Frontiers in Cellular Neuroscience最新文献_第4页

Voltage-gated potassium channels as a potential therapeutic target for the treatment of neurological and psychiatric disorders. 电压门控钾通道是治疗神经和精神疾病的潜在治疗靶点。

IF 4.2 3区医学

Frontiers in Cellular Neuroscience Pub Date : 2024-10-01 eCollection Date: 2024-01-01 DOI: 10.3389/fncel.2024.1449151

Isabel E Faulkner, Rachael Z Pajak, Michael K Harte, Jocelyn D Glazier, Reinmar Hager

{"title":"Voltage-gated potassium channels as a potential therapeutic target for the treatment of neurological and psychiatric disorders.","authors":"Isabel E Faulkner, Rachael Z Pajak, Michael K Harte, Jocelyn D Glazier, Reinmar Hager","doi":"10.3389/fncel.2024.1449151","DOIUrl":"https://doi.org/10.3389/fncel.2024.1449151","url":null,"abstract":"Voltage-gated potassium channels are a widely distributed subgroup of potassium channels responsible for the efflux of potassium in the repolarisation of the cell membrane, and hence contribute to the latency and propagation of action potentials. As they are causal to synaptic transmission, alterations to the structure of these channels can lead to a variety of neurological and psychiatric diseases. The Kv3 subfamily of voltage-gated potassium channels are found on many neurons in the brain, including inhibitory interneurons where they contribute to fast-frequency firing. Changes to the firing ability of these interneurons can lead to an imbalance of inhibitory and excitatory neurotransmission. To date, we have little understanding of the mechanism by which excitatory and inhibitory inputs become imbalanced. This imbalance is associated with cognitive deficits seen across neurological and neuropsychiatric disorders, which are currently difficult to treat. In this review, we collate evidence supporting the hypothesis that voltage-gated potassium channels, specifically the Kv3 subfamily, are central to many neurological and psychiatric disorders, and may thus be considered as an effective drug target. The collective evidence provided by the studies reviewed here demonstrates that Kv3 channels may be amenable to novel treatments that modulate the activity of these channels, with the prospect of improved patient outcome.","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11473391/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461927","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Anatomical and molecular development of the human primary visual cortex. 人类初级视觉皮层的解剖学和分子发育。

IF 4.2 3区医学

Frontiers in Cellular Neuroscience Pub Date : 2024-09-30 eCollection Date: 2024-01-01 DOI: 10.3389/fncel.2024.1427515

Kathryn M Murphy, Leanne Monteiro

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Anti-neuroinflammatory effects of conjugated linoleic acid isomers, c9,t11 and t10,c12, on activated BV-2 microglial cells. 共轭亚油酸异构体 c9,t11 和 t10,c12 对活化的 BV-2 小胶质细胞的抗神经炎作用。

IF 4.2 3区医学

Frontiers in Cellular Neuroscience Pub Date : 2024-09-27 eCollection Date: 2024-01-01 DOI: 10.3389/fncel.2024.1442786

Clara Porcedda, Claudia Manca, Gianfranca Carta, Franca Piras, Sebastiano Banni, Valeria Sogos, Elisabetta Murru

