Brené S, Lindefors N, Herrera-Marschitz M, Persson H
Department of Medical Chemistry, Karolinska Institute, Stockholm, Sweden.
Eur J Neurosci. 1993 Jul 1;5(7):839-45. doi: 10.1111/j.1460-9568.1993.tb00936.x.
In this report we have studied the influence of hippocampal neurons on neuropeptide mRNA expression in both dorsal and ventral striatum in the rat. Intrahippocampal unilateral kainic acid injections were performed in control animals and in animals with a unilateral 6-hydroxydopamine-induced dopamine deafferentation of the striatum. In situ hybridization combined with quantitative image analysis was used to study the expression of preprotachykinin A mRNA encoding the neuropeptides substance P and neurokinin A. The 6-hydroxydopamine-induced lesion caused a decrease of preprotachykinin A mRNA levels in the ipsilateral dorsal striatum and in both sides of the ventral striatum. In normal rats, the intrahippocampal kainic acid injection caused a twofold increase in preprotachykinin A mRNA in the limbic parts of the striatum, which are innervated by the hippocampus. No effect of the kainic acid injection was seen in the lateral parts of the dorsal striatum, a region which does not appear to be innervated by the hippocampus. Animals with a 6-hydroxydopamine lesion showed a similar kainic acid-mediated increase in preprotachykinin A mRNA in parts of the ventral striatum. In the dopamine-lesioned dorsal striatum and ventral striatum the decreased preprotachykinin A mRNA levels were normalized by the intrahippocampal kainic acid injection. These results show that kainic acid-mediated excitation of hippocampal neurons causes a dopamine-independent induction of preprotachykinin A mRNA expression in parts of the ventral striatum, and reverses the dopamine deafferentation-induced decrease of preprotachykinin A mRNA in both dorsal and ventral striatum. Combined, our results suggest that hippocampal neurons can regulate preprotachykinin A mRNA expression in both the ventral and the dorsal striatum.
在本报告中，我们研究了海马神经元对大鼠背侧和腹侧纹状体中神经肽mRNA表达的影响。对对照动物以及纹状体单侧6-羟基多巴胺诱导多巴胺去传入的动物进行海马内单侧注射 kainic 酸。采用原位杂交结合定量图像分析技术，研究编码神经肽P物质和神经激肽A的前速激肽原A mRNA的表达。6-羟基多巴胺诱导的损伤导致同侧背侧纹状体以及腹侧纹状体两侧的前速激肽原A mRNA水平降低。在正常大鼠中，海马内注射kainic酸导致受海马支配的纹状体边缘部分的前速激肽原A mRNA增加两倍。在背侧纹状体外侧部分未观察到kainic酸注射的影响，该区域似乎不受海马支配。6-羟基多巴胺损伤的动物在腹侧纹状体部分也显示出类似的kainic酸介导的前速激肽原A mRNA增加。在多巴胺损伤的背侧纹状体和腹侧纹状体中，海马内注射kainic酸使降低的前速激肽原A mRNA水平恢复正常。这些结果表明，kainic酸介导的海马神经元兴奋导致腹侧纹状体部分区域前速激肽原A mRNA表达的多巴胺非依赖性诱导，并逆转了多巴胺去传入诱导的背侧和腹侧纹状体中前速激肽原A mRNA的降低。综合来看，我们的结果表明海马神经元可以调节腹侧和背侧纹状体中前速激肽原A mRNA的表达。
