Hamani C, Tenório F, Mendez-Otero R, Mello L E
Departmento de Fisiologia da EPM-UNIFESP, São Paulo-SP, Brazil.
Hippocampus. 1999;9(3):303-13. doi: 10.1002/(SICI)1098-1063(1999)9:3<303::AID-HIPO9>3.0.CO;2-Z.
Recent evidence suggests an important role for NO in cholinergic models of epilepsy. Nicotinamide adenine dinucleotide phosphate diaphorase (NADPHd), a marker of NO containing neurons, was shown to intensely colocalize with GABA in double-labeling studies performed in the hippocampal formation (exception made for the pyramidal cell layer) (Valtschanoff et al., J Comp Neurol 1993:331:111-121). In this sense, it further characterizes an extremely important cell category due to the relevant involvement of inhibitory systems in the mechanisms of genesis and propagation of seizures. Here, we assessed the histochemistry for NADPHd in the hippocampal complex of chronic pilocarpine-epileptic animals. NADPHd-positive cells were lost in almost every hippocampal subfield in pilocarpine-treated rats. The central portion of the polymorphic layer of the dentate gyrus (hilus) presented one of the highest losses of NADPHd-positive cells (55-79%) in the hippocampus. A significant loss of NADPHd-positive cells was seen in strata oriens, pyramidale, and radiatum CA1, CA2, and CA3 subfields. NADPHd staining in the subicular pyramidal cell layer was not different from that observed in controls. A significant loss of NADPHd-stained cells was observed in entorhinal cortex layers II and III in the epileptic group. For entorhinal cortex layers V and VI, however, results varied from an almost complete tissue destruction to an overexpression of NADPHd-positive cells, as well as an increase in neuropil staining. In summary, loss of NADPHd staining was not uniform throughout the hippocampal formation. There has been a growing support for the notion that GABAergic neurons in the hippocampal formation are not equally sensitive to insults. Our results suggest that, as a marker for a subpopulation of GABAergic neurons, NADPHd helps in further refining the characterization of the different neuronal populations sensitive to epileptic activity.
最近的证据表明，一氧化氮（NO）在癫痫的胆碱能模型中发挥着重要作用。烟酰胺腺嘌呤二核苷酸磷酸黄递酶（NADPHd）是含NO神经元的标志物，在海马结构（锥体细胞层除外）进行的双重标记研究中显示，它与γ-氨基丁酸（GABA）强烈共定位（瓦尔查诺夫等人，《比较神经学杂志》1993年：331：111 - 121）。从这个意义上说，由于抑制系统在癫痫发作的发生和传播机制中具有重要作用，它进一步刻画了一类极其重要的细胞。在此，我们评估了慢性匹罗卡品癫痫动物海马复合体中NADPHd的组织化学情况。在匹罗卡品处理的大鼠中，几乎每个海马亚区的NADPHd阳性细胞都减少了。齿状回多形层（门区）的中央部分是海马中NADPHd阳性细胞损失率最高的区域之一（55 - 79%）。在CA1、CA2和CA3亚区的海马伞、锥体层和辐射层中，可见NADPHd阳性细胞显著减少。海马下锥体细胞层的NADPHd染色与对照组观察到的情况无差异。在癫痫组的内嗅皮层II层和III层中，观察到NADPHd染色细胞显著减少。然而，对于内嗅皮层V层和VI层，结果各不相同，从几乎完全的组织破坏到NADPHd阳性细胞的过度表达，以及神经纤维染色增加。总之，NADPHd染色在整个海马结构中的减少并不均匀。越来越多的人支持这样一种观点，即海马结构中的γ-氨基丁酸能神经元对损伤的敏感性并不相同。我们的结果表明，作为γ-氨基丁酸能神经元亚群的标志物，NADPHd有助于进一步细化对不同癫痫活动敏感神经元群体的特征描述。
