Glutamate and GABA in the balance: convergent pathways sustain seizures during status epilepticus.
Seizures rapidly become self-sustaining and pharmacoresistant to benzodiazepines during status epilepticus (SE). A decrease in the number of postsynaptic gamma-aminobutyric acid (GABA)(A) receptors with SE causes a loss of synaptic inhibition, whereas increases in postsynaptic glutamatergic receptors further upset the balance between excitation and inhibition. Although extracellular GABA levels may increase during SE and contribute to postsynaptic GABA(A) receptor desensitization, other pathways involving glutamatergic activation ultimately may be responsible for the persistent down-regulation of postsynaptic GABA(A) receptors and erosion of synaptic inhibition.
Naylor
David E
DE
Department of Neurology, Los Angeles Biomedical Research Institute at Harbor-UCLA Medical Center, University of California at Los Angeles, Torrance, California 90509, USA. dnaylor@ucla.edu
D000818:Animals; D004195:Disease Models, Animal; D018698:Glutamic Acid / Q000502:physiology*; D011963:Receptors, GABA-A / Q000502:physiology; D017470:Receptors, Glutamate / Q000502:physiology; D013226:Status Epilepticus / Q000209:etiology / Q000503:physiopathology*; D009435:Synaptic Transmission / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000502:physiology*
D011963:Receptors, GABA-A; D017470:Receptors, Glutamate; D018698:Glutamic Acid; D005680:gamma-Aminobutyric Acid