Involvement of NO and superoxide radicals in the neurotransmission mechanism.

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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.