IBRO Neuroscience Reports最新文献_第4页

Medullary dorsal horn neurons activated during voluntary diving express neurotransmitter receptors for glutamate and substance P 自愿潜水时激活的髓背角神经元表达谷氨酸和P物质的神经递质受体

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2025-12-13 DOI: 10.1016/j.ibneur.2025.12.004

P.F. McCulloch, K.M. DiNovo

The diving response is a cardiorespiratory reflex characterized by apnea, bradycardia and increased peripheral vascular resistance when animals submerge underwater. Afferent information initiating this reflex response projects from the nasal mucosa via trigeminal nerves to activate second-order afferent neurons within the medullary dorsal horn (MDH). The present study investigated the synapse between these trigeminal nerves and MDH neurons, specifically what neurotransmitter receptors are expressed by MDH neurons activated during diving. Male Sprague-Dawley rats were trained to dive repetitively through an underwater maze, and Fos was used as a measure of neuronal activation. Immunohistochemistry combined with epifluorescent microscopy was used to determine which ionotropic glutamate receptor subunits, or if the Substance P receptor NK-1, were co-expressed by activated MDH neurons. Results indicate repetitive diving primarily activates small oval-shaped MDH neurons, and these Fos-positive MDH neurons co-express AMPA glutamate receptor subunits GluA1 and GluA2/3, KA glutamate receptor subunit GluK5, and NMDA glutamate receptor subunit GluN1. Since these subunits are constituent parts of their respective receptor structure, these findings reveal the formation of AMPA, KA, and NMDA glutamate receptors on the cellular membrane of these activated MDH neurons. In addition, MDH neurons activated by repetitive diving co-express the Substance P receptor NK-1. This research indicates that MDH neurons activated by diving express neurotransmitter receptors for both glutamate and SP. This supports the assertion that trigeminal nerves innervating the nasal passages release glutamate and SP within their central synapses in the brainstem and can function as part of the afferent limb of a cardiorespiratory reflex.

潜水反应是一种以动物潜水时呼吸暂停、心动过缓和周围血管阻力增加为特征的心肺反射。引发这种反射反应的传入信息通过三叉神经从鼻黏膜投射，激活髓质背角（MDH）内的二级传入神经元。本研究研究了这些三叉神经与MDH神经元之间的突触，特别是MDH神经元在潜水时激活时表达的神经递质受体。雄性Sprague-Dawley大鼠被训练在水下迷宫中反复潜水，Fos被用作神经元激活的测量指标。利用免疫组织化学结合荧光显微镜检测激活的MDH神经元共表达了哪些嗜离子性谷氨酸受体亚基，或者P物质受体NK-1。结果表明，重复潜水主要激活小的卵圆形MDH神经元，这些fos阳性MDH神经元共表达AMPA谷氨酸受体亚基GluA1和GluA2/3， KA谷氨酸受体亚基GluK5和NMDA谷氨酸受体亚基GluN1。由于这些亚基是各自受体结构的组成部分，这些发现揭示了这些活化的MDH神经元细胞膜上AMPA， KA和NMDA谷氨酸受体的形成。此外，重复潜水激活的MDH神经元共同表达P物质受体NK-1。本研究表明，通过潜水激活的MDH神经元表达谷氨酸和SP的神经递质受体。这支持了支配鼻通道的三叉神经在其脑干中枢突触内释放谷氨酸和SP的说法，并可作为心血管反射传入肢体的一部分发挥作用。

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引用次数: 0

The influence of mesenchymal stem cells on the severity of hypoxic-ischemic brain damage in neonatal rats via serum cytokines. 间充质干细胞通过血清细胞因子对新生大鼠缺氧缺血性脑损伤严重程度的影响。

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2025-12-05 eCollection Date: 2025-12-01 DOI: 10.1016/j.ibneur.2025.12.002

Sifeng Yue, Feng Lin, Zenghong Huang, Xinyi Liang, Shuchun Lü, Yuan Tan

Background: Neonatal hypoxic-ischemic brain damage (Hypoxic‑Ischemic Brain Damage, HIBD) is a severe neurological disorder caused by perinatal asphyxia. Its severe long-term sequelae impose a heavy burden on families and society. Therefore, effective early diagnosis and intervention for HIBD are crucial for improving prognosis.

Objective: To investigate the correlation between serum levels of interleukin-6 (IL-6), interleukin-18 (IL-18), and tumor necrosis factor-α (TNF-α) and the severity of hypoxic-ischemic brain damage (HIBD) in neonatal SD rats, as well as the effects of mesenchymal stem cells (MSCs) on serum cytokine levels and the repair of HIBD in rats.

