Kainic acid induced seizures cause a marked increase in the expression of neurokinin-3 receptor mRNA 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 this study we investigated mRNA levels encoding the receptor for NKB, the neurokinin-3 receptor (NK-3R), after limbic seizures induced by kainic acid (KA) in the rat. NK-3R mRNA levels were determined by nuclease protection assay at various time intervals after i.p. injection of KA 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 amygdala, levels of the transcript were decreased (by 50% and more) at all intervals investigated. The decreases in mRNA levels in the amygdala 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.[1]References
- Kainic acid induced seizures cause a marked increase in the expression of neurokinin-3 receptor mRNA in the rat cerebellum. Röder, C., Bellmann, R., McCarson, K.E., Krause, J.E., Sperk, G. Neurosci. Lett. (1994) [Pubmed]
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