Ketamine and MK-801 prevent degeneration of thalamic neurons induced by focal cortical seizures.
Ketamine and MK-801 act at phencyclidine receptors to block transmitter activity through the N-methyl-D-aspartate (NMDA) subtype of glutamate (GLU) receptor. These agents also block the potent excitotoxic actions of NMDA and are of interest for their potential ability to protect against neurodegenerative processes mediated by the excitotoxic action of endogenous Glu at NMDA receptors. Here we show that degeneration of thalamic neurons caused by persistent seizure activity in the corticothalamic tract (putative glutamergic transmitter pathway) is prevented by systemic administration of ketamine or MK-801, despite the failure of these agents to eliminate persistent electrographic seizure activity recorded from cortex and thalamus.
Clifford
D B
DB
Department of Neurology, Washington University School of Medicine, St. Louis, Missouri 63110.
Zorumski
C F
CF
Olney
J W
JW
D000818:Animals; D000927:Anticonvulsants / Q000494:pharmacology*; D001640:Bicuculline / Q000494:pharmacology; D002540:Cerebral Cortex / Q000503:physiopathology*; D003986:Dibenzocycloheptenes / Q000494:pharmacology*; D016291:Dizocilpine Maleate; D004569:Electroencephalography; D007649:Ketamine / Q000494:pharmacology*; D009410:Nerve Degeneration / Q000187:drug effects*; D009474:Neurons / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D011919:Rats, Inbred Strains; D012640:Seizures / Q000503:physiopathology*; D013788:Thalamus / Q000187:drug effects / Q000502:physiology / Q000503:physiopathology*
D000927:Anticonvulsants; D003986:Dibenzocycloheptenes; D007649:Ketamine; D016291:Dizocilpine Maleate; D001640:Bicuculline