Methods: 250 7-day-old SD rats were selected and a HIBD model was established using the Rice-Vannucci method. The rats were randomly divided into 5 groups: 1) control group; 2) mild HIBD group; 3) severe HIBD group; 4) mild HIBD + MSCs group; 5) severe HIBD + MSCs group. The MSCs intervention group rats were injected with MSCs into the lumbar spine 1 and 8 days after modeling. Longa scores were evaluated at 0, 3, 7, 11, and 15 days after modeling, and serum levels of IL-6, IL-18, and TNF-α were detected. Brain tissue was stained with hematoxylin-eosin (HE) for Longa scoring. The correlation between serum cytokines and the severity of brain injury was analyzed, and the regulatory effect of MSCs intervention on cytokine expression levels and its role in neural injury repair were further explored.

Results: (1) The Longa scores and serum levels of IL-6, IL-18, and TNF-α in the mild HIBD group and severe HIBD group were significantly higher than those in the control group at all stages (P < 0.05), and the severe HIBD group had significantly higher levels than the mild HIBD group at all stages (P < 0.05). (2) After treatment, HE staining showed that the brain tissue damage in the mild HIBD group and mild HIBD + MSCs group improved, and the Longa scores and serum levels of IL-6, IL-18, and TNF-α decreased significantly at all time points (D3, D7, D11, D15) after treatment compared to those before treatment (D0). The Longa scores and serum levels of IL-6, IL-18, and TNF-α in the mild HIBD + MSCs group and severe HIBD + MSCs group decreased significantly at each time point (D3, D7, D11, D15) after treatment compared to those before treatment (D0).

Conclusion: The serum levels of IL-6, IL-18, and TNF-α in rats are positively correlated with the severity of HIBD and can reflect the degree of brain tissue injury. They can be used for disease assessment; mesenchymal stem cell treatment can significantly reduce the serum levels of IL-6, IL-18, and TNF-α in HIBD rats, alleviate inflammatory responses, improve symptoms, and repair brain injury.

背景：新生儿缺氧缺血性脑损伤（Hypoxic - Ischemic brain damage， HIBD）是一种由围产期窒息引起的严重神经系统疾病。其严重的长期后遗症给家庭和社会带来沉重的负担。因此，对HIBD进行有效的早期诊断和干预对改善预后至关重要。目的：探讨新生SD大鼠血清白细胞介素-6 （IL-6）、白细胞介素-18 （IL-18）、肿瘤坏死因子-α (TNF-α)水平与缺氧缺血性脑损伤（HIBD）严重程度的相关性，以及间充质干细胞（MSCs）对大鼠血清细胞因子水平及HIBD修复的影响。方法：选取7日龄SD大鼠250只，采用Rice-Vannucci法建立HIBD模型。将大鼠随机分为5组：1)对照组；2)轻度HIBD组；3)重度HIBD组；4)轻度HIBD + MSCs组；5)重度HIBD + MSCs组。MSCs干预组大鼠在造模后1天和8天分别向腰椎注射MSCs。分别于造模后0、3、7、11、15 d评估Longa评分，并检测血清中IL-6、IL-18、TNF-α水平。脑组织采用苏木精-伊红（HE）染色进行Longa评分。分析血清细胞因子与脑损伤严重程度的相关性，进一步探讨MSCs干预对细胞因子表达水平的调节作用及其在神经损伤修复中的作用。结果：(1)轻、重度HIBD组各阶段的Longa评分及血清中IL-6、IL-18、TNF-α水平均显著高于对照组（P ）结论：大鼠血清中IL-6、IL-18、TNF-α水平与HIBD的严重程度呈正相关，可反映脑组织损伤程度。它们可用于疾病评估；间充质干细胞治疗可显著降低HIBD大鼠血清IL-6、IL-18、TNF-α水平，减轻炎症反应，改善症状，修复脑损伤。

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引用次数: 0

Levodopa exerts neuroprotective effects by suppressing microglial proinflammatory activation in a rat hemi-Parkinson's disease model. 左旋多巴通过抑制大鼠半帕金森病模型的小胶质细胞促炎激活发挥神经保护作用。

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2025-12-04 eCollection Date: 2025-12-01 DOI: 10.1016/j.ibneur.2025.12.001

Noriyuki Miyaue, Mohammed E Choudhury, Ikuko Takeda, Junya Tanaka, Ayane Takenaga, Haruto Yamamoto, Yuki Nishikawa, Naoki Abe, Masahiro Nagai, Tasuku Nishihara

