Abstract
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.
Highlights
Synaptic connections are important defining features of neurons
The same time the presynaptic differentiation is coordinated through the PDZ-domain-binding motif of β-neurexin which interacts with the CASK (Hata et al, 1996) and Mint (Biederer and Südhof, 2000) proteins at the presynaptic site -both associated with Munc18 protein that is Family Neuroligin Cadherin
That action induced neurodegeneration of cells in dentate gyrus and CA3 region of hippocampus and promoted the early onset of focal seizures (Duveau and Fritschy, 2010). Another studies focused on the impact of PSA-neural cell adhesion molecule (NCAM) on pathophysiology of epilepsy demonstrated that loss of PSA-NCAM decreased the number of hippocampal newborn cells in kindling-associated changes of hippocampal neuronal network
Summary
Synaptic connections are important defining features of neurons. They continue to be formed and eliminated throughout the development and postnatal period allowing neurons spreading and processing complex patterns of impulses that underlie cognition. The alignment of both synaptic constituents must be coordinated in time during junction formation, neurotransmitters released from the pre-synaptic membrane could act on receptors located at the post-synaptic site in order to ensure fine flow of information between neurons (Harris and Littleton, 2015). Trans-synaptic CAMs govern different aspects of synaptic plasticity. They organize synapse formation, control synapse morphology, and receptor function, as well as are engaged in synaptic elimination (Bhaskar et al, 2010; Siddiqui and Craig, 2011). An aim of this review is to recapitulate current understanding of trans-synaptic interactions in pathophysiology of inter-neuronal connections that underlies epileptogenesis and epilepsy
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