scholarly journals Microglia: An Active Player in the Regulation of Synaptic Activity

2013 ◽  
Vol 2013 ◽  
pp. 1-9 ◽  
Author(s):  
Kyungmin Ji ◽  
Jeremy Miyauchi ◽  
Stella E. Tsirka
Keyword(s):  
Central Nervous System ◽  
Critical Role ◽  
Innate Immune ◽  
Synaptic Activity ◽  
Cell Type ◽  
Synaptic Development ◽  
Active Player ◽  
The Central Nervous System ◽  
Shed Light

Synaptic plasticity is critical for elaboration and adaptation in the developing and developed brain. It is well established that astrocytes play an important role in the maintenance of what has been dubbed “the tripartite synapse”. Increasing evidence shows that a fourth cell type, microglia, is critical to this maintenance as well. Microglia are the resident macrophages of the central nervous system (CNS). Because of their well-characterized inflammatory functions, research has primarily focused on their innate immune properties. The role of microglia in the maintenance of synapses in development and in homeostasis is not as well defined. A number of significant findings have shed light on the critical role of microglia at the synapse. It is becoming increasingly clear that microglia play a seminal role in proper synaptic development and elimination.

scholarly journals Snapin deficiency is associated with developmental defects of the central nervous system

2010 ◽  
Vol 31 (2) ◽  
pp. 151-158 ◽  
Author(s):  
Bing Zhou ◽  
Yi-Bing Zhu ◽  
Lin Lin ◽  
Qian Cai ◽  
Zu-Hang Sheng
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Protein Quality ◽  
Third Ventricle ◽  
Critical Role ◽  
Developmental Defects ◽  
Lysosomal Function ◽  
Quality Control Process ◽  
The Central Nervous System

The autophagy–lysosomal pathway is an intracellular degradation process essential for maintaining neuronal homoeostasis. Defects in this pathway have been directly linked to a growing number of neurodegenerative disorders. We recently revealed that Snapin plays a critical role in co-ordinating dynein-driven retrograde transport and late endosomal–lysosomal trafficking, thus maintaining efficient autophagy–lysosomal function. Deleting snapin in neurons impairs lysosomal proteolysis and reduces the clearance of autolysosomes. The role of the autophagy–lysosomal system in neuronal development is, however, largely uncharacterized. Here, we report that snapin deficiency leads to developmental defects in the central nervous system. Embryonic snapin−/− mouse brain showed reduced cortical plates and intermediate zone cell density, increased apoptotic death in the cortex and third ventricle, enhanced membrane-bound LC3-II staining associated with autophagic vacuoles and an accumulation of polyubiquitinated proteins in the cortex and hippocampus. Thus our results provide in vivo evidence for the essential role of late endocytic transport and autophagy–lysosomal function in maintaining neuronal survival and development of the mammalian central nervous system. In addition, our study supports the existence of a functional interplay between the autophagy–lysosome and ubiquitin–proteasome systems in the protein quality-control process.

scholarly journals The Role of CARD9 Deficiency in Neutrophils

2021 ◽  
Vol 2021 ◽  
pp. 1-5
Author(s):  
Ruanmei Sheng ◽  
Xiaoming Zhong ◽  
Zhiwen Yang ◽  
Xuemin Wang
Keyword(s):  
Critical Role ◽  
Myeloid Cell ◽  
Immune Defense ◽  
Innate Immune ◽  
Innate Immune Defense ◽  
The Central Nervous System ◽  
Clinical Advances ◽  
Insight Into ◽  
Increased Susceptibility

Neutrophils play a critical role in innate immune defense and directly contribute to infectious and autoimmune ailments. Great efforts are underway to better understand the nature of neutrophilic inflammation. Of note, CARD9, a myeloid cell-specific signaling protein that mainly expresses in macrophages and dendritic cells, is also present in neutrophils, emerging as a critical mediator for intercellular communication. CARD9–deficiency neutrophils display an increased susceptibility to fungal infection that primarily localize to the central nervous system, subcutaneous, and skin tissue. Additionally, CARD9–deficiency neutrophils are associated with some autoimmune diseases and even provide protection against a few bacteria. Here, the review summarizes recent preclinical and clinical advances that have provided a novel insight into the pathogenesis of CARD9 deficiency in neutrophils.

scholarly journals The Role of Extracellular Vesicles in Demyelination of the Central Nervous System

2020 ◽  
Vol 21 (23) ◽  
pp. 9111
Author(s):  
José Antonio López-Guerrero ◽  
Inés Ripa ◽  
Sabina Andreu ◽  
Raquel Bello-Morales
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Extracellular Vesicles ◽  
Viral Infections ◽  
Membrane Vesicles ◽  
Synaptic Activity ◽  
Demyelinating Diseases ◽  
Parkinson’S Diseases ◽  
The Central Nervous System

