Limbic seizures cause pronounced changes in the expression of neurokinin B in the hippocampus of the rat.

Abstract

Immunohistological and in situ hybridization techniques were used to study the influence of kainic acid-induced seizures and of pentylenetetrazol kindling on neurokinin B immunoreactivity and neurokinin B mRNA in the rat hippocampus. Pronounced increases in neurokinin B immunoreactivity were observed in the terminal field of mossy fibres 10-60 days after intraperitoneal injection of kainic acid. These slow but persistent increases in immunoreactivity were accompanied by markedly enhanced expression of neurokinin B mRNA in the granule cells and in hilar interneurons adjacent to the granule cell layer. These changes were preceded by transient increases in neurokinin B mRNA and immunoreactivity in CA1 pyramidal cell layer two and 10 days after kainic acid, which, however, subsided later on. Pentylenetetrazol kindling caused similar increases in neurokinin B mRNA expression in granule cells and in CA1 pyramidal cells, but not in hilar interneurons. In CA1, increased neurokinin B message was present two days after termination of the kindling procedure but not after 10 days. Sixty days after kainic acid injection, neurokinin B immunoreactivity extended to the inner-third of the molecular layer of the dentate gyrus. After pentylenetetrazol kindling, a neurokinin B-immunoreactive band was observed in the infrapyramidal region of CA3. Lesions of the dentate granule cells by local injection of colchicine in kainic acid-treated rats abolished the supragranular neurokinin B-positive staining, whereas it was almost unchanged after transection of the ventral hippocampal commissure. These observations suggest that neurokinin B immunoreactivity may be located in ipsilateral mossy fibres undergoing collateral sprouting to the inner molecular layer or to the infrapyramidal region in CA3, respectively. Preprotachykinin A mRNA, which encodes for neurokinin A and substance P, and substance P immunoreactivity were not changed in the hippocampus of epileptic rats compared with untreated animals. The observed changes in neurokinin B immunoreactivity and mRNA indicate that specific functional and morphological changes may be induced in hippocampal neurons by recurrent limbic seizures.

• Authors: J Marksteiner, R Wahler, R Bellmann, M Ortler, J E Krause, G Sperk
• Journal: Neuroscience (Neuroscience) Vol. 49 Issue 2 Pg. 383-95 (Jul 1992) ISSN: 0306-4522 [Print] United States
• PMID: 1279453 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Research Support, U.S. Gov't, P.H.S.)

Chemical References

• RNA, Messenger
• Tachykinins
• Substance P
• Neurokinin B
• Kainic Acid
• Pentylenetetrazole

Topics

• Animals
• Hippocampus (drug effects, metabolism)
• Immunohistochemistry
• Kainic Acid (pharmacology)
• Limbic System (pathology)
• Male
• Neurokinin B (biosynthesis)
• Nucleic Acid Hybridization
• Pentylenetetrazole
• RNA, Messenger (biosynthesis, metabolism)
• Rats
• Rats, Sprague-Dawley
• Seizures (chemically induced, metabolism, pathology)
• Substance P (immunology, metabolism)
• Tachykinins (physiology)