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Inhibition of neuronal nitric oxide synthase prevents iron-induced cerebellar Purkinje cell loss in the rat

100%

Gulturk S., Kozan R., Bostanci M. O., Sefil F., Bagirici F.

Acta Neurobiologiae Experimentalis

2008

vol. 68

issue 1

26-31

Iron plays an important role in maintaining normal brain function. However, in many neurodegenerative diseases abnormal iron accumulation in specific brain regions has been consistently reported. In this study, we investigated the neurotoxic effect of the intracerebroventricularly injected iron on the cerebellar Purkinje cells in the rat and the role of nitric oxide (NO) in this process. The role of NO in rats administered iron (FeCl36H2O) was examined with the use of a donor of NO, L-arginine (L-Arg), and a central selective inhibitor of NO synthase, 7-nitroindazole (7-NI). For this reason, rats were divided into 5 groups: control, iron-injected, iron plus L-Arg, iron plus 7-NI, and iron plus L-Arg plus 7-NI. Means (value ? standard deviation) of the total numbers of Purkinje cells in the cerebellum were estimated as 337 ? 23, 209 ? 16, 167 ? 19, 305 ? 26, and 265 ? 14 thousands in the control, iron, iron plus L-Arg, iron plus 7-NI, and iron plus L-Arg plus 7-NI groups, respectively. Iron treatment alone and the combination of iron and L-Arg caused a significant reduction in the total number of cerebellar Purkinje cells. Therefore, L-Arg increased the Purkinje cell loss induced by treatment with iron. These data show that inhibition of the neuronal NOS by 7-NI can prevent some of the deleterious effects of iron on cerebellar Purkinje cells. Presence of L-arginine decreased the neuroprotective effect of 7-NI.

Striking pattern of Purkinje cell loss in cerebellum of an ataxic mutant mouse, tottering

86%

Sawada K., Azad A. K., Sakata-Haga H., Lee N.-S., Jeong Y.-G., Fukui Y.

Acta Neurobiologiae Experimentalis

2009

vol. 69

issue 1

138-145

Tottering mouse is an ataxic mutant that carries a mutation in a gene encoding for the ?1A subunit of P/Q-type Ca2+ channel (Cav2.1). This study revisited to examine whether a Purkinje cell loss occurred in the cerebellum of tottering mice. In tottering mice, Calbindin D-28k negative gaps were apparent in the vermis but not in the hemisphere. Calbindin D-28k immunofluorescence with DAPI staining demonstrated the absence of Purkinje cells in the Calbindin D-28k negative gaps. The Purkinje cell loss seemed to be observed prominently in the zebrin II negative compartments of the anterior vermis, but in the zebrin II positive compartments of the posterior vermis. Quite consistent with the histopathological observations, quantitation of the density of Calbindin D-28k and zebrin II immunopositive Purkinje cells in the tottering cerebellum revealed that the Purkinje cells were selectively lost in the zebrin II immunonegative compartments of the lobules I and II but in the zebrin II immunopositive compartments in the lobule IX. Those results predict that the susceptibility to the Cav2.1 gene defect is different among Purkinje cell phenotypes of the tottering cerebellum rather than the expression pattern of mutated Cav2.1 channels. This may result in the reproducible parasagittal pattern of Purkinje cell loss.

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2 Acta Neurobiologiae Experimentalis

1 2009

1 2008

1 Azad A. K.

1 Bagirici F.

1 Bostanci M. O.

1 Fukui Y.

1 Gulturk S.

1 Jeong Y.-G.

1 Kozan R.

1 Lee N.-S.

1 Sakata-Haga H.

1 Sawada K.

1 Sefil F.

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Inhibition of neuronal nitric oxide synthase prevents iron-induced cerebellar Purkinje cell loss in the rat

Striking pattern of Purkinje cell loss in cerebellum of an ataxic mutant mouse, tottering