Epileptic Seizures: Glia-Neuron Interactions For Better or For Worse.

07:00 EST 2nd December 2019 | BioPortfolio

Summary of "Epileptic Seizures: Glia-Neuron Interactions For Better or For Worse."

Investigations of the mechanisms generating epileptic seizures have primarily focused on neurons. However, more systemic research of brain circuits has highlighted an important role of non-neuronal cells such as glia in the genesis and spreading of generalized seizures in the brain.


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This article was published in the following journal.

Name: Current biology : CB
ISSN: 1879-0445
Pages: R1248-R1251


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Medical and Biotech [MESH] Definitions

Cell adhesion molecules that mediate neuron-neuron adhesion and neuron-astrocyte adhesion. They are expressed on neurons and Schwann cells, but not astrocytes and are involved in neuronal migration, neurite fasciculation, and outgrowth. Ng-CAM is immunologically and structurally distinct from NCAM.

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A factor identified in the brain that influences the growth and differentiation of NEURONS and NEUROGLIA. Glia maturation factor beta is the 17-kDa polypeptide product of the GMFB gene and is the principal component of GLIA MATURATION FACTOR.

Specialized junctions at which a neuron communicates with a target cell. At classical synapses, a neuron's presynaptic terminal releases a chemical transmitter stored in synaptic vesicles which diffuses across a narrow synaptic cleft and activates receptors on the postsynaptic membrane of the target cell. The target may be a dendrite, cell body, or axon of another neuron, or a specialized region of a muscle or secretory cell. Neurons may also communicate via direct electrical coupling with ELECTRICAL SYNAPSES. Several other non-synaptic chemical or electric signal transmitting processes occur via extracellular mediated interactions.

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