Levodopa is a central medicine used for the treatment of Parkinson's disease (PD) as a dopamine (DA) precursor that increases DA levels in the striatum. Microglia, resident macrophages in the brain, become activated in response to the progressive degeneration of nigral dopaminergic neurons in PD pathology, while releasing proinflammatory mediators that are harmful to dopaminergic neurons. DA has been shown to prevent proinflammatory activation of microglia. This study showed that DA decreases lipopolysaccharide-induced proinflammatory reactions and increases tissue repairing factors of microglia in cultured rat microglia. Levodopa was administered to 6-hydroxydopmaine (6-OHDA)-induced PD model rats for 7 days, and motor deficits were evaluated after a two-week withdrawal period. The levodopa-treated PD model rats showed a better motor function than the vehicle-treated rats. The administration of levodopa for 7 days led to an increase in DA levels and a suppression of microglial activation in the striatum, which was maintained, even at two weeks after withdrawal. These results suggest that levodopa may act in the PD brain, not only as a DA precursor, but also as an immunosuppressant to reduce neuroinflammation accompanied by PD pathology.

左旋多巴是一种用于治疗帕金森病（PD）的中枢药物，作为多巴胺（DA）前体，可增加纹状体中的DA水平。在PD病理中，小胶质细胞作为驻留在大脑中的巨噬细胞，在对黑质多巴胺能神经元进行性退行性变的反应中被激活，同时释放对多巴胺能神经元有害的促炎介质。DA已被证明可以防止小胶质细胞的促炎激活。本研究表明，DA可降低脂多糖诱导的小胶质细胞促炎反应，增加小胶质细胞的组织修复因子。左旋多巴给予6-羟多巴胺（6-OHDA）诱导的PD模型大鼠7天，停药两周后评估运动障碍。左旋多巴处理的PD模型大鼠运动功能明显优于对照组。左旋多巴给药7天导致DA水平升高，纹状体中小胶质细胞的激活受到抑制，即使在停药后两周也能保持这种抑制。这些结果表明，左旋多巴可能在PD脑中不仅作为DA前体，而且作为免疫抑制剂减少PD病理伴随的神经炎症。

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引用次数: 0

Citalopram-induced decrease of CLOCK-ir and BMAL1-ir kisspeptin neurons in the anteroventral periventricular nucleus of adult male mice 西酞普兰诱导成年雄性小鼠前腹侧脑室周围核CLOCK-ir和BMAL1-ir kisspeptin神经元减少

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2025-12-01 DOI: 10.1016/j.ibneur.2025.09.014

Manish Putteeraj , Tomoko Soga , Ishwar S. Parhar

A complex network exists between the reproductive, circadian and the serotonergic system. Modulation of brain serotonin levels triggers sexual irregularities and alters circadian behaviour. This study investigated the presence of an endogeneous clock within kisspeptin neurons in the anteroventral periventricular nucleus (AVPV) and arcuate nucleus (ARC); and their modulation by a serotonin reuptake inhibitor, citalopram (CIT), in adult male mice. Treatment consisted of daily (chronic) intra-peritoneal administration of CIT (10 mg/kg) or saline for 4 weeks in adult male mice. Gene expression study using RT-PCR was conducted at two timepoints during the dark phase (ZT14) and the light phase (ZT4). Higher expression of Kiss1, Per1 and Per2 mRNA was observed at ZT14, anti-phase to Bmal1 mRNA showing higher expression at ZT4 in the AVPV. Morphological analysis confined to ZT14 showed the presence of CLOCK and BMAL1 proteins in kisspeptin neurons. Chronic CIT-treatment did not induce any change in Kiss1 mRNA expression in the AVPV. However, a significant reduction in CLOCK-ir and BMAL1-ir kisspeptin neurons was observed in CIT-treated male mice at ZT14 in the AVPV using double immunohistochemistry. In brief, a time-dependent expression of Per1, Per2 and Bmal1 exists in the AVPV and chronic CIT orchestrates a decrease in CLOCK-ir and BMAL1-ir kisspeptin neurons. These data suggests rhythmic imbalances in kisspeptin neurons as a potential mediator of reproductive irregularities.

