The effects of body temperature on kainic acid-induced seizures and se
izure-related brain damage were examined in rats. In rats with status
epilepticus induced by intraperitoneal injection of 12 mg/kg of kainic
acid (KA), ictal discharges were decreased by 50% when body temperatu
re was lowered to 28 degrees C and nearly abolished when body temperat
ure was lowered to 23 degrees C. In rats with mild hypothermia (28 deg
rees C), the duration of ictal discharges following KA injection was s
ignificantly lower than in rats with normal body temperature. No detec
table hippocampal cell loss was observed in rats with hypothermia to 2
8 degrees C whereas gross cell loss in the hippocampus was observed in
all rats with KA injection at normal body temperature. In contract to
hypothermia, hyperthermia markedly aggravated the seizures and hippoc
ampal damage induced by KA. Following elevation of body temperature to
42 degrees C KA (12 mg/kg) resulted in severe seizures and all rats d
ied of tonic seizures within 2 h. Furthermore, 6 mg/kg of KA administe
red to rats with a body temperature of 41-42 degrees C, resulted in up
to 4 h of continuous ictal discharges whereas no continuous ictal dis
charges were observed after the same injections in rats with normal bo
dy temperature. Histological examination in rats receiving 6 mg/kg of
KA revealed severe cell loss in the hippocampus in rats with hyperther
mia but not in rats with normal temperature. These results demonstrate
that body temperature plays an important role in the control of epile
ptic seizures and seizure-related brain damage. These data suggest tha
t hypothermia may be useful in reducing seizures and associated brain
damage and that hyperthermia should be avoided in status epilepticus.