{"title":"Anti-neuroinflammatory effects of conjugated linoleic acid isomers, c9,t11 and t10,c12, on activated BV-2 microglial cells.","authors":"Clara Porcedda, Claudia Manca, Gianfranca Carta, Franca Piras, Sebastiano Banni, Valeria Sogos, Elisabetta Murru","doi":"10.3389/fncel.2024.1442786","DOIUrl":"https://doi.org/10.3389/fncel.2024.1442786","url":null,"abstract":"Conjugated linoleic acid (CLA) isomers exhibit anti-inflammatory properties within the central nervous system (CNS). This study investigated the effects of CLA isomers c9,t11 and t10,c12 on fatty acid (FA) and N-acylethanolamine (NAE) profiles and their association with pro-inflammatory molecule expression in BV-2 microglia cell line, the CNS's resident immune cells responsible for maintaining neuronal activity and immune homeostasis. BV-2 cells were treated with 25 μM of c9,t11-CLA, t10,c12-CLA, or oleic acid (OA) for 24 h, followed by lipopolysaccharide (LPS) stimulation. After treatment, the cell's FA and NAE profiles and pro-inflammatory molecule expression were analyzed. Our results demonstrated that CLA isomers mitigate LPS-induced morphological changes in BV-2 cells and reduce gene expression and protein levels of inflammatory markers. This effect was linked to an upregulation of acyl-CoA oxidase 1, a key enzyme in the anti-inflammatory peroxisomal beta-oxidation pathway that efficiently metabolizes CLA isomers. Notably, t10,c12-CLA significantly suppressed stearoyl-CoA desaturase 1, impacting monounsaturated fatty acid synthesis. The NAEs profile was remarkably altered by CLA isomers, with a significant release of the anti-neuroinflammatory mediator docosahexaenoic acid (DHA)-derived N-acylethanolamine (DHAEA). In conclusion, our findings suggest that the anti-neuroinflammatory effects of CLA isomers are due to their unique influences on FA metabolism and the modulation of bioactive FA-derived NAEs, highlighting a potential strategy for nutritional intervention in conditions characterized by neuroinflammation.","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11466893/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142461922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Corrigendum: Contribution of thyrotropin-releasing hormone to cerebellar long-term depression and motor learning. 更正：促甲状腺激素释放激素对小脑长期抑制和运动学习的贡献

IF 4.2 3区医学

Frontiers in Cellular Neuroscience Pub Date : 2024-09-26 eCollection Date: 2024-01-01 DOI: 10.3389/fncel.2024.1495155

Masashi Watanave, Yasunori Matsuzaki, Yasuyo Nakajima, Atsushi Ozawa, Masanobu Yamada, Hirokazu Hirai

引用次数: 0

Editorial: Gateways to the brain: vascular-glial-immune network in health and disease. 社论：通往大脑的门户：健康与疾病中的血管-神经胶质-免疫网络。

IF 4.2 3区医学

Frontiers in Cellular Neuroscience Pub Date : 2024-09-26 eCollection Date: 2024-01-01 DOI: 10.3389/fncel.2024.1461604

Diana Matias, Patrícia P Garcez, Helena Florindo, Luis Graça, Luiz Gustavo Dubois

引用次数: 0

The gut-eye axis: the retinal/ocular degenerative diseases and the emergent therapeutic strategies. 肠眼轴：视网膜/眼部变性疾病与新兴治疗策略。

IF 4.2 3区医学

Frontiers in Cellular Neuroscience Pub Date : 2024-09-26 eCollection Date: 2024-01-01 DOI: 10.3389/fncel.2024.1468187

Sonda Kammoun, Mona Rekik, Aryj Dlensi, Samir Aloulou, Walid Smaoui, Sahla Sellami, Khaled Trigui, Rahma Gargouri, Imen Chaari, Hayet Sellami, Dhawia Elatoui, Nahed Khemakhem, Ines Hadrich, Sourour Neji, Balkiss Abdelmoula, Nouha Bouayed Abdelmoula

{"title":"The gut-eye axis: the retinal/ocular degenerative diseases and the emergent therapeutic strategies.","authors":"Sonda Kammoun, Mona Rekik, Aryj Dlensi, Samir Aloulou, Walid Smaoui, Sahla Sellami, Khaled Trigui, Rahma Gargouri, Imen Chaari, Hayet Sellami, Dhawia Elatoui, Nahed Khemakhem, Ines Hadrich, Sourour Neji, Balkiss Abdelmoula, Nouha Bouayed Abdelmoula","doi":"10.3389/fncel.2024.1468187","DOIUrl":"10.3389/fncel.2024.1468187","url":null,"abstract":"The interplay between human microbiota and various physiological systems has garnered significant attention in recent years. The gut microbiota plays a critical role in maintaining physiological homeostasis and influences various aspects of human health, particularly via the gut brain axis. Since 2017, the challenging concept of the gut-retina axis has emerged thanks to a network analysis emphasizing the potential role of the gut microbiota disruption in the development of the age-related macular degeneration and further retinal damages. Many other ocular disorders have been linked to the dysbiosis of the gut microbiota, including uveitis and glaucoma. It has been shown that age related macular degeneration can be prevented or reversed using a diet that induces changes in the gut microbiota. The potential link between the gut microbiota as well as others types of microbiota such as the ocular surface microbiota and the development/progression of age related as well as inherited retinal degenerations and other degenerative eye diseases, has recently been broadened. Therefore, the pathogenesis of several eye diseases has recently been associated with a larger perception called the gut eye axis. This mini-review examines the potential mechanisms underlying the gut eye axis and suggests implications for the management of eye diseases. By understanding the modulation of the gut microbiota and its impact on eye disease, this mini-review provides insight into potential therapeutic interventions and avenues for future research.","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11464360/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142399880","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Dysregulated mTOR networks in experimental sporadic Alzheimer's disease. 实验性散发性阿尔茨海默病中失调的 mTOR 网络。

