2025 Aug · PMID 40836213 · Full text
BACKGROUND: Glaucoma is a leading cause of blindness characterized by retinal ganglion cell (RGC) degeneration. SA-10, a dual-acting compound with ROS scavenging and NO-donating properties, was evaluated to enhance RGC s...
BACKGROUND: Glaucoma is a leading cause of blindness characterized by retinal ganglion cell (RGC) degeneration. SA-10, a dual-acting compound with ROS scavenging and NO-donating properties, was evaluated to enhance RGC survival and function in models of oxidative stress, ischemia/reperfusion (I/R) injury, and neurotrophic factor (NF) deprivation. METHODS: SA-10-loaded nanoparticles (SA-10-NP) with a size of 279.6 ± 20.9 nm, polydispersity index of 0.34, and encapsulation efficiency of 80.6% were synthesized and tested for sustained release over 28 days. I/R injury was induced by elevating intraocular pressure to 120 mmHg for 60 min in C57BL/6J mice, followed by SA-10-NP treatment (1% w/v). Retinal ganglion cell function and survival were evaluated using PERG and PVEP. Oxidative stress in primary RGCs and retinal explants was induced using endothelin-3 (ET-3), and the effects of SA-10 (10 µM) on ROS levels were assessed. In ex vivo human retinal explants (HREs), SA-10 treatment effects on oxidative stress markers NRF2 and HMOX1 were analyzed. RESULTS: SA-10-NP improved PERG amplitudes (112.96% in females, p < 0.01) and PVEP amplitudes (67.53% in females, p < 0.01), preserving RGC density in both central and mid-peripheral regions. Immunohistochemistry showed upregulation of Hmox1 and downregulation of TNF-α in the SA-10-NP-treated group. SA-10 significantly reduced ROS levels in primary RGCs and retinal explants exposed to endothelin-3 (ET-3), decreasing fluorescence intensity by 25.9% (p < 0.01) and 14.7% (p < 0.0001), respectively. SA-10 upregulated oxidative stress markers (NRF2 and HMOX1) and enhanced RGC survival in NF-deprived HREs. CONCLUSIONS: SA-10 demonstrated significant ROS reduction and preserved RGC survival and function in both I/R mouse models and HREs, with immunohistochemistry confirming upregulation of Hmox1 and downregulation of TNF-α in the SA-10-NP-treated group. SA-10-NP provided sustained drug delivery and bioavailability, showcasing strong neuroprotective effects and offering a potential therapeutic strategy for glaucomatous optic neuropathy and other neurodegenerative conditions.
Visual change-related brain potentials elicited by changes in doll hair color in school-aged children.
Kozaki M, Mizuno R, Suzuki M … +3 more , Koike Y, Doi N, Inui K
BMC Neurosci · 2025 Aug · PMID 40790464 · Full text
Change-related brain responses are specifically elicited when the regularity of a continuous sensory stimulus is disrupted and are recorded by electroencephalography or magnetoencephalography. These responses are one of...
Change-related brain responses are specifically elicited when the regularity of a continuous sensory stimulus is disrupted and are recorded by electroencephalography or magnetoencephalography. These responses are one of the higher brain functions representing memory-based comparison processes between the current and previous sensory states. The present study aimed to record change-related visual evoked potentials in children aged 6-10 years. Pictures of a doll were presented for 1.5 s, and participants were given the task of quickly pressing a button when glasses appeared on the doll, which occurred in 5% of trials. In the remaining 95% of trials, one third used pictures with no change, while the others used a similar picture but with a hair color change, from rose to yellow or from brown to pink, 1000 ms after the stimulus onset. The results obtained showed that in all 37 children tested, the abrupt change in hair color elicited clear biphasic responses consisting of occipital positivity at approximately 130 ms (P130) followed by negativity at 250 ms. The P130 latency decreased linearly up to 92 months of age and remained stable thereafter, suggesting that this method may serve as an objective tool for assessing brain development in children. In addition, it could potentially be used to evaluate whether and how specific toys influence neural processing at different developmental stages.
Effects of subanesthetic dose of ketamine on motor and cognitive outcomes of harmaline-induced essential tremor model: a focus on Lingo-1 and inflammatory pathways.
Ilaghi M, Pirmoradi Z, Esmaili Z … +7 more , Hosseinalipour S, Rouhi L, Soltanizadeh A, Nakhaie M, Sharififar K, Razavinasab M, Shabani M
BMC Neurosci · 2025 Aug · PMID 40751128 · Full text
INTRODUCTION: Essential tremor (ET) is a common neurodegenerative disorder characterized by action tremors and various non-motor symptoms. This study investigated the potential therapeutic effects of ketamine, an NMDA re...
