A Model of Developmental Synapse Elimination in the Central Nervous System: Possible Mechanisms and Functional Consequences

Author(s):  
Ann M. Lohof ◽  
Yannick Bailly ◽  
Nicole Delhaye-Bouchaud ◽  
Jean Mariani
1998 ◽  
pp. 253-284 ◽  
Author(s):  
David Lyons ◽  
Christopher T. Whitlow ◽  
Hilary R. Smith ◽  
Linda J. Porrino

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 529
Author(s):  
Elena V. Ryabova ◽  
Pavel A. Melentev ◽  
Artem E. Komissarov ◽  
Nina V. Surina ◽  
Ekaterina A. Ivanova ◽  
...  

Glia are crucial for the normal development and functioning of the nervous system in many animals. Insects are widely used for studies of glia genetics and physiology. Drosophila melanogaster surface glia (perineurial and subperineurial) form a blood–brain barrier in the central nervous system and blood–nerve barrier in the peripheral nervous system. Under the subperineurial glia layer, in the cortical region of the central nervous system, cortex glia encapsulate neuronal cell bodies, whilst in the peripheral nervous system, wrapping glia ensheath axons of peripheral nerves. Here, we show that the expression of the evolutionarily conserved swiss cheese gene is important in several types of glia. swiss cheese knockdown in subperineurial glia leads to morphological abnormalities of these cells. We found that the number of subperineurial glia nuclei is reduced under swiss cheese knockdown, possibly due to apoptosis. In addition, the downregulation of swiss cheese in wrapping glia causes a loss of its integrity. We reveal transcriptome changes under swiss cheese knockdown in subperineurial glia and in cortex + wrapping glia and show that the downregulation of swiss cheese in these types of glia provokes reactive oxygen species acceleration. These results are accompanied by a decline in animal mobility measured by the negative geotaxis performance assay.


Author(s):  
Jungjoo Park ◽  
Eunji Jung ◽  
Seung-Hee Lee ◽  
Won-Suk Chung

AbstractGlia contribute to synapse elimination through phagocytosis in the central nervous system. Despite important roles during development and neurological disorders, the “eat-me” signal that initiates glia-mediated phagocytosis of synapses remains largely elusive. Here, by generating inducible conditional knockout mice of Cdc50a, we induced stable exposure of phosphatidylserine in the neuronal outer membrane. Surprisingly, acute Cdc50a deletion in neurons causes specific loss of inhibitory post-synapses without affecting other synapses, thereby generating excessive excitability with appearance of seizure. Ablating microglia or deleting microglial Mertk rescues the loss of inhibitory post-synapses, indicating that microglial phagocytosis is responsible for inhibitory post-synapse elimination. Moreover, inhibitory post-synapses in normal juvenile brains also use phosphatidylserine for synapse pruning by microglia, suggesting that phosphatidylserine may serve as a general “eat-me” signal for inhibitory post-synapse elimination.One Sentence SummaryCdc50a dependent phosphatidylserine exposure functions as an “eat-me” signal for microglia-dependent inhibitory post-synapse elimination


2009 ◽  
Vol 19 (2) ◽  
pp. 154-161 ◽  
Author(s):  
Masanobu Kano ◽  
Kouichi Hashimoto

Author(s):  
Paul G. DeCaen ◽  
Alfred L. George ◽  
Christopher H. Thompson

This chapter presents information about the structure, function, and molecular genetics of voltage-gated sodium channels expressed in the central nervous system. Sodium channels are essential for the generation and propagation of neuronal action potentials. Recent advances in structural biology have provided atomic-scale descriptions of sodium channel structure that can be related to specific functional properties. We further discuss cellular and subcellular localization, as well as the primary physiological functions mediated by sodium channels within the central nervous system. Finally, this chapter examines the association of various sodium channel isoforms with common brain disorders, including epilepsy, autism, and migraine, and explains the range of functional consequences of disease-associated mutations that are correlated with diverse human phenotypes.


Author(s):  
Gladys Harrison

With the advent of the space age and the need to determine the requirements for a space cabin atmosphere, oxygen effects came into increased importance, even though these effects have been the subject of continuous research for many years. In fact, Priestly initiated oxygen research when in 1775 he published his results of isolating oxygen and described the effects of breathing it on himself and two mice, the only creatures to have had the “privilege” of breathing this “pure air”.Early studies had demonstrated the central nervous system effects at pressures above one atmosphere. Light microscopy revealed extensive damage to the lungs at one atmosphere. These changes which included perivascular and peribronchial edema, focal hemorrhage, rupture of the alveolar septa, and widespread edema, resulted in death of the animal in less than one week. The severity of the symptoms differed between species and was age dependent, with young animals being more resistant.


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