A slow NMDA-mediated synaptic potential underlies seizures originating from midbrain.
After bath-perfusion with gamma-aminobutyric acid antagonists, slices of the rat's inferior colliculus were studied electrophysiologically. Synchronized epileptiform events were found to occur. The most prominent intracellular event was a sustained 30 mV depolarization which was pharmacologically and electrophysiologically characterized as an N-methyl-D-aspartate-mediated event. We propose that elicitation of this slow synaptic potential is the a priori basis of seizures arising in this midbrain nucleus.
Pierson
M G
MG
Wadsworth Center for Laboratories and Research, New York State Department of Health, Albany 12201-0509.
Smith
K L
KL
Swann
J W
JW
D015763:2-Amino-5-phosphonovalerate; D000818:Animals; D001224:Aspartic Acid / Q000031:analogs & derivatives* / Q000502:physiology; D001640:Bicuculline / Q000494:pharmacology; D066298:In Vitro Techniques; D007245:Inferior Colliculi / Q000187:drug effects / Q000378:metabolism / Q000503:physiopathology*; D016202:N-Methylaspartate; D010852:Picrotoxin / Q000494:pharmacology; D051381:Rats; D012640:Seizures / Q000378:metabolism*; D014633:Valine / Q000031:analogs & derivatives / Q000494:pharmacology
D015763:2-Amino-5-phosphonovalerate; D001224:Aspartic Acid; D001640:Bicuculline; D016202:N-Methylaspartate; D010852:Picrotoxin; D014633:Valine