Pathophysiology of Trans-Synaptic Adhesion Molecules: Implications for Epilepsy

被引:15
|
作者
Gorlewicz, Adam [1 ]
Kaczmarek, Leszek [1 ]
机构
[1] Polish Acad Sci, Nencki Inst Expt Biol, Neurobiol Lab, Warsaw, Poland
关键词
synaptic plasticity; autism spectrum disorders; epileptogenesis; neuronal development; neuropsychiatric disorders; LONG-TERM POTENTIATION; DEPENDENT PROTEOLYTIC CLEAVAGE; REPEAT TRANSMEMBRANE PROTEINS; TISSUE-PLASMINOGEN ACTIVATOR; REGULATES DENDRITIC SPINE; CELL-ADHESION; N-CADHERIN; SYNAPSE FORMATION; MATRIX METALLOPROTEINASES; MENTAL-RETARDATION;
D O I
10.3389/fcell.2018.00119
中图分类号
Q2 [细胞生物学];
学科分类号
071009 ; 090102 ;
摘要
Chemical synapses are specialized interfaces between neurons in the brain that transmit and modulate information, thereby integrating cells into multiplicity of interacting neural circuits. Cell adhesion molecules (CAMs) might form trans-synaptic complexes that are crucial for the appropriate identification of synaptic partners and further for the establishment, properties, and dynamics of synapses. When affected, trans-synaptic adhesion mechanisms play a role in synaptopathies in a variety of neuropsychiatric disorders including epilepsy. This review recapitulates current understanding of trans-synaptic interactions in pathophysiology of interneuronal connections. In particular, we discuss here the possible implications of trans-synaptic adhesion dysfunction for epilepsy.
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页数:17
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