INTRODUCTION: Essential tremor (ET) is a common neurodegenerative disorder characterized by action tremors and various non-motor symptoms. This study investigated the potential therapeutic effects of ketamine, an NMDA receptor antagonist with known GABA modulatory and anti-inflammatory properties, in a harmaline-induced model of ET in mice. We also evaluated the changes in expression of inflammatory interleukin 6 (IL-6) as well as Leucine rich repeat and Immunoglobin-like domain-containing protein 1 (Lingo-1), a prominent gene involved in the pathogenesis of ET. METHODS: Male Swiss Webster mice were divided into four groups: control, harmaline (10 mg/kg), ketamine (8 mg/kg), and harmaline + ketamine. Tremor severity, muscle strength, locomotor activity, anxiety-like behavior, and passive avoidance learning were assessed. Cerebellar expression of Lingo-1 and IL-6 was analyzed using real-time PCR. RESULTS: Ketamine did not significantly reduce harmaline-induced tremors but improved muscle strength deficits in the wire grip test. In the open field test, ketamine normalized some harmaline-induced changes in locomotor activity and grooming behavior. No significant differences were observed in passive avoidance learning across groups. At the molecular level, ketamine did not mitigate the harmaline-induced increase in IL-6 expression, and Lingo-1 expression was not significantly altered by either harmaline or ketamine treatment. CONCLUSION: Our findings suggest that ketamine has limited efficacy in the harmaline ET model, showing some improvements in motor function and anxiety-like behavior but failing to address core tremor symptoms or modulate inflammatory and Lingo-1 pathways. These results highlight the complex nature of ET pathophysiology and the need for further research into targeted therapeutic approaches.
Structural changes of tubulin by interacting with Δ-tetrahydrocannabinol: in-vitro and theoretical studies.
Mohammadkhani M, Jarah M, Gholami D … +2 more , Riazi G, Rezazadeh H
BMC Neurosci · 2025 Jul · PMID 40739185 · Full text
BACKGROUND: There is growing evidence of the contribution of microtubule dynamics to dendritic spine changes, synaptic plasticity, axonal transportation, and cell polarity. Besides, one of the well-studied effects of Can...
BACKGROUND: There is growing evidence of the contribution of microtubule dynamics to dendritic spine changes, synaptic plasticity, axonal transportation, and cell polarity. Besides, one of the well-studied effects of Cannabis on human behavior is memory disability. As Δ-tetrahydrocannabinol (Δ-THC) is the most pivotal chemical of Cannabis, we investigated the effect of Δ-THC on microtubule dynamicity and the structural study of tubulin (microtubule monomer). RESULTS: Our results show that Δ-THC changes microtubule dynamicity compared to the control group. The turbidity assay results demonstrated that Δ-THC reduces microtubule polymerization in a concentration-dependent manner. Circular Dichroism spectroscopy also studied the structural changes of the purified tubulin, which revealed significant changes in the secondary structure of the tubulin. Furthermore, Silico studies predicted one binding site for Δ-THC on β-tubulin. CONCLUSIONS: We concluded that Δ-THC could reduce the microtubule's stability, which may conversely affect brain function by microtubule dynamic changes caused by secondary structural changes of tubulin and preventing tubulin-tubulin interaction.
Valproate-vitamin E co-treatment preserved cortico-callosal white matter integrities in cypermethrin co-exposed pentylene tetrazole induced seizure.
Imam A, Ajibola OE, Akorede AA … +2 more , Ijomone OM, Ajao MS
BMC Neurosci · 2025 Jul · PMID 40739166 · Full text
BACKGROUND: Epilepsy is characterized by recurrent seizures and neurological consequences, which may be associated with impaired myelin and glial integrity, and exacerbated by environmental neurotoxicants. Environmental...
BACKGROUND: Epilepsy is characterized by recurrent seizures and neurological consequences, which may be associated with impaired myelin and glial integrity, and exacerbated by environmental neurotoxicants. Environmental neurotoxicants, such as Cypermethrin (CPM), may heighten these impairments, worsening seizure outcomes. This study investigates the effects of Cypermethrin (CPM) on Pentylenetetrazole (PTZ)-induced seizures and the Vitamin E (Vit E) and valproate (VAP) co-interventions on myelin and glial integrity. METHODS: Histochemical and immunohistochemical analyses for hematoxylin and eosin (H&E), myelin basic protein (MBP), ionized calcium-binding adaptor molecule 1 (IBA1), glial fibrillary acidic protein (GFAP), and oligodendrocyte transcription factor 2 (OLIG-2) were conducted on cerebral white matter and corpus callosum tissues. The density of stained cells and immunoreactivity obtained with ImageJ was subjected to one-way analysis of variance. RESULTS: Immunohistochemistry revealed that cypermethrin exposure in PTZ-induced seizure rats led to marked neuronal, oligodendroglial, and myelin loss, accompanied by substantial glial activation in both cerebral white matter and corpus callosum. Interventional ingestions of VAP and Vit E, especially when combined, substantially reduced both microglial activation and reactive astrogliosis, thereby consequently preventing oligodendrocyte and neuronal loss, thus preserving both cerebral white matter and callosal myelin. CONCLUSIONS: These findings highlight the potential of pyrethroid insecticides to exacerbate the neurological consequences of epilepsy, specifically causing myelin damage via glial activation. Also, the putative therapeutic synergy of antioxidant supplementation in epilepsy and neurotoxicity management was obvious.
