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Frontiers in Molecular Neuroscience

Mario Stampanoni Bassi, Sara Garofalo, Girolama A Marfia, Luana Gilio, Ilaria Simonelli, Annamaria Finardi, Roberto Furlan, Giulia M Sancesario, Jonny Di Giandomenico, Marianna Storto, Francesco Mori, Diego Centonze, Ennio Iezzi
Cognitive deficits are frequently observed in multiple sclerosis (MS), mainly involving processing speed and episodic memory. Both demyelination and gray matter atrophy can contribute to cognitive deficits in MS. In recent years, neuroinflammation is emerging as a new factor influencing clinical course in MS. Inflammatory cytokines induce synaptic dysfunction in MS. Synaptic plasticity occurring within hippocampal structures is considered as one of the basic physiological mechanisms of learning and memory. In experimental models of MS, hippocampal plasticity is profoundly altered by proinflammatory cytokines...
2017: Frontiers in Molecular Neuroscience
Liang Kong, Yan Zhao, Wen-Juan Zhou, Hui Yu, Shuai-Wen Teng, Qi Guo, Zheyu Chen, Yue Wang
The metabolism of glucose is a nearly exclusive source of energy for maintaining neuronal survival, synaptic transmission and information processing in the brain. Two glucose metabolism pathways have been reported, direct neuronal glucose uptake and the astrocyte-neuron lactate shuttle (ANLS), which can be involved in these functions simultaneously or separately. Although ANLS in the dorsal hippocampus (DH) has been proved to be required for memory consolidation, the specific metabolic pathway involved during memory acquisition remains unclear...
2017: Frontiers in Molecular Neuroscience
Chih-Chung Lin, Chien-Chung Yang, Li-Der Hsiao, Ssu-Yu Chen, Chuen-Mao Yang
Neurodegenerative disorders and brain damage are initiated by excessive production of reactive oxygen species (ROS), which leads to tissue injury, cellular death and inflammation. In cellular anti-oxidant systems, heme oxygenase-1 (HO-1) is an oxidative-sensor protein induced by ROS generation or carbon monoxide (CO) release. CO releasing molecules (CORMs), including CORM-3, exert anti-oxidant and anti-inflammatory effects. However, the molecular mechanisms of CORM-3-induced HO-1 expression and protection against interleukin (IL)-1β-induced inflammatory responses have not been fully elucidated in rat brain astrocytes (RBA-1)...
2017: Frontiers in Molecular Neuroscience
Xuemei Xie, Li Peng, Jin Zhu, Yang Zhou, Lingyu Li, Yanlin Chen, Shanshan Yu, Yong Zhao
Nurr1 is a member of the nuclear receptor 4 family of orphan nuclear receptors that is decreased in inflammatory responses and leads to neurons death in Parkinson's disease. Abnormal expression of Nurr1 have been attributed to various signaling pathways, but little is known about microRNAs (miRNAs) regulation of Nurr1 in ischemia/reperfusion injury. To investigate the post transcriptional regulatory networks of Nurr1, we used a miRNA screening approach and identified miR-145-5p as a putative regulator of Nurr1...
2017: Frontiers in Molecular Neuroscience
Rongchen Huang, Min Chen, Leiqing Yang, Mahendra Wagle, Su Guo, Bing Hu
Axon regeneration, fundamental to nerve repair, and functional recovery, relies on rapid changes in gene expression attributable to microRNA (miRNA) regulation. MiR-133b has been proved to play an important role in different organ regeneration in zebrafish, but its role in regulating axon regeneration in vivo is still controversial. Here, combining single-cell electroporation with a vector-based miRNA-expression system, we have modulated the expression of miR-133b in Mauthner-cells (M-cells) at the single-cell level in zebrafish...
2017: Frontiers in Molecular Neuroscience
Felix L Struebing, Jiaxing Wang, Ying Li, Rebecca King, Olivia C Mistretta, Arthur W English, Eldon E Geisert
In both the central nervous system (CNS) and the peripheral nervous system (PNS), axonal injury induces changes in neuronal gene expression. In the PNS, a relatively well-characterized alteration in transcriptional activation is known to promote axonal regeneration. This transcriptional cascade includes the neurotrophin Bdnf and the transcription factor Sox11. Although both molecules act to facilitate successful axon regeneration in the PNS, this process does not occur in the CNS. The present study examines the differential expression of Sox11 and Bdnf mRNA isoforms in the PNS and CNS using three experimental paradigms at different time points: (i) the acutely injured CNS (retina after optic nerve crush) and PNS (dorsal root ganglion after sciatic nerve crush), (ii) a CNS regeneration model (retina after optic nerve crush and induced regeneration); and (iii) the retina during a chronic form of central neurodegeneration (the DBA/2J glaucoma model)...