在生殖系统、昼夜节律系统和血清素能系统之间存在着一个复杂的网络。大脑血清素水平的调节会引发性行为不规律，并改变昼夜节律行为。本研究调查了腹侧脑室周围核（AVPV）和弓状核（ARC）中kisspeptin神经元内的内源性时钟的存在；以及成年雄性小鼠血清素再摄取抑制剂西酞普兰（CIT）对它们的调节作用。治疗方法为每日（慢性）腹腔注射CIT（10 mg/kg）或生理盐水，连续4周。采用RT-PCR技术在暗期（ZT14）和亮期（ZT4）两个时间点进行基因表达研究。Kiss1、Per1和Per2 mRNA在ZT14表达较高，Bmal1 mRNA的反相在ZT4表达较高。形态学分析显示，kisspeptin神经元中存在CLOCK和BMAL1蛋白。慢性cit治疗未引起AVPV中Kiss1 mRNA表达的任何变化。然而，双免疫组化观察发现，cit处理的雄性小鼠在AVPV的ZT14时，CLOCK-ir和BMAL1-ir kisspeptin神经元显著减少。简而言之，在AVPV中存在Per1， Per2和Bmal1的时间依赖性表达，慢性CIT协调CLOCK-ir和Bmal1 -ir kisspeptin神经元的减少。这些数据表明kisspeptin神经元的节律性失衡是生殖不规则的潜在中介。

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引用次数: 0

Electroacupuncture enhances nerve regeneration and functional recovery in a rat model of median nerve transection 电针促进正中神经横断大鼠神经再生和功能恢复

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2025-12-01 DOI: 10.1016/j.ibneur.2025.11.002

Hongyu Zhou , Jin He , Ainizier Yalikun , Hui Chen , Yu Si Aierken Rehemulatu , Li li

Objective

To investigate the therapeutic efficacy and underlying mechanisms of electroacupuncture (EA) in promoting peripheral nerve regeneration following delayed repair of a median nerve transection in a rat model.

Methods

Thirty male Sprague-Dawley rats were randomly assigned to five groups: sham operation, model (1- and 2-weeks post-transection), and EA treatment (1- and 2-weeks post-repair). Median nerve transection was performed, followed by delayed microsurgical repair. EA was applied at Jianyu (LI15) and Neiguan (PC6) acupoints following nerve repair. Nerve regeneration and tissue response were evaluated through histological staining (Hematoxylin and Eosin [H&E], Luxol Fast Blue [LFB], Masson’s Trichrome [Masson]), immunofluorescence (S100β, Sox10), western blotting (phosphorylated phosphoinositide 3-kinase [p-PI3K], receptor for advanced glycation end products [RAGE], triggering receptor expressed on myeloid cells 2 [TREM2]), enzyme-linked immunosorbent assay (ELISA; interleukin-6 [IL-6], C-X-C motif chemokine ligand 3 [CXCL3], matrix metalloproteinase-3 [MMP3], reactive oxygen species [ROS], superoxide dismutase [SOD], malondialdehyde [MDA]), and transcriptome sequencing with gene set enrichment analysis (GSEA)

Results

EA significantly enhanced axonal regeneration and remyelination, reduced inflammatory infiltration, and suppressed fibrotic collagen deposition. EA treatment markedly downregulated p-PI3K and RAGE expression and upregulated TREM2, indicating inhibition of inflammatory signaling and promotion of M2 macrophage polarization. Serum biomarkers showed reduced levels of IL-6, ROS, and MDA, along with increased SOD activity. Transcriptomic analysis revealed EA-induced activation of reparative and metabolic pathways, including lysosome function, endocytosis, and protein processing, while reversing injury-induced suppression of oxidative phosphorylation and ribosomal function.

Conclusion

EA facilitates peripheral nerve regeneration through multi-target regulation of inflammation, oxidative stress, and neuroglial activity. These findings support the translational potential of EA as a complementary therapeutic strategy following nerve repair for upper limb peripheral nerve injuries.

