Marksteiner J, Wahler R, Bellmann R, Ortler M, Krause J E, Sperk G
Department of Pharmacology, University of Innsbruck, Austria.
Neuroscience. 1992 Jul;49(2):383-95. doi: 10.1016/0306-4522(92)90104-a.
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.
采用免疫组织化学和原位杂交技术，研究了海藻酸诱导的癫痫发作和戊四氮点燃对大鼠海马中神经激肽B免疫反应性和神经激肽B mRNA的影响。腹腔注射海藻酸后10 - 60天，在苔藓纤维终末区观察到神经激肽B免疫反应性显著增加。这些免疫反应性缓慢但持续的增加伴随着颗粒细胞和颗粒细胞层相邻的门区中间神经元中神经激肽B mRNA表达的明显增强。在海藻酸注射后2天和10天，CA1锥体细胞层中神经激肽B mRNA和免疫反应性短暂增加，随后消退。戊四氮点燃导致颗粒细胞和CA1锥体细胞中神经激肽B mRNA表达有类似增加，但门区中间神经元中未增加。在CA1区,点燃程序终止后2天神经激肽B信息增加，但10天后未增加。海藻酸注射60天后，神经激肽B免疫反应性扩展到齿状回分子层的内三分之一。戊四氮点燃后，在CA3的锥体下区域观察到一条神经激肽B免疫反应带。在海藻酸处理的大鼠中，局部注射秋水仙碱损伤齿状颗粒细胞可消除颗粒上神经激肽B阳性染色，而切断腹侧海马连合后几乎未改变。这些观察结果表明，神经激肽B免疫反应性可能分别位于同侧苔藓纤维，这些苔藓纤维向分子层内侧或CA3的锥体下区域进行侧支发芽。与未处理动物相比，癫痫大鼠海马中编码神经激肽A和P物质的前速激肽原A mRNA和P物质免疫反应性没有变化。观察到的神经激肽B免疫反应性和mRNA的变化表明，边缘系统反复癫痫发作可能在海马神经元中诱导特定的功能和形态学变化。
