Delayed expression of NADPH-diaphorase in rat brain after administration of the cholinotoxin AF64A |
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Authors: | M Yu Stepanichev M L Libe I A Chernyshevskaya A G Moiseenok N V Gulyaeva |
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Institution: | (1) Institute of Higher Nervous Activity and Neurophysiology, Russian Academy of Sciences, ul. Butlerova 5a, Moscow, 117485, Russia;(2) Institute of Pharmacology and Biochemistry, National Academy of Sciences of Belarus, Grodno, 230017, Belarus |
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Abstract: | Administration of cholinotoxin etylcholine aziridinium (AF64A) into the brain selectively induces nonrever-sible cholinergic deficit. Wistar rats were injected intracerebroventricularly bilaterally with AF64A at doses of 1–3 nmol/ventricle. 28 days later the number of neurons survived was counted in dorsolateral, intermediate and medial groups of cells of the medial septum. AF64A induced a decrease in neuronal density and expression of cholineacetyl transferase at all doses used as well as in all regions studied. Brain sections were also stained for NADPH-diaphorase representing neuronal NO-synthase. Effects of AF64A on NADPH-diaphorase expression depended on the region studied. The number of NADPH-diaphorase-positive cells increased in the medial cellular group where more cholineacetly transferase-positive cells survived. In contrast, decrease in NADPH-diaphorase expression in