2017: Frontiers in Molecular Neuroscience
Yanyun Sun, Xi Chen, Xinyu Zhang, Xianzhi Shen, Mengwei Wang, Xiaona Wang, Wen-Cao Liu, Chun-Feng Liu, Jie Liu, Wenlan Liu, Xinchun Jin
[This corrects the article on p. 257 in vol. 10, PMID: 28855859.].
2017: Frontiers in Molecular Neuroscience
Fabian Arenas, Carmen Garcia-Ruiz, Jose C Fernandez-Checa
Cholesterol is a critical component of membrane bilayers where it plays key structural and functional roles by regulating the activity of diverse signaling platforms and pathways. Particularly enriched in brain, cholesterol homeostasis in this organ is singular with respect to other tissues and exhibits a heterogeneous regulation in distinct brain cell populations. Due to the key role of cholesterol in brain physiology and function, alterations in cholesterol homeostasis and levels have been linked to brain diseases and neurodegeneration...
2017: Frontiers in Molecular Neuroscience
Nemat Khan, Arjun Muralidharan, Maree T Smith
Recent preclinical and proof-of-concept clinical studies have shown promising analgesic efficacy of selective small molecule angiotensin II type 2 (AT2) receptor antagonists in the alleviation of peripheral neuropathic pain. However, their cellular and molecular mechanism of action requires further investigation. To address this issue, groups of adult male Sprague-Dawley rats with fully developed unilateral hindpaw hypersensitivity, following chronic constriction injury (CCI) of the sciatic nerve, received a single intraperitoneal bolus dose of the small molecule AT2 receptor antagonist, EMA300 (10 mg kg-1), or vehicle...
2017: Frontiers in Molecular Neuroscience
Mauricio A Retamal, Manuel A Riquelme, Jimmy Stehberg, Julio Alcayaga
In this review article, we summarize the current insight on the role of Connexin- and Pannexin-based channels as modulators of sensory neurons. The somas of sensory neurons are located in sensory ganglia (i.e., trigeminal and nodose ganglia). It is well known that within sensory ganglia, sensory neurons do not form neither electrical nor chemical synapses. One of the reasons for this is that each soma is surrounded by glial cells, known as satellite glial cells (SGCs). Recent evidence shows that connexin43 (Cx43) hemichannels and probably pannexons located at SGCs have an important role in paracrine communication between glial cells and sensory neurons...
2017: Frontiers in Molecular Neuroscience
Dorota Wyczechowska, Hui-Yi Lin, Andrea LaPlante, Duane Jeansonne, Adam Lassak, Christopher H Parsons, Patricia E Molina, Francesca Peruzzi
HIV-associated neurocognitive disorders (HAND) affects more than half of persons living with HIV-1/AIDS (PLWHA). Identification of biomarkers representing the cognitive status of PLWHA is a critical step for implementation of successful cognitive, behavioral and pharmacological strategies to prevent onset and progression of HAND. However, the presence of co-morbidity factors in PLWHA, the most common being substance abuse, can prevent the identification of such biomarkers. We have optimized a protocol to profile plasma miRNAs using quantitative RT-qPCR and found a miRNA signature with very good discriminatory ability to distinguish PLWHA with cognitive impairment from those without cognitive impairment...
2017: Frontiers in Molecular Neuroscience
Ignacio M Larrayoz, Hilda Ferrero, Eva Martisova, Francisco J Gil-Bea, María J Ramírez, Alfredo Martínez
Memory decline is common in elderly individuals and is the hallmark of Alzheimer's disease (AD). Memory failure follows the loss of synaptic contacts in the cerebral cortex and hippocampus, caused in part by cytoskeleton disruption. Adrenomedullin (AM) and its gene-related peptide, proadrenomedullin N-terminal 20 peptide (PAMP), are microtubule-associated proteins (MAP) whose expression has been identified as a potential biomarker for predicting progression from predementia to clinical AD. Here we analyze the connection between AM levels and memory preservation...
2017: Frontiers in Molecular Neuroscience
Jaewook Kim, Yeon-Kyun Shin
Ca2+-triggered SNARE-mediated membrane fusion is essential for neuronal communication. The speed of this process is of particular importance because it sets a time limit to cognitive and physical activities. In this work, we expand the proteoliposome-to-supported bilayer (SBL) fusion assay by successfully incorporating synaptotagmin 1 (Syt1), a major Ca2+ sensor. We report that Syt1 and Ca2+ together can elicit more than a 50-fold increase in the number of membrane fusion events when compared with membrane fusion mediated by SNAREs only...