目的探讨电针促进大鼠正中神经延迟修复后周围神经再生的疗效及机制。方法30只雄性Sprague-Dawley大鼠随机分为5组：假手术组、模型组（切除后1周和2周）和EA治疗组（修复后1周和2周）。行正中神经横断，延迟显微手术修复。神经修复后，在建俞穴（LI15）和内关穴（PC6）应用电针。通过组织染色（苏木精和伊红[H&；E], Luxol Fast Blue [LFB], Masson 's Trichrome [Masson]），免疫荧光（S100β, Sox10）， western blotting（磷酸化磷酸肌肽3-激酶[p-PI3K]，晚期糖基化终产物受体[RAGE]，髓细胞上表达的触发受体2 [TREM2]），酶联免疫吸附试验(ELISA；白细胞介素-6 （IL-6）、C-X-C基序趋化因子配体3 （CXCL3）、基质金属蛋白酶-3 （MMP3）、活性氧（ROS）、超氧化物歧化酶（SOD）、丙二醛（MDA）)等)转录组测序及基因集富集分析（GSEA）结果sea显著促进轴突再生和髓鞘再生，减少炎症浸润，抑制纤维化胶原沉积。EA治疗显著下调p-PI3K和RAGE表达，上调TREM2，表明抑制炎症信号，促进M2巨噬细胞极化。血清生物标志物显示IL-6、ROS和MDA水平降低，SOD活性升高。转录组学分析显示，ea诱导的修复和代谢途径的激活，包括溶酶体功能、内吞作用和蛋白质加工，同时逆转损伤诱导的氧化磷酸化和核糖体功能的抑制。结论ea通过多靶点调控炎症、氧化应激和神经胶质活性促进周围神经再生。这些发现支持EA作为上肢周围神经损伤神经修复后的补充治疗策略的转化潜力。

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引用次数: 0

Losartan attenuates depression-like behavior in epileptic rats by regulating the TGF-β/Smad signaling 氯沙坦通过调节TGF-β/Smad信号通路减轻癫痫大鼠抑郁样行为

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2025-12-01 DOI: 10.1016/j.ibneur.2025.12.003

Penghui Cao , Shichuan Shen , Ziyan Fang , Junjie Tan , Jinwei Wang , Nannan Pan

Objective

This study aims to investigate the role of the TGF-β/Smad Signaling in depression comorbidity in epileptic individuals and to evaluate the effect of losartan on depressive symptoms.

Methods

Li-Popilocarpine was used to induce status epilepticus (SE) in rats. The rats in which SE was successfully induced were randomly divided into the SE saline group and the SE losartan group. Then, the rats in the different groups were given the corresponding interventions for 20 days. After the intervention, the depression levels of the rats in each group were evaluated. Upon completion of the intervention, brain tissue was collected for comprehensive assessment of TGF-β mRNA levels, TGF-β/Smad Signaling-related protein expression, and GFAP⁺ astrocyte density in the rat hippocampus.

Results

The depression-like behavior of SE rats was more obvious than that of control rats. TGF-β mRNA, p-Smad2, p-Smad3 and GFAP⁺ astrocyte expression levels were significantly greater in SE rats than in control rats. Compared with the SE-saline group, the depression-like behavior of the SE-losartan group improved. The expression levels of TGF-β mRNA p-Smad2, p-Smad3 and GFAP⁺ astrocyte expression in the SE-losartan group rats were lower than those in the SE-saline group.

Conclusion

The TGF-β/Smad Signaling is an important Signaling leading to depression-like behavior in epileptic rats. Losartan is a drug that can significantly improve the depression-like behavior of epileptic rats by regulating the TGF-β/Smad Signaling. Findings in this study support losartan as a repurposable central nervous system drug for comorbid depression in epilepsy, warranting further clinical investigation.

目的探讨TGF-β/Smad信号在癫痫患者抑郁共病中的作用，评价氯沙坦对抑郁症状的影响。方法采用si - popilocarpine诱导大鼠癫痫持续状态（SE）。将SE诱导成功的大鼠随机分为SE生理盐水组和SE氯沙坦组。然后给予不同组大鼠相应干预，疗程20 d。干预后评估各组大鼠抑郁水平。干预结束后，收集脑组织，综合评估大鼠海马中TGF-β mRNA水平、TGF-β/Smad信号相关蛋白表达、GFAP⁺星形胶质细胞密度。结果SE大鼠抑郁样行为较对照组明显。TGF-β mRNA、p-Smad2、p-Smad3和GFAP +星形胶质细胞表达水平在SE大鼠中显著高于对照组大鼠。与se -生理盐水组比较，se -氯沙坦组抑郁样行为有所改善。se -氯沙坦组大鼠TGF-β mRNA p-Smad2、p-Smad3和GFAP +星形胶质细胞表达水平低于se -生理盐水组。结论TGF-β/Smad信号通路是癫痫大鼠抑郁样行为的重要信号通路。氯沙坦是一种通过调节TGF-β/Smad信号显著改善癫痫大鼠抑郁样行为的药物。本研究结果支持氯沙坦作为一种可用于癫痫共病抑郁的中枢神经系统药物，值得进一步的临床研究。

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引用次数: 0

TMEM206 gene knockout improves balance performance in SCA1 transgenic mice 敲除TMEM206基因可改善SCA1转基因小鼠的平衡性能

