Status epilepticus-induced hippocampal damage is modulated by glucose availability.
Kainic acid administration induces status epilepticus seizures in the rat which damage CA1 and CA3 hippocampal neurons. Rats made hypoglycemic prior to seizure had enhanced volumes of damage, when compared to normo- or hyperglycemic rats. The mild hypoglycemia was not in the range which, itself, typically produces hippocampal damage. This suggests that limited energy availability compromised the ability of neurons to survive seizures. Our data also suggest that the CA1 damage seen after status epilepticus is not hypoxic-ischemic in origin, since elevating pre-seizure glucose concentrations to a range which typically exacerbates hypoxic-ischemic CA1 damage did not augment status-epilepticus CA1 damage.
Sapolsky
R M
RM
Department of Biological Sciences, Stanford University, CA 94305.
Stein
B A
BA
D000818:Animals; D001786:Blood Glucose / Q000378:metabolism*; D006624:Hippocampus / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D007003:Hypoglycemia / Q000378:metabolism; D007608:Kainic Acid; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains; D013226:Status Epilepticus / Q000139:chemically induced / Q000378:metabolism* / Q000473:pathology
D001786:Blood Glucose; D007608:Kainic Acid