Administration of
kainic acid (15 mg/kg, i.p.) or
pentetrazole (75 mg/kg, i.p.) to rats evoked recurrent limbic or
tonic-clonic seizures, respectively. Radioimmunoassay showed that the level of
alpha-neoendorphin (
prodynorphin-derived
peptide) in the hippocampus was decreased after 3 h (by c. 60%) and 72 h (by c. 40%), but was not changed after 24 h following
kainic acid administration. The basal release of
alpha-neoendorphin from hippocampal slices of
kainic acid-treated rats was decreased after 3, 24 and 72 h following the
drug injection by c. 50%. The K(+)-stimulated release was decreased after 3 and 24 h (by c. 300 and 200%, respectively) and was back to the control level after 72 h. An in situ hybridization study showed that
kainic acid strongly enhanced the
prodynorphin messenger RNA levels in the dentate gyrus after 3 and 24 h (by c. 200%), whereas after 72 h it tended to decrease. Twenty four hours after
pentetrazole injection the hippocampal level of
alpha-neoendorphin was elevated (by c. 33%) and remained unchanged after 3 and 72 h. No significant changes in the basal or K(+)-stimulated
alpha-neoendorphin release from hippocampal slices of
pentetrazole-treated rats were found at any time points measured. Three and 24 h after
pentetrazole administration the level of
prodynorphin mRNA in the dentate gyrus was slightly decreased (by c. 30%), but was back to the control values after 72 h. Hence seizure-related changes in hippocampal
prodynorphin neuron activity seem to depend on the experimental model of
epilepsy.(ABSTRACT TRUNCATED AT 250 WORDS)