Contribution of GABA(B) receptor-mediated inhibition to the expression and termination of group I mGluR-induced ictaform bursts.
Huszár
Péter
P
Department of Physiology and Pharmacology, State University of New York Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, NY 11203, USA.
Merlin
Lisa R
LR
D000818:Animals; D003292:Convulsants / Q000494:pharmacology; D004569:Electroencephalography / Q000187:drug effects; D004827:Epilepsy / Q000139:chemically induced / Q000503:physiopathology; D018756:GABA Antagonists / Q000494:pharmacology; D005998:Glycine / Q000031:analogs & derivatives* / Q000494:pharmacology; D006168:Guinea Pigs; D066298:In Vitro Techniques; D008564:Membrane Potentials / Q000187:drug effects; D009943:Organophosphorus Compounds / Q000494:pharmacology; D010852:Picrotoxin / Q000494:pharmacology; D017966:Pyramidal Cells / Q000187:drug effects / Q000502:physiology; D018080:Receptors, GABA-B / Q000187:drug effects / Q000502:physiology*; D018094:Receptors, Metabotropic Glutamate / Q000819:agonists*; D012118:Resorcinols / Q000494:pharmacology
D003292:Convulsants; D018756:GABA Antagonists; D005998:Glycine; D009943:Organophosphorus Compounds; D010852:Picrotoxin; D018080:Receptors, GABA-B; D018094:Receptors, Metabotropic Glutamate; D012118:Resorcinols; C104077:metabotropic glutamate receptor type 1; C079215:3,5-dihydroxyphenylglycine; C066430:CGP 35348