Cellular and Molecular Neurobiology最新文献

Differential Neuronal Activation of Nociceptive Pathways in Neuropathic Pain After Spinal Cord Injury.

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-30 DOI: 10.1007/s10571-025-01532-6

Ziyu He, Jun Zhang, Jia Xu, Yu Wang, Xiaolong Zheng, Wei Wang

{"title":"Differential Neuronal Activation of Nociceptive Pathways in Neuropathic Pain After Spinal Cord Injury.","authors":"Ziyu He, Jun Zhang, Jia Xu, Yu Wang, Xiaolong Zheng, Wei Wang","doi":"10.1007/s10571-025-01532-6","DOIUrl":"10.1007/s10571-025-01532-6","url":null,"abstract":"Neuropathic pain, a prevalent complication following spinal cord injury (SCI), severely impairs the life quality of patients. No ideal treatment exists due to incomplete knowledge on underlying neural processes. To explore the SCI-induced effect on nociceptive circuits, the protein expression of c-Fos was analyzed as an indicator of neuronal activation in a rat contusion model exhibiting below-level pain. Additional stimuli were delivered to mimic the different peripheral sensory inputs in daily life. Following noxious rather than innocuous or no stimulation, a greater number of spinal dorsal horn (DH) neurons were activated after SCI, mainly in the deep DH. SCI facilitated the activation of excitatory but not inhibitory DH neurons. Moreover, excitatory interneurons expressing protein kinase C gamma (PKCγ) in laminae II-III, which are known to play a role in mechanical allodynia after peripheral nerve injury, responded in larger amounts to both innocuous and noxious stimulation following SCI. Accordingly, more spinal projection neurons in lamina I were activated. Within supraspinal nuclei processing pain, differentially enhanced activation in response to noxious stimulation was detected after SCI, with a significant increase in the locus coeruleus and medial thalamus, a slight increase in the periaqueductal gray and dorsal raphe, and no change in the lateral parabrachial nucleus or primary sensory cortex. These findings indicated differential hyperexcitability along the sensory neuroaxis following SCI, with a particular emphasis on the involvement of specific neuron subtypes, such as spinal PKCγ interneurons and locus coeruleus noradrenergic neurons, which may serve as crucial targets for potential therapies.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"18"},"PeriodicalIF":3.6,"publicationDate":"2025-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11782389/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143064063","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction: Myosin IIA Regulated Tight Junction in Oxygen Glucose-Deprived Brain Endothelial Cells Via Activation of TLR4/PI3K/Akt/JNK1/2/14-3-3ε/NF-κB/MMP9 Signal Transduction Pathway.

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-28 DOI: 10.1007/s10571-025-01531-7

Yanni Lv, Wen Liu, Zhaohui Ruan, Zixuan Xu, Longsheng Fu

引用次数: 0

Correction: Docosahexaenoic Acid Alleviates Oxidative Stress-Based Apoptosis Via Improving Mitochondrial Dynamics in Early Brain Injury After Subarachnoid Hemorrhage.

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-25 DOI: 10.1007/s10571-025-01530-8

Tongyu Zhang, Pei Wu, John H Zhang, Yuchen Li, Shancai Xu, Chunlei Wang, Ligang Wang, Guang Zhang, Jiaxing Dai, Shiyi Zhu, Yao Liu, Binbing Liu, Cesar Reis, Huaizhang Shi

引用次数: 0

AMPA Receptors in Synaptic Plasticity, Memory Function, and Brain Diseases. AMPA受体在突触可塑性、记忆功能和脑部疾病中的作用。

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-22 DOI: 10.1007/s10571-024-01529-7