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2025-12-01 DOI: 10.1016/j.ibneur.2025.11.012

Jia-Hui Zhang , Yu Qin , Shun-Chang Sun

TMEM206 was identified as a conserved chloride channel that underlies widely expressed, proton-activated, outwardly rectifying chloride currents. Spinocerebellar ataxia type 1 (SCA1) is one of polyglutamine diseases, and is characterized as a progressive and autosomal dominant genetic disease, which is caused by an increasing number of CAG repeats in the ataxin-1 gene. TMEM206 was confirmed to interact with ataxin-1. This study suggests that TMEM206-ataxin-1 interaction might involve in the pathological mechanisms of SCA1. To elucidate the mechanisms of SCA1 involved in proton-activated chloride channel gating, we bred TMEM206 knockout mice using SCA1 model mice. Motor coordination and balance in mice was evaluated using rotarod test and grip strength. These studies showed that genetic depletion of TMEM206 has slight impacts on the SCA1 mice weight, and partially improves motor incoordination in Atxn1^154Q/2Q mice. No alteration in grip strength was found in Atxn1^154Q/2Q mice with depletion of the TMEM206 gene. Our studies indicate that the TMEM206 knockout appears to emerge as a potential therapy method for SCA1 mice.

TMEM206被认为是一个保守的氯离子通道，是广泛表达、质子激活、向外整流氯离子电流的基础。脊髓小脑性共济失调1型（SCA1）是多谷氨酰胺疾病之一，是一种进行性常染色体显性遗传病，由ataxin-1基因CAG重复数增加引起。TMEM206被证实与ataxin-1相互作用。本研究提示TMEM206-ataxin-1相互作用可能参与SCA1的病理机制。为了阐明SCA1参与质子激活氯通道门控的机制，我们用SCA1模型小鼠培育TMEM206基因敲除小鼠。用旋转杆试验和握力评价小鼠的运动协调和平衡能力。这些研究表明，TMEM206基因缺失对SCA1小鼠体重有轻微影响，并部分改善Atxn1154Q/2Q小鼠的运动不协调。在TMEM206基因缺失的Atxn1154Q/2Q小鼠中没有发现握力的改变。我们的研究表明，TMEM206基因敲除似乎是一种潜在的治疗SCA1小鼠的方法。

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引用次数: 0

Behavioral and physiological benefits of alpha-pinene in adult rats experiencing chronic stress: A focus on depression and oxidative stress α -蒎烯在经历慢性应激的成年大鼠中的行为和生理益处：关注抑郁和氧化应激

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2025-12-01 DOI: 10.1016/j.ibneur.2025.11.014

Seyed Shahriyar Hosseini , Zohreh Ghotbeddin , Seyed Reza Fatemi Tabatabaei , Kaveh Rahimi

To investigate the protective effects of alpha-pinene, an antioxidant compound, on depressive-like behaviors, social interactions, and biochemical markers in adult rats exposed to chronic stress through maternal separation during early development. Forty-nine Wistar rats were divided into seven groups: control (receiving solvent only), two alpha-pinene treatment groups (5 and 10 mg/kg), a stress group (maternal separation for 6 h daily for 21 days), two combined treatment groups (alpha-pinene with stress), and a positive control group (imipramine hydrochloride, 10 mg/kg). Behavioral assessments included forced swimming tests, sucrose preference tests, elevated plus maze tests, and social interaction tests. Serum corticosterone levels and oxidative stress markers (MDA and GPx activity) in brain tissue were measured. The stress group showed significant increases in immobility time, anxiety behaviors, and serum corticosterone levels, with decreased sucrose preference and altered social interactions. Biochemical analysis revealed increased MDA levels and decreased GPx activity in the stress group, indicating heightened oxidative stress. Alpha-pinene treatment at both doses significantly improved behavioral outcomes, reduced corticosterone levels, decreased MDA levels, and increased GPx activity in stressed rats, with effects comparable to imipramine. Alpha-pinene significantly protects against chronic stress-induced behavioral and biochemical alterations in rats. These findings suggest that alpha-pinene may improve behavioral performance through antioxidant mechanisms and by modulating HPA axis activity, as evidenced by reduced corticosterone levels. This study provides preliminary evidence for alpha-pinene's potential therapeutic value in stress-related disorders.

