Klimaschewski L, Obermüller N, Majewski M, Bachmann S, Heym C
Institute for Anatomy and Cell Biology, University of Heidelberg, Im Neuenheimer Feld 307, D-69120 Heidelberg, Germany.
Cell Tissue Res. 1996 Sep;285(3):419-25. doi: 10.1007/s004410050658.
Nitric oxide synthase (NOS) expression is increased in peripheral sensory and central motor neurons after axotomy. By applying double-labelling immunofluorescence and non-radioactive in situ hybridization, we have investigated the regulation of NOS in axotomized sympathetic rat superior cervical ganglia. Furthermore, co-localization of NOS with vasoactive intestinal peptide, which is also induced by axotomy, has been examined. Very few (<0.1%) NOS-expressing neurons are observed in control ganglia. Some large cell bodies located at the exit of the internal carotid nerve are additionally immunoreactive for vasoactive intestinal peptide. One week following postganglionic axotomy, the number of NOS-immunoreactive and NOS mRNA-expressing neurons increases but does not exceed 2% of the whole neuronal population. About 20% of these neurons are also immunoreactive for vasoactive intestinal peptide. Preganglionic nerve fibre meshworks that are immunoreactive for NOS in untreated ganglia disappear after ganglionic decentralization, whereas some presumably postganglionic fibres remain visible after combined axotomy and decentralization. The findings are indicative of an increased synthesis of NOS in a small subset of postganglionic neurons of the rat superior cervical ganglion, possibly because of the loss of target-derived factors that inhibit nitric oxide synthesis under normal conditions.
轴突切断后,外周感觉神经元和中枢运动神经元中的一氧化氮合酶(NOS)表达增加。通过应用双标记免疫荧光和非放射性原位杂交技术,我们研究了大鼠颈上神经节轴突切断后一氧化氮合酶的调节情况。此外,还检测了一氧化氮合酶与同样由轴突切断诱导产生的血管活性肠肽的共定位情况。在对照神经节中,观察到表达一氧化氮合酶的神经元极少(<0.1%)。位于颈内神经出口处的一些大细胞体对血管活性肠肽也呈免疫反应阳性。节后轴突切断一周后,一氧化氮合酶免疫反应阳性和表达一氧化氮合酶mRNA的神经元数量增加,但不超过整个神经元群体的2%。这些神经元中约20%对血管活性肠肽也呈免疫反应阳性。在未处理的神经节中,对一氧化氮合酶呈免疫反应阳性的节前神经纤维网在神经节去传入后消失,而在轴突切断和去传入联合处理后,一些推测为节后的纤维仍可见。这些发现表明,大鼠颈上神经节节后神经元的一个小亚群中一氧化氮合酶的合成增加,这可能是由于在正常情况下抑制一氧化氮合成的靶源性因子丧失所致。