A study on nitric oxide synathae positive neurons in the retina of spontaneously hypertensive rat

Abstract

The changes of the nitric oxide synthase(NOS) positive neurons number were studied with using NADPH-diaphorase histochemical staining method in the retina of spontaneously hypertensive rats(SHR)and Wistar Kyoto rats(WKY).The results showed that NOS positive neurons located in both the inner nuclear layer and the ganglion cell layer,In the SHR most are amacrine cells and displaced amacrine cells disributed in ganglion cell layer,and a little number of ganglion cells are positive. The perikarya of amacrine cell are stained intensely and some NOS positive long processes were seen, The density of NOS positive cells in the central area is higher than the peripheral area of the retina. However,in the WKY lower density and weaker NOS positive amacrine cells were identified and their processes are shorter and fine. Nitric oxide(NO)may be s anew class of neurotransmitter and serves as an important neuronal messenger. However,NO is also responsible for NMDA-type glutamate neurotoxicity. The enhanced expression of NOS in the retinal amacrine cells of the SHR probably suggests that nitric oxide related to the damage of the neurons under ischemic and hypoxic condition.

本實驗用ＮＡＤＰＨ－黃遞酶（ＮＤＰ）組織化學染色法觀察了自發性高血壓大鼠（ＳＨＲ）和京都種大鼠（ＷＫＹ，正常對照）視網膜內一氧化氮合酶（ＮＯＳ）的變化。結果顯示，ＮＯＳ陽性神經元位于內核層和視網膜節細胞層。ＳＨＲ組視網膜ＮＯＳ陽性細胞屬無長突細胞和移位無長突細胞。偶見陽性的節細胞。ＮＯＳ陽性無長突細胞和節細胞胞質顯強陽性反應，可見較長而清晰的突起。ＮＯＳ陽性神經元的分布密度大，且在視網膜中央區（視神經盤附近）的分布密度略大于周圍區。在ＷＫＹ正常對照組，ＮＯＳ陽性無長突細胞和節細胞的反應不如ＳＨＲ組強，突起較短且纖細。ＮＯＳ陽性細胞的分布密度低于ＳＨＲ組。自發性高血壓大鼠視網膜無長突細胞內一氧化氮合酶表達增加，提示一氧化氮在視網膜缺氧缺血的情況下，可能參與神經細胞損傷的過程，具有神經毒性。