研究α -蒎烯（一种抗氧化化合物）对早期发育期间暴露于母体分离慢性应激的成年大鼠抑郁样行为、社会互动和生化指标的保护作用。49只Wistar大鼠分为7组：对照组（仅给予溶剂）、2个α -蒎烯处理组（5和10 mg/kg）、应激组（每天6 h，连续21 d）、2个联合处理组（α -蒎烯加应激）和阳性对照组（盐酸丙咪嗪，10 mg/kg）。行为评估包括强迫游泳测试、蔗糖偏好测试、升高+迷宫测试和社会互动测试。测定脑组织血清皮质酮水平和氧化应激标志物（MDA、GPx活性）。应激组的不动时间、焦虑行为和血清皮质酮水平显著增加，对蔗糖的偏好降低，社会互动改变。生化分析显示应激组MDA水平升高，GPx活性降低，提示氧化应激升高。两种剂量的α -蒎烯治疗显著改善应激大鼠的行为结果，降低皮质酮水平，降低MDA水平，增加GPx活性，其效果与丙咪嗪相当。α -蒎烯显著保护大鼠免受慢性应激诱导的行为和生化改变。这些发现表明，α -蒎烯可能通过抗氧化机制和调节HPA轴活性来改善行为表现，正如皮质酮水平降低所证明的那样。本研究为α -蒎烯在应激相关疾病中的潜在治疗价值提供了初步证据。

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引用次数: 0

Posterior fossa arachnoid cysts in multiple system atrophy 后窝蛛网膜囊肿多系统萎缩

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2025-12-01 DOI: 10.1016/j.ibneur.2025.11.015

Audrey M. Blazek Ramsay M.D, Eoin P. Flanagan M.B.,B.Ch., Elizabeth A. Coon M.D., Lauren M. Jackson M.D.

Background

Multiple system atrophy (MSA) is an α-synucleinopathy characterized by prominent cerebellar or parkinsonian features. This is pathologically due to the deposition of α-synuclein in glial cells, the mechanism by which s not entirely clear. We describe three patients with posterior fossa arachnoid cysts later diagnosed with clinically established MSA, suggesting the co-existence of two rare pathologies through a shared mechanism versus by chance.

Cases

Patients ranged from 45 to 67 years of age at presentation, each describing 2–3 years of progressive symptoms. All displayed cerebellar findings and various non-motor features of orthostatic hypotension, genitourinary failure, and dream enactment behavior confirmed on diagnostic testing or on a clinical basis. All imaging demonstrated posterior fossa arachnoid cysts and supportive features of MSA, notably pontine and cerebellar atrophy.

Conclusions

The probability of having both MSA and a posterior fossa arachnoid cyst based on population study-derived point prevalence and assuming independence of the events is 1.09 e-6. We suspect that while uncommon, concurrence of the diseases is due to chance. It is plausible that space-occupying lesions, when already present, may contribute to neurodegenerative disease progression.

多系统萎缩（MSA）是一种以小脑或帕金森特征为特征的α-突触核蛋白病。这在病理上是由于α-突触核蛋白在胶质细胞中的沉积，其机制尚不完全清楚。我们描述了三例后窝蛛网膜囊肿患者，后来被诊断为临床建立的MSA，表明两种罕见病理通过共同机制而不是偶然共存。病例患者发病时年龄从45岁到67岁不等，每位患者症状进展2-3年。所有患者均表现出小脑病变和各种非运动特征，如体位性低血压、泌尿生殖系统功能衰竭和梦境行为，均经诊断测试或临床证实。所有影像显示后颅窝蛛网膜囊肿和MSA的支持特征，特别是脑桥和小脑萎缩。结论基于人群研究得出的点患病率和假设事件的独立性，MSA和后窝蛛网膜囊肿的概率为1.09 e-6。我们怀疑，虽然罕见，但这些疾病的同时发生是偶然的。当占位性病变已经存在时，可能会导致神经退行性疾病的进展，这是合理的。