IF 4.2 3区医学

Frontiers in Cellular Neuroscience Pub Date : 2024-09-25 eCollection Date: 2024-01-01 DOI: 10.3389/fncel.2024.1432359

Suzanne M de la Monte, Ming Tong

{"title":"Dysregulated mTOR networks in experimental sporadic Alzheimer's disease.","authors":"Suzanne M de la Monte, Ming Tong","doi":"10.3389/fncel.2024.1432359","DOIUrl":"10.3389/fncel.2024.1432359","url":null,"abstract":"Background: Beyond the signature amyloid-beta plaques and neurofibrillary tangles, Alzheimer's disease (AD) has been shown to exhibit dysregulated metabolic signaling through insulin and insulin-like growth factor (IGF) networks that crosstalk with the mechanistic target of rapamycin (mTOR). Its broad impact on brain structure and function suggests that mTOR is likely an important therapeutic target for AD.Objective: This study characterizes temporal lobe (TL) mTOR signaling abnormalities in a rat model of sporadic AD neurodegeneration.Methods: Long Evans rats were given intracerebroventricular injections of streptozotocin (ic-STZ) or saline (control), and 4 weeks later, they were administered neurobehavioral tests followed by terminal harvesting of the TLs for histopathological study and measurement of AD biomarkers, neuroinflammatory/oxidative stress markers, and total and phosphorylated insulin/IGF-1-Akt-mTOR pathway signaling molecules.Results: Rats treated with ic-STZ exhibited significantly impaired performance on Rotarod (RR) and Morris Water Maze (MWM) tests, brain atrophy, TL and hippocampal neuronal and white matter degeneration, and elevated TL pTau, AβPP, Aβ, AChE, 4-HNE, and GAPDH and reduced ubiquitin, IL-2, IL-6, and IFN-γ immunoreactivities. In addition, ic-STZ reduced TL pY1135/1136-IGF-1R, Akt, PTEN, pS380-PTEN, pS2448-mTOR, p70S6K, pT412-p70S6K, p/T-pT412-p70S6K, p/T-Rictor, and p/T-Raptor.Conclusion: Experimental ic-STZ-induced sporadic AD-type neurodegeneration with neurobehavioral dysfunctions associated with inhibition of mTOR signaling networks linked to energy metabolism, plasticity, and white matter integrity.","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11461251/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142389273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

GABAergic dysfunction in postmortem dorsolateral prefrontal cortex: implications for cognitive deficits in schizophrenia and affective disorders. 死后背外侧前额叶皮层的 GABA 能功能障碍：对精神分裂症和情感障碍的认知缺陷的影响。

IF 4.2 3区医学

Frontiers in Cellular Neuroscience Pub Date : 2024-09-24 eCollection Date: 2024-01-01 DOI: 10.3389/fncel.2024.1440834