Cristina A Muñoz de León-López, Marta Carretero-Rey, Zafar U Khan

{"title":"AMPA Receptors in Synaptic Plasticity, Memory Function, and Brain Diseases.","authors":"Cristina A Muñoz de León-López, Marta Carretero-Rey, Zafar U Khan","doi":"10.1007/s10571-024-01529-7","DOIUrl":"10.1007/s10571-024-01529-7","url":null,"abstract":"Tetrameric AMPA-type ionotropic glutamate receptors are primary transducers of fast excitatory synaptic transmission in the central nervous system, and their properties and abundance at the synaptic surface are crucial determinants of synaptic efficacy in neuronal communication across the brain. The induction of long-term potentiation (LTP) leads to the insertion of GluA1-containing AMPA receptors at the synaptic surface, whereas during long-term depression (LTD), these receptors are internalized into the cytoplasm of the spine. Disruptions in the trafficking of AMPA receptors to and from the synaptic surface attenuate both forms of synaptic plasticity. Homeostatic scaling up and scaling down, which are additional types of plasticity similar to LTP and LTD, are also regulated by the insertion and removal of GluA1-containing AMPA receptors from the synaptic surface. The trafficking of AMPA receptors is an intricate process assisted by various proteins. Furthermore, AMPA receptors are critical for the formation and consolidation of various types of memory, and alterations in their function are intimately associated with cognitive dysfunction in aging and several neurological and psychiatric diseases. In this review, we will provide an overview of the current understanding of how AMPA receptors regulate various forms of synaptic plasticity, their contribution to memory functions, and their role in aging and brain diseases.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"14"},"PeriodicalIF":3.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11754374/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000766","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Genetically Predicted Leucine Level Mediates Association Between CD4/CD8br T Lymphocytes and Insomnia. 基因预测的亮氨酸水平介导CD4/CD8br T淋巴细胞与失眠的关系

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-22 DOI: 10.1007/s10571-025-01533-5

Sumei Luo, Jianyin Yin, Jie Zhang, Pan Li, Tao Wen, Ke Li, Jing Tang, Xiaohong Wang, Aiyuan Li, Liang Chen

{"title":"Genetically Predicted Leucine Level Mediates Association Between CD4/CD8br T Lymphocytes and Insomnia.","authors":"Sumei Luo, Jianyin Yin, Jie Zhang, Pan Li, Tao Wen, Ke Li, Jing Tang, Xiaohong Wang, Aiyuan Li, Liang Chen","doi":"10.1007/s10571-025-01533-5","DOIUrl":"10.1007/s10571-025-01533-5","url":null,"abstract":"Immune and metabolic factors play an important role in the onset and development of insomnia. This study aimed to investigate the causal relationship between insomnia and immune cells and metabolites. Data for 731 immune cell phenotypes, 1400 metabolites, and insomnia in this study were obtained from the GWAS open-access database. Two-way Mendelian randomization was used to (1) detect the causal relationship between immune cells and insomnia and (2) identify potential mediating metabolites. Mendelian randomization analysis identified eight immune cell phenotypes with a causal relationship to insomnia, and two immune cell phenotypes were protective factors for insomnia, namely CD8br %T cells and CD80 on CD62L + myeloid dendritic cells. The other six immune cell phenotypes were risk factors for insomnia, i.e., CD4/CD8br, CD16-CD56 on NKT, CCR2 on myeloid dendritic cells, CD40 on monocytes, CD38 on CD3-CD19-, and CD25 on CD45RA + CD4 not Treg. Further Mendelian randomization revealed 11 metabolites that were causally related to insomnia. Five metabolites were protective factors for insomnia, i.e., 3-hydroxy-3-methylglutarate, cholate, dodecanedioate, N-formylmethionine, and x-26054. Six metabolites were risk factors for insomnia, 3-amino-2-piperidone, 6-oxopiperdine-2-carboxylate, caffeine to theophylline ratio, leucine, maltose, and x-24736. In addition, our analysis showed that leucine mediated the association between CD4/CD8br and insomnia. From genetic information, we confirmed the causal relationship between insomnia, eight immune cell phenotypes, and eleven metabolite levels. Notably, we found a relationship between leucine-mediated CD4/CD8br and insomnia, providing evidence supporting the causal relationship between immune cell and insomnia, with plasma metabolites serving as mediators.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"15"},"PeriodicalIF":3.6,"publicationDate":"2025-01-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11754360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000771","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Aging and MPTP Sensitivity Depend on Molecular and Ultrastructural Signatures of Astroglia and Microglia in Mice Substantia Nigra. 衰老和MPTP敏感性取决于小鼠黑质星形胶质细胞和小胶质细胞的分子和超微结构特征。

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-20 DOI: 10.1007/s10571-024-01528-8

