Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:1.6.99.1 (NADPH-diaphorase)
 3,903 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The distribution of NADPH diaphorase (NADPH-d)/nitric oxide synthase (NOS) neurons was evaluated during the postnatal development of the primary somatosensory cortex (SI) of the rat. Both cell counts and area measurements of barrel fields were carried out throughout cortical maturation. In addition, NADPH-d and cytochrome oxidase (CO) activities were also compared in both coronal and tangential sections of rat SI between postnatal days (P) 10 and 90. Throughout this period, the neuropil distributions of both enzymes presented a remarkable similarity and have not changed noticeably. Their distribution pattern show the PMBSF as a two-compartmented structure, displaying a highly reactive region (barrel hollows) flanked by less reactive regions (barrel septa). The number of NADPH-d neurons increased significantly in the barrel fields between P10 and P23, with peak at P23. The dendritic arborization of NADPH-d neurons became more elaborated during barrel development. In all ages evaluated, the number of NADPH-d cells was always higher in septa than in the barrel hollows. Both high neuropil reactivity and differential distribution of NADPH-d neurons during SI development suggest a role for nitric oxide throughout barrel field maturation.
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PMID:A morphometric study of the progressive changes on NADPH diaphorase activity in the developing rat's barrel field. 1528 99

Astrogliosis, oligodendroglial death and motor deficits have been observed in the offspring of female rats that had their uterine arteries clamped at the 18(th) gestational day. Since nitric oxide has important roles in several inflammatory and developmental events, here we evaluated NADPH-diaphorase (NADPH-d) distribution in the cerebellum of rats submitted to this hypoxia-ischemia (HI) model. At postnatal (P) day 9, Purkinje cells of SHAM and non-manipulated (NM) animals showed NADPH-d+ labeling both in the cell body and dendritic arborization in folia 1 to 8, while HI animals presented a weaker labeling in both cellular structures. NADPH-d+ labeling in the molecular (ML), and in both the external and internal granular layer, was unaffected by HI at this age. At P23, labeling in Purkinje cells was absent in all three groups. Ectopic NADPH-d+ cells in the ML of folia 1 to 4 and folium 10 were present exclusively in HI animals. This labeling pattern was maintained up to P90 in folium 10. In the cerebellar white matter (WM), at P9 and P23, microglial (ED1+) NADPH-d+ cells, were observed in all groups. At P23, only HI animals presented NADPH-d labeling in the cell body and processes of reactive astrocytes (GFAP+). At P9 and P23, the number of NADPH-d+ cells in the WM was higher in HI animals than in SHAM and NM ones. At P45 and at P90 no NADPH-d+ cells were observed in the WM of the three groups. Our results indicate that HI insults lead to long-lasting alterations in nitric oxide synthase expression in the cerebellum. Such alterations in cerebellar differentiation might explain, at least in part, the motor deficits that are commonly observed in this model.
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PMID:Prenatal hypoxic-ischemic insult changes the distribution and number of NADPH-diaphorase cells in the cerebellum. 2254 5