{"title":"Posterior fossa arachnoid cysts in multiple system atrophy","authors":"Audrey M. Blazek Ramsay M.D, Eoin P. Flanagan M.B.,B.Ch., Elizabeth A. Coon M.D., Lauren M. Jackson M.D.","doi":"10.1016/j.ibneur.2025.11.015","DOIUrl":"10.1016/j.ibneur.2025.11.015","url":null,"abstract":"<div><h3>Background</h3><div>Multiple system atrophy (MSA) is an α-synucleinopathy characterized by prominent cerebellar or parkinsonian features. This is pathologically due to the deposition of α-synuclein in glial cells, the mechanism by which s not entirely clear. We describe three patients with posterior fossa arachnoid cysts later diagnosed with clinically established MSA, suggesting the co-existence of two rare pathologies through a shared mechanism versus by chance.</div></div><div><h3>Cases</h3><div>Patients ranged from 45 to 67 years of age at presentation, each describing 2–3 years of progressive symptoms. All displayed cerebellar findings and various non-motor features of orthostatic hypotension, genitourinary failure, and dream enactment behavior confirmed on diagnostic testing or on a clinical basis. All imaging demonstrated posterior fossa arachnoid cysts and supportive features of MSA, notably pontine and cerebellar atrophy.</div></div><div><h3>Conclusions</h3><div>The probability of having both MSA and a posterior fossa arachnoid cyst based on population study-derived point prevalence and assuming independence of the events is 1.09 e-6. We suspect that while uncommon, concurrence of the diseases is due to chance. It is plausible that space-occupying lesions, when already present, may contribute to neurodegenerative disease progression.</div></div>","PeriodicalId":13195,"journal":{"name":"IBRO Neuroscience Reports","volume":"19 ","pages":"Pages 1034-1037"},"PeriodicalIF":2.9,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145690386","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Circulating microRNA-219 in stroke: Lack associations with clinical parameters and post-stroke epilepsy risk 卒中中循环microRNA-219：与临床参数和卒中后癫痫风险缺乏关联

IF 2.9 Q3 NEUROSCIENCES

IBRO Neuroscience Reports

Pub Date : 2025-12-01 DOI: 10.1016/j.ibneur.2025.11.013

Zeynab Fahimi , Mohammad Kazemi , Habibollah Rahimi , Maryam Afarini , Hossein Motedayyen , Mahyar Noorbakhsh

Background

Post-stroke epilepsy (PSE) is a significant complication in stroke survivors, yet early diagnostic biomarkers remain unclear. This study investigated whether circulating microRNA-219 (miR-219) could serve as a reliable biomarker for early detection of PSE.

Methods

Serum samples (2 mL) were collected from 40 stroke patients and 20 healthy controls. Circulating miR-219 was measured using real-time PCR. The predictive performance of miR-219 and the PoSERS model for PSE was evaluated using ROC analysis. Demographic and clinical information, including age, gender, stroke subtype, and lesion location, was recorded.

Results

Significant differences were observed in stroke subtype (ischemic vs. hemorrhagic) and lesion location (cortical vs. subcortical) between patients with and without PSE (P < 0.05). Triglyceride (TG), HbA1C, and cholesterol levels also differed significantly (P < 0.05). Circulating miR-219 was significantly elevated in stroke patients compared to controls (P < 0.05). However, no significant differences in miR-219 levels were observed between patients with and without PSE. Similar trends were observed when comparing survivors vs. non-survivors, ischemic vs. hemorrhagic stroke, and cortical vs. subcortical lesions. MiR-219 had no predictive value for PSE (AUC=0.49), unlike the PoSERS model (AUC=0.72).

Conclusions

Although a significant difference in circulating miR-219 was observed between stroke patients and healthy subjects, it cannot serve as a biomarker to predict the development of PSE. Given the limited sample size, the predictive potential of miR-219 should be confirmed in future studies with larger sample sizes.

卒中后癫痫（PSE）是卒中幸存者的重要并发症，但早期诊断生物标志物尚不清楚。本研究探讨了循环microRNA-219 （miR-219）是否可以作为早期检测PSE的可靠生物标志物。方法采集40例脑卒中患者血清（2 mL）和20例健康对照。采用实时PCR检测循环miR-219。采用ROC分析评估miR-219和PoSERS模型对PSE的预测性能。记录人口统计学和临床信息，包括年龄、性别、脑卒中亚型和病变部位。结果PSE患者与非PSE患者在卒中亚型（缺血性vs出血性）和病变部位（皮质vs皮质下）上存在显著差异（P <； 0.05）。甘油三酯（TG）、糖化血红蛋白（HbA1C）和胆固醇水平也有显著差异（P <； 0.05）。与对照组相比，卒中患者循环miR-219显著升高（P <； 0.05）。然而，miR-219水平在PSE患者和非PSE患者之间没有显著差异。在比较幸存者与非幸存者、缺血性卒中与出血性卒中、皮质病变与皮质下病变时，也观察到类似的趋势。与PoSERS模型（AUC=0.72）不同，MiR-219对PSE没有预测价值（AUC=0.49）。结论虽然在卒中患者和健康人之间循环miR-219存在显著差异，但它不能作为预测PSE发展的生物标志物。由于样本量有限，miR-219的预测潜力应在未来更大样本量的研究中得到证实。

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引用次数: 0