Involvement of NO and superoxide radicals in the neurotransmission mechanism.

新纹状体生长抑素神经元对锰超氧化物歧化酶（Mn-SOD）具有很强的免疫反应性，这些神经元与一氧化氮合酶（NOS）神经元相同。这些新纹状体神经元选择性抵抗各种神经毒性损伤，如缺血、nmda介导的神经毒性和亨廷顿氏病。虽然其抵抗的原因尚不清楚，但有人认为SOD可能阻止过氧亚硝酸盐阴离子的形成，从而减少新纹状体NOS神经元的细胞死亡。目前尚不清楚海马体中的这些神经元是否以类似于新纹状体的方式抵抗神经毒性损伤。本研究通过双免疫染色法和酶组织化学染色法证实，海马中NOS细胞群与Mn-SOD神经元几乎总是不同的；尽管Mn-SOD和nos -免疫反应神经元的分布相似，但几乎所有后一种神经元在所有亚区均无或弱Mn-SOD免疫反应。因此，Mn-SOD不太可能参与海马NOS神经元前氧亚硝酸盐通路的抑制。然而，不能排除这种NO-SOD相互作用可能发生在抗缺血损伤的CA3锥体细胞中，因为它们对Mn-SOD表现出很强的免疫反应性。由于锥体细胞不表现出一氧化氮免疫反应性，因此它们可能从邻近细胞或含有一氧化氮的神经突中接受相当数量的一氧化氮。相反，Mn-SOD在CA1锥体细胞中免疫染色较弱，而CA1锥体细胞极易受到缺血损伤。细胞内Mn-SOD含量的差异可能是CA1和CA3锥体细胞神经毒性程度差异的部分原因。

Strong immunoreactivity for manganese superoxide dismutase (Mn-SOD)is seen in neostriatal somatostatin neurons, these being identical to nitric oxide synthase (NOS) neurons. These neostriatal neurons are selectively resistant to various kinds of neurotoxic insults, such as ischemia, NMDA-mediated neurotoxicity, and Huntington's disease. Although the reason for their resistance is not known, it has been suggested that SOD may prevent the formation of the peroxynitrite anion and may thus reduce cell death among NOS neurons in the neostriatum. It remained unclear whether such neurons in the hippocampus are resistant to neurotoxic insults in a manner similar to that shown in the neostriatum. The present study demonstrated, by using a double immunostaining method and a enzyme histochemical staining method, that the NOS cell population in the hippocampus is almost always different from that of Mn-SOD neurons ; virtually all of the latter neurons had no or weak Mn-SOD immunoreactivity in all subfields, although Mn-SOD-and NOS-immunoreactive neurons showed a similar distribution. Therefore, it is unlikely that Mn-SOD participates in the inhibition of the preoxynitrite pathway in hippocampal NOS neurons. However, it can not be ruled out that such NO-SOD interaction may occur in CA3 pyramidal cells being resistant to ischemic insults, since they show strong immunoreactivity for Mn-SOD.As pyramidal cells do not exhibit NOS-immunoreactivity, it is possible that thay may receive a considerale amount of NO from neighboring cells or from neurites containing NOS.In contrast, Mn-SOD is weakly immunostained in CA1 pyramidal cells, which cells are very vulnerable to ischemic insults. Differences in the intracellular amounts of Mn-SOD may be, in part responsible for the differences in the degree of neurotoxicity between CA1 and CA3 pyramidal cells.