Effects of repetitive mechanical tactile stimulation interventions with stationary and moving patterns on paired-pulse depression.
Watanabe H, Kojima S, Otsuru N … +1 more , Onishi H
BMC Neurosci · 2025 Jul · PMID 40713502 · Full text
BACKGROUND: Repetitive somatosensory stimulation (RSS) reduces paired-pulse depression (PPD), reflecting GABAergic inhibition in the primary somatosensory cortex (S1). This effect may vary by tactile stimulation pattern....
BACKGROUND: Repetitive somatosensory stimulation (RSS) reduces paired-pulse depression (PPD), reflecting GABAergic inhibition in the primary somatosensory cortex (S1). This effect may vary by tactile stimulation pattern. Therefore, this study aimed to clarify the effects of RSS intervention with stationary and moving pattern tactile stimulation on PPD. RESULTS: In a crossover study of 15 healthy males, RSS with a stationary pattern showed a non-significant trend toward increased PPD (corrected p = 0.088), while the moving pattern showed no effect. A strong negative correlation was found between baseline PPD and its change rate (r = - 0.837, p < 0.001), indicating that greater baseline S1 inhibition predicted a larger reduction after RSS. CONCLUSION: RSS effects on GABAergic inhibition in S1 depend on the tactile stimulation pattern, emphasizing the importance of tactile stimulus design in modulating somatosensory cortex activity.
Mir-199a-3p aggravates neuroinflammation in an Alzheimer's disease transgenic mouse model by promoting M1-polarization microgliaMir-199a-3p M1.
Wang C, Bu X, Cao M … +7 more , Lian Y, Ling H, You M, Yi J, Gao X, Wu D, Li Y
BMC Neurosci · 2025 Jul · PMID 40707875 · Full text
Chronic neuroinflammation, driven by M1-polarized microglia, is a core pathological mechanism of Alzheimer's disease (AD). Elevated expression levels of miR-199a-3p and pro-inflammatory cytokines were detected in the hip...
Chronic neuroinflammation, driven by M1-polarized microglia, is a core pathological mechanism of Alzheimer's disease (AD). Elevated expression levels of miR-199a-3p and pro-inflammatory cytokines were detected in the hippocampi of AD transgenic mice and in LPS-stimulated BV2 microglial cells. We hypothesized that miR-199a-3p exacerbates neuroinflammation by promoting M1 microglial polarization in AD progression. M1 （AD） 。 AD LPS BV2 miR-199a-3p 。 miR-199a-3p AD M1 。 OBJECTIVE: To explore the role of miR-199a-3p in AD-associated neuroinflammation. miR-199a-3p AD 。 METHODS: AD transgenic (APPswe/PSEN1dE9) mice and LPS-treated BV2 cells were used to assess miR-199a-3p effects in vivo and in vitro. Inflammatory cytokines and markers for microglial cell typing were detected. Transcriptome sequencing was performed on miR-199a-3p-modulated BV2 cells, and the sequencing data were cross-analyzed with public databases to predict miR-199a-3p-mediated pathways.AD （APPswe/PSEN1dE9） LPS BV2 miR-199a-3p 。。 miR-199a-3p BV2 ，， miR-199a-3p 。 RESULTS: Intracerebroventricular administration of miR-199a-3p agomir exacerbated amyloid deposition and impaired cognitive function in AD mice, and promoted microglial polarization toward the M1 phenotype. Conversely, treatment with miR-199a-3p antagomir attenuated AD pathology and suppressed M1 polarization. In LPS treated BV2 cells, miR-199a-3p mimics promoted M1 polarization, while inhibitors reversed this effect. Transcriptome analysis revealed that miR-199a-3p downregulated WDR76, subsequently suppressing cell cycle-associated pathways, IL-17 signaling, and FOXO pathways, resulting in an increase in the proportion of M1 type microglia. miR-199a-3p agomir AD ， M1 。， miR-199a-3p AD M1 。 LPS BV2 ，miR-199a-3p M1 ，。，miR-199a-3p WDR76，、 IL-17 FOXO ， M1 。 CONCLUSION: MiR-199a-3p aggravates neuroinflammation of AD by promoting M1-polarization microglia. These findings highlight miR-199a-3p as a potential therapeutic target for AD.