It is being increasingly demonstrated that extracellular vesicles (EVs) are deeply involved in the physiology of the central nervous system (CNS). Processes such as synaptic activity, neuron-glia communication, myelination and immune response are modulated by EVs. Likewise, these vesicles may participate in many pathological processes, both as triggers of disease or, on the contrary, as mechanisms of repair. EVs play relevant roles in neurodegenerative disorders such as Alzheimer’s or Parkinson’s diseases, in viral infections of the CNS and in demyelinating pathologies such as multiple sclerosis (MS). This review describes the involvement of these membrane vesicles in major demyelinating diseases, including MS, neuromyelitis optica, progressive multifocal leukoencephalopathy and demyelination associated to herpesviruses.

scholarly journals Molecular genetic defects in congenital hypothyroidism

2004 ◽  
pp. U39-U44 ◽  
Author(s):  
A Gruters ◽  
H Krude ◽  
H Biebermann
Keyword(s):  
Central Nervous System ◽  
Congenital Hypothyroidism ◽  
Molecular Genetic ◽  
Critical Role ◽  
Genetic Defects ◽  
Cns Development ◽  
Central Hypothyroidism ◽  
Molecular Defects ◽  
The Central Nervous System

Recently molecular genetic defects in some cases of congenital hypothyroidism (CH) as well as of rare cases of central hypothyroidism have been identified. These studies have led to the description of so far unexplained forms of these disorders. In some patients with CH early diagnosis by newborn screening and early treatment was not able to lead to a normal mental development. This could subsequently be explained by molecular defects of transcription factors (FOXE-1/FKHL15, NKX2.1) which are important not only for the embryonic development of the thyroid gland but also for other organs including the central nervous system (CNS). These findings will help in understanding the critical role of thyroid hormones in the pre-and postnatal CNS development. However, many questions regarding the molecular defects and their consequences in the majority of patients with CH still remain open and will be addressed in this article.

scholarly journals The Dichotomous Role of Inflammation in the CNS: A Mitochondrial Point of View

Biomolecules ◽  
2020 ◽  
Vol 10 (10) ◽  
pp. 1437
Author(s):  
Bianca Vezzani ◽  
Marianna Carinci ◽  
Simone Patergnani ◽  
Matteo P. Pasquin ◽  
Annunziata Guarino ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Epileptic Seizures ◽  
Point Of View ◽  
Innate Immune ◽  
Molecular Signaling ◽  
Therapeutic Approaches ◽  
Neuroinflammatory Response ◽  
The Central Nervous System

Innate immune response is one of our primary defenses against pathogens infection, although, if dysregulated, it represents the leading cause of chronic tissue inflammation. This dualism is even more present in the central nervous system, where neuroinflammation is both important for the activation of reparatory mechanisms and, at the same time, leads to the release of detrimental factors that induce neurons loss. Key players in modulating the neuroinflammatory response are mitochondria. Indeed, they are responsible for a variety of cell mechanisms that control tissue homeostasis, such as autophagy, apoptosis, energy production, and also inflammation. Accordingly, it is widely recognized that mitochondria exert a pivotal role in the development of neurodegenerative diseases, such as multiple sclerosis, Parkinson’s and Alzheimer’s diseases, as well as in acute brain damage, such in ischemic stroke and epileptic seizures. In this review, we will describe the role of mitochondria molecular signaling in regulating neuroinflammation in central nervous system (CNS) diseases, by focusing on pattern recognition receptors (PRRs) signaling, reactive oxygen species (ROS) production, and mitophagy, giving a hint on the possible therapeutic approaches targeting mitochondrial pathways involved in inflammation.

scholarly journals The central nervous system and experimental diabetes mellitus

1995 ◽  
Vol 41 (1) ◽  
pp. 39-45
Author(s):  
H. A. Shvyrkova
Keyword(s):  
Diabetes Mellitus ◽  
Central Nervous System ◽  
Nervous System ◽  
Experimental Studies ◽  
Synaptic Activity ◽  
Experimental Diabetes Mellitus ◽  
Patients With Diabetes ◽  
Development And Differentiation ◽  
The Central Nervous System

After the publication of data on the detection of insulin in brain tissue, interest in studying the role of insulin in the central nervous system (CNS) and changes in the central nervous system in diabetes mellitus increased sharply. In patients with diabetes, a high frequency of mental disorders has been established. Complications of the nervous system in children whose mothers were pregnant with diabetes during pregnancy are described in literature. The role of insulin in the development and differentiation of neurons, potentiation of synaptic activity, the exchange of catecholamines, transcription of genes in nerve cells has been identified, which allows a better understanding of the mechanism of diabetic encephalopathy. This review analyzes the results of experimental studies of the central nervous system in diabetes.

Sign in / Sign up

Export Citation Format

Share Document