Hannah Hughes, Lillian J Brady, Kirsten E Schoonover

{"title":"GABAergic dysfunction in postmortem dorsolateral prefrontal cortex: implications for cognitive deficits in schizophrenia and affective disorders.","authors":"Hannah Hughes, Lillian J Brady, Kirsten E Schoonover","doi":"10.3389/fncel.2024.1440834","DOIUrl":"https://doi.org/10.3389/fncel.2024.1440834","url":null,"abstract":"The microcircuitry within superficial layers of the dorsolateral prefrontal cortex (DLPFC), composed of excitatory pyramidal neurons and inhibitory GABAergic interneurons, has been suggested as the neural substrate of working memory performance. In schizophrenia, working memory impairments are thought to result from alterations of microcircuitry within the DLPFC. GABAergic interneurons, in particular, are crucially involved in synchronizing neural activity at gamma frequency, the power of which increases with working memory load. Alterations of GABAergic interneurons, particularly parvalbumin (PV) and somatostatin (SST) subtypes, are frequently observed in schizophrenia. Abnormalities of GABAergic neurotransmission, such as deficiencies in the 67 kDA isoform of GABA synthesis enzyme (GAD67), vesicular GABA transporter (vGAT), and GABA reuptake transporter 1 (GAT1) in presynaptic boutons, as well as postsynaptic alterations in GABA A receptor subunits further contribute to impaired inhibition. This review explores GABAergic abnormalities of the postmortem DLPFC in schizophrenia, with a focus on the roles of interneuron subtypes involved in cognition, and GABAergic neurotransmission within presynaptic boutons and postsynaptic alterations. Where available, comparisons between schizophrenia and affective disorders that share cognitive pathology such as bipolar disorder and major depressive disorder will be made. Challenges in directly measuring GABA levels are addressed, emphasizing the need for innovative techniques. Understanding GABAergic abnormalities and their implications for neural circuit dysfunction in schizophrenia is crucial for developing targeted therapies.","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11458443/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142389276","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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

Editorial: Microglia in neurodegenerative diseases. 社论：神经退行性疾病中的小胶质细胞。

IF 4.2 3区医学

Frontiers in Cellular Neuroscience Pub Date : 2024-09-24 eCollection Date: 2024-01-01 DOI: 10.3389/fncel.2024.1473576

Ting Li, Ana María Espinosa-Oliva

引用次数: 0

Activation of arginine vasopressin receptor 1a reduces inhibitory synaptic currents at reciprocal synapses in the mouse accessory olfactory bulb. 激活精氨酸加压素受体1a可降低小鼠附属嗅球互惠突触的抑制性突触电流

IF 4.2 3区医学

Frontiers in Cellular Neuroscience Pub Date : 2024-09-24 eCollection Date: 2024-01-01 DOI: 10.3389/fncel.2024.1466817

Mutsuo Taniguchi, Yoshihiro Murata, Masahiro Yamaguchi, Hideto Kaba

{"title":"Activation of arginine vasopressin receptor 1a reduces inhibitory synaptic currents at reciprocal synapses in the mouse accessory olfactory bulb.","authors":"Mutsuo Taniguchi, Yoshihiro Murata, Masahiro Yamaguchi, Hideto Kaba","doi":"10.3389/fncel.2024.1466817","DOIUrl":"10.3389/fncel.2024.1466817","url":null,"abstract":"Central arginine vasopressin (AVP) facilitates social recognition and modulates many complex social behaviors in mammals that, in many cases, recognize each other based on olfactory and/or pheromonal signals. AVP neurons are present in the accessory olfactory bulb (AOB), which is the first relay in the vomeronasal system and has been demonstrated to be a critical site for mating-induced mate recognition (olfactory memory) in female mice. The transmission of information from the AOB to higher centers is controlled by the dendrodendritic recurrent inhibition, i.e., inhibitory postsynaptic currents (IPSCs) generated in mitral cells by recurrent dendrodendritic inhibitory inputs from granule cells. These reports suggest that AVP might play an important role in regulating dendrodendritic inhibition in the AOB. To test this hypothesis, we examined the effects of extracellularly applied AVP on synaptic responses measured from mitral and granule cells in slice preparations from 23--36-day-old Balb/c mice. To evoke dendrodendritic inhibition in a mitral cell, depolarizing voltages of -70 to 0 mV (10 ms duration) were applied to a mitral cell using a conventional whole-cell configuration. We found that AVP significantly reduced the IPSCs. The suppressive effects of AVP on the IPSCs was diminished by an antagonist for vasopressin receptor 1a (V1aR) (Manning compound), but not by an antagonist for vasopressin receptor 1b (SSR149415). An agonist for V1aRs [(Phe2)OVT] mimicked the action of AVP on IPSCs. Additionally, AVP significantly suppressed voltage-activated currents in granule cells without affecting the magnitude of the response of mitral cells to gamma-aminobutyric acid (GABA). The present results suggest that V1aRs play a role in reciprocal transmission between mitral cells and granule cells in the mouse AOB by reducing GABAergic transmission through a presynaptic mechanism in granule cells.","PeriodicalId":12432,"journal":{"name":"Frontiers in Cellular Neuroscience","volume":null,"pages":null},"PeriodicalIF":4.2,"publicationDate":"2024-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11462548/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142389271","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"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