Anatomical and behavioral characterization of three hemiplegic animal models.
Liu M, Xu L, Cheng G … +3 more , Yang Y, Yang L, Wang Y
BMC Neurosci · 2025 Jul · PMID 40691765 · Full text
BACKGROUND: Hemiplegia is characterized by muscle weakness on one side of the body, often resulting from damage to the brain, spinal cord, or associated nerves. This condition commonly occurs due to strokes, traumatic br...
BACKGROUND: Hemiplegia is characterized by muscle weakness on one side of the body, often resulting from damage to the brain, spinal cord, or associated nerves. This condition commonly occurs due to strokes, traumatic brain injuries (TBI), or spinal cord injuries (SCI), which can damage corticospinal neurons (CSNs) and the corticospinal tract (CST). However, there is still a notable lack of comprehensive studies that systematically characterize the anatomical and behavioral aspects of these hemiplegic animal models. OBJECTIVE: This study aimed to validate and compare existing models of TBI, stroke, and SCI in order to identify the most suitable preclinical hemiplegia models for future research. METHOD: Using viral-based retrograde tracing, we first mapped the cortical distribution of CSNs responsible for hindlimb movement. Anterograde and retrograde viral tracing techniques were then employed to label and evaluate the damage to CSNs and the CST in three models: photothrombotic stroke, Feeney's weight-drop TBI, and T10 hemi-section SCI. We also conducted behavioral tests to assess spontaneous motor function recovery, including open field and rotarod tests for gross motor function, as well as beam walking and irregular ladder walking tasks for assessing skilled motor function. RESULTS: Our findings revealed that the CSNs controlling hindlimb movement are concentrated in the hindlimb region of the primary somatosensory cortex (S1HL). In the TBI and stroke models, there was complete destruction of ipsilateral CSNs in the S1HL and loss of CST fibers governing hindlimb movement. In the SCI model, ipsilateral CST fibers below T10 were also lost. After 8 weeks post-injury, all three groups of hemiplegic mice showed improvements in motor function, with gross motor function returning to normal levels; however, the recovery of skilled motor function was only modest. Notably, the degree of improvement in fine motor skills varied among the hemiplegia models, with mice subjected to brain injury (stroke and TBI) demonstrating significantly greater recovery in fine motor skills compared to those with SCI. CONCLUSION: We confirmed and validated previous hemiplegia models by damaging CSNs or CST controlling hindlimb movement. Post-injury, gross motor function gradually returned to normal levels across all groups, whereas recovery of skilled motor function was limited. Furthermore, there were significant differences in the recovery of skilled motor function between brain injury models and the SCI model. These hemiplegic mouse models are valuable tools for studying post-injury skilled motor functions. CLINICAL TRIAL NUMBER: Not applicable.
A pharmacological and brain imaging study of human vasopressin AVP1BR receptor functional polymorphisms.
Alacreu-Crespo A, Olié E, Manière M … +5 more , Deverdun J, Lebars E, Corbani M, Guillon G, Courtet P
BMC Neurosci · 2025 Jul · PMID 40676548 · Full text
In humans, vasopressin AVP1BR receptor (hV) plays key roles in hypothalamic-pituitary-adrenal (HPA) axis regulation and social behavior. Three hV polymorphisms, rs35369693 (K65N), rs28632197 (R364H) and rs33990840 (G191R...
In humans, vasopressin AVP1BR receptor (hV) plays key roles in hypothalamic-pituitary-adrenal (HPA) axis regulation and social behavior. Three hV polymorphisms, rs35369693 (K65N), rs28632197 (R364H) and rs33990840 (G191R), have been related to psychiatric disorders with altered HPA axis function and social behavior. The aim of this study was to explore hV pharmacological properties as a function of the polymorphism in transfected cells and the brain functioning in an emotional task in volunteers harboring different AVP1BR polymorphisms. Transfection rate, fluorescent imaging and inositol phosphate (IPs) accumulation were evaluated in HEK293 cells that expressed different hV variants: K65/G191/R364 (wild type), G191R, K65N and/or R364H. Brain functional activity was investigated in 35 healthy men with different hV variants during an fMRI implicit emotional recognition paradigm. IPs accumulation after arginine vasopressin stimulation was much reduced in cells expressing hV K65N and/or R364H, and increased in cells expressing G191R. Basal IPs accumulation, transfection rate, and fluorescent binding to plasma membrane were similar for all polymorphisms. During the anger vs. neutral face visualization task, activation of motor areas, visual areas, frontal sub-gyral area, hippocampus, and putamen was higher in homozygotes for the K65/R364 haplotype than in heterozygotes. Analyses did not include participants with the G191 polymorphism because of its low frequency. Different hV polymorphisms could be candidates as biomarkers of psychiatric disorders. Moreover, hV may be a pharmacological target if these polymorphisms are considered.
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