P L Abhilash, Upasna Bharti, Santhosh Kumar Rashmi, Mariamma Philip, T R Raju, Bindu M Kutty, B K Chandrasekhar Sagar, Phalguni Anand Alladi

{"title":"Aging and MPTP Sensitivity Depend on Molecular and Ultrastructural Signatures of Astroglia and Microglia in Mice Substantia Nigra.","authors":"P L Abhilash, Upasna Bharti, Santhosh Kumar Rashmi, Mariamma Philip, T R Raju, Bindu M Kutty, B K Chandrasekhar Sagar, Phalguni Anand Alladi","doi":"10.1007/s10571-024-01528-8","DOIUrl":"10.1007/s10571-024-01528-8","url":null,"abstract":"Both astroglia and microglia show region-specific distribution in CNS and often maladapt to age-associated alterations within their niche. Studies on autopsied substantia nigra (SN) of Parkinson's disease (PD) patients and experimental models propose gliosis as a trigger for neuronal loss. Epidemiological studies propose an ethnic bias in PD prevalence, since Caucasians are more susceptible than non-whites. Similarly, different mice strains are variably sensitive to MPTP. We had earlier likened divergent MPTP sensitivity of C57BL/6 J and CD-1 mice with differential susceptibility to PD, based on the numbers of SN neurons. We examined whether the variability was incumbent to inter-strain differences in glial features of male C57BL/6 J and CD-1 mice. Stereological counts showed relatively more microglia and fewer astrocytes in the SN of normal C57BL/6 J mice, suggesting persistence of an immune-vigilant state. MPTP-induced microgliosis and astrogliosis in both strains suggest their involvement in pathogenesis. ELISA of pro-inflammatory cytokines in the ventral-midbrain revealed augmentation of TNF-α and IL-6 at middle age in both strains that reduced at old age, suggesting middle age as a critical, inflamm-aging-associated time point. TNF-α levels were high in C57BL/6 J, through aging and post-MPTP, while IL-6 and IL-1β were upregulated at old age. CD-1 had higher levels of anti-inflammatory cytokine TGF-β. MPTP challenge caused upregulation of enzymes MAO-A, MAO-B, and iNOS in both strains. Post-MPTP enhancement in fractalkine and hemeoxygenase-1 may be neuron-associated compensatory signals. Ultrastructural observations of elongated astroglial/microglial mitochondria vis-à-vis the shrunken ones in neurons suggest a scale-up of their functions with neurotoxic consequences. Thus, astroglia and microglia may modulate aging and PD susceptibility.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"13"},"PeriodicalIF":3.6,"publicationDate":"2025-01-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11753320/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143000764","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Correction: Sevoflurane Induces Learning and Memory Impairment in Young Mice Through a Reduction in Neuronal Glucose Transporter 3. 更正：七氟醚通过减少神经元葡萄糖转运蛋白3诱导幼鼠学习和记忆障碍。

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-16 DOI: 10.1007/s10571-024-01520-2

Jinpiao Zhu, Zongze Zhang, Junke Jia, Lirong Wang, Qiuyue Yang, Yanlin Wang, Chang Chen

引用次数: 0

Correction: Expression of CGRP in the Trigeminal Ganglion and Its Effect on the Polarization of Macrophages in Rats with Temporomandibular Arthritis. 修正：CGRP在三叉神经节的表达及其对颞下颌关节炎大鼠巨噬细胞极化的影响。

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-09 DOI: 10.1007/s10571-024-01527-9

Junli Tao, Xiaohui Wang, Jie Xu

引用次数: 0

A Focal Traumatic Injury to the Neonatal Rodent Spinal Cord Causes an Immediate and Massive Spreading Depolarization Sustained by Chloride Ions, with Transient Network Dysfunction. 幼鼠脊髓局灶性创伤损伤引起氯离子维持的立即和大量扩张性去极化，并伴有短暂的网络功能障碍。

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2025-01-02 DOI: 10.1007/s10571-024-01516-y

Atiyeh Mohammadshirazi, Graciela L Mazzone, Benjamín A Zylberberg, Giuliano Taccola