2017: Frontiers in Molecular Neuroscience
Benoit Lizen, Charlotte Moens, Jinane Mouheiche, Thomas Sacré, Marie-Thérèse Ahn, Lucie Jeannotte, Ahmad Salti, Françoise Gofflot
Hoxa5 is a member of the Hox gene family that plays critical roles in successive steps of the central nervous system formation during embryonic and fetal development. In the mouse, Hoxa5 was recently shown to be expressed in the medulla oblongata and the pons from fetal stages to adulthood. In these territories, Hoxa5 transcripts are enriched in many precerebellar neurons and several nuclei involved in autonomic functions, while the HOXA5 protein is detected mainly in glutamatergic and GABAergic neurons. However, whether HOXA5 is functionally required in these neurons after birth remains unknown...
2017: Frontiers in Molecular Neuroscience
Marwa Elamin, David N Ruskin, Susan A Masino, Paola Sacchetti
The ketogenic diet's (KD) anticonvulsant effects have been well-documented for nearly a century, including in randomized controlled trials. Some patients become seizure-free and some remain so after diet cessation. Many recent studies have explored its expanded therapeutic potential in diverse neurological disorders, yet no mechanism(s) of action have been established. The diet's high fat, low carbohydrate composition reduces glucose utilization and promotes the production of ketone bodies. Ketone bodies are a more efficient energy source than glucose and improve mitochondrial function and biogenesis...
2017: Frontiers in Molecular Neuroscience
Qingwei Lai, Wantong Du, Jian Wu, Xiao Wang, Xinyu Li, Xuebin Qu, Xiuxiang Wu, Fuxing Dong, Ruiqin Yao, Hongbin Fan
Recently, it is reported that monocarboxylate transporter 1 (MCT1) plays crucial role in oligodendrocyte differentiation and myelination. We found that MCT1 is strongly expressed in oligodendrocyte but weakly expressed in oligodendrocyte precursors (OPCs), and the underlying mechanisms remain elusive. Histone deacetylases (HDACs) activity is required for induction of oligodendrocyte differentiation and maturation. We asked whether HDACs are involved in the regulation of MCT1 expression. This work revealed that the acetylation level of histone H3K9 (H3K9ac) was much higher in mct1 gene (Slc16a1) promoter in OPCs than that in oligodendrocyte...
2017: Frontiers in Molecular Neuroscience
Ji Won Um
Glial cells are essential for every aspect of normal neuronal development, synapse formation, and function in the central nervous system (CNS). Astrocytes secrete a variety of factors that regulate synaptic connectivity and circuit formation. Microglia also modulate synapse development through phagocytic activity. Most of the known actions of CNS glial cells are limited to roles at excitatory synapses. Nevertheless, studies have indicated that both astrocytes and microglia shape inhibitory synaptic connections through various mechanisms, including release of regulatory molecules, direct contact with synaptic terminals, and utilization of mediators in the extracellular matrix...
2017: Frontiers in Molecular Neuroscience
Ryan N Delgado, Daniel A Lim
Throughout embryonic development and into postnatal life, regionally distinct populations of neural progenitor cells (NPCs) collectively generate the many different types of neurons that underlie the complex structure and function of the adult mammalian brain. At very early stages of telencephalic development, NPCs become organized into regional domains that each produce different subsets of neurons. This positional identity of NPCs relates to the regional expression of specific, fate-determining homeodomain transcription factors...
2017: Frontiers in Molecular Neuroscience
Yan Zhu, Juline Beudez, Ning Yu, Thomas Grutter, Hong-Bo Zhao
The P2X2 receptor is an ATP-gated ion channel, assembled by three subunits. Recently, it has been found that heterozygous mutations of P2X2 V60L and G353R can cause autosomal dominant nonsyndromic hearing loss. However, the underlying mechanism remains unclear. The fact that heterozygous mutations cause deafness suggests that the mutations may have dominant-negative effect (DNE) on wild-type (WT) P2X2 isoforms and/or other partners leading to hearing loss. In this study, the effect of these dominant deafness P2X2 mutations on WT P2X2 was investigated...
2017: Frontiers in Molecular Neuroscience
Ksenija Zega, Vukasin M Jovanovic, Zagorka Vitic, Magdalena Niedzielska, Laura Knaapi, Marin M Jukic, Juha Partanen, Roland F Friedel, Roland Lang, Claude Brodski
Hydrocephalus can occur in children alone or in combination with other neurodevelopmental disorders that are often associated with brain overgrowth. Despite the severity of these disorders, the molecular and cellular mechanisms underlying these pathologies and their comorbidity are poorly understood. Here, we studied the consequences of genetically inactivating in mice dual-specificity phosphatase 16 (Dusp16), which is known to negatively regulate mitogen-activated protein kinases (MAPKs) and which has never previously been implicated in brain development and disorders...
2017: Frontiers in Molecular Neuroscience
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