KAINIC ACID-INDUCED SEIZURES CAUSE A MARKED INCREASE IN THE EXPRESSION OF NEUROKININ-3 RECEPTOR MESSENGER-RNA IN THE RAT CEREBELLUM

Marked changes in the expression of the tachykinin peptide neurokinin B (NKB) have been recently observed in animal models of epilepsy. In t his study we investigated mRNA levels encoding the receptor for NKB, t he neurokinin-3 receptor (NK-3R), after limbic seizures induced by kai nic acid (KA) in the rat. NK-3R mRNA levels were determined by nucleas e protection assay at various time intervals after i.p. injection of K A in the rat. Increases of more than 200% were observed in NK-3R mRNA in the cerebellum after 7 and 30 days. In the hippocampus a moderate, reversible increase (of 70%, 1 day after KA) was seen. In the frontal cortex a reduction of NK-3R mRNA (2 days after KA) was found. In the a mygdala, levels of the transcript were decreased (by 50% and more) at all intervals investigated. The decreases in mRNA levels in the amygda la are consistent with the severe damage observed in this brain area. The increases in NK-3R mRNA in the cerebellum point to the development of receptor supersensitivity and suggest a functional role of NKB in this animal model of epilepsy.