{"title":"A Focal Traumatic Injury to the Neonatal Rodent Spinal Cord Causes an Immediate and Massive Spreading Depolarization Sustained by Chloride Ions, with Transient Network Dysfunction.","authors":"Atiyeh Mohammadshirazi, Graciela L Mazzone, Benjamín A Zylberberg, Giuliano Taccola","doi":"10.1007/s10571-024-01516-y","DOIUrl":"10.1007/s10571-024-01516-y","url":null,"abstract":"In clinics, physical injuries to the spinal cord cause a temporary motor areflexia below lesion, known as spinal shock. This topic is still underexplored due to the lack of preclinical spinal cord injury (SCI) models that do not use anesthesia, which would affect spinal excitability. Our innovative design considered a custom-made micro impactor that provides localized and calibrated strikes to the ventral surface of the thoracic spinal cord of the entire CNS isolated from neonatal rats. Before and after injury, multiple ventral root (VR) recordings continuously traced respiratory rhythm, baseline spontaneous activities, and electrically induced reflex responses. As early as 200 ms after the lowering of the impactor, an immediate transient depolarization spread from the injury site to the whole spinal cord with distinct segmental velocities. Stronger strikes induced higher potentials causing, close by the site of injury, a transient drop in spinal cord oxygenation (SCO2) and a massive cell death with a complete functional disconnection of input along the cord. Below the impact site, expiratory rhythm and spontaneous lumbar activity were suppressed. On lumbar VRs, reflex responses transiently halted but later recovered to control values, while electrically induced fictive locomotion remained perturbed. Moreover, low-ion modified Krebs solutions differently influenced impact-induced depolarizations, the magnitude of which amplified in low Cl-. Overall, our novel ex vivo platform traces the immediate functional consequences of impacts to the spinal cord during development. This basic study provides insights on the SCI pathophysiology, unveiling an immediate chloride dysregulation.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"10"},"PeriodicalIF":3.6,"publicationDate":"2025-01-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11695467/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142913268","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Differences in Blood and Cerebrospinal Fluid Between Parkinson's Disease and Related Diseases. 帕金森病及相关疾病患者血液和脑脊液的差异

IF 3.6 4区医学

Cellular and Molecular Neurobiology Pub Date : 2024-12-27 DOI: 10.1007/s10571-024-01523-z

Jie Ma, Zhijian Tang, Yaqi Wu, Jun Zhang, Zitao Wu, Lulu Huang, Shengwen Liu, Yu Wang

{"title":"Differences in Blood and Cerebrospinal Fluid Between Parkinson's Disease and Related Diseases.","authors":"Jie Ma, Zhijian Tang, Yaqi Wu, Jun Zhang, Zitao Wu, Lulu Huang, Shengwen Liu, Yu Wang","doi":"10.1007/s10571-024-01523-z","DOIUrl":"10.1007/s10571-024-01523-z","url":null,"abstract":"It is difficult to distinguish Parkinson's disease (PD) in the early stage from those of various disorders including atypical Parkinson's syndrome (APS), vascular parkinsonism (VP), and even essential tremor (ET), because of the overlap of symptoms. Other, more challenging problems will arise when Parkinson's disease develops into Parkinson's disease dementia (PDD) in the middle and late stages. At this time, the differential diagnosis of PDD and DLB becomes thorny. These complicate the diagnostic process for PD, which traditionally heavily relies on symptomatic assessment and treatment response. Recent advances have identified several biomarkers in the blood and cerebrospinal fluid (CSF), including α-synuclein, lysosomal enzymes, fatty acid-binding proteins, and neurofilament light chain, whose concentration differs in PD and the related diseases. However, not all these molecules can effectively discriminate PD from related disorders. This review advocates for a paradigm shift toward biomarker-based diagnosis to effectively distinguish between PD and similar conditions. These biomarkers may reflect the diversity that exist among different diseases and provide an effective way to accurately understand their mechanisms. This review focused on blood and CSF biomarkers of PD that may have differential diagnostic value and the related molecular measurement methods with high diagnostic performance due to emerging technologies.","PeriodicalId":9742,"journal":{"name":"Cellular and Molecular Neurobiology","volume":"45 1","pages":"9"},"PeriodicalIF":3.6,"publicationDate":"2024-12-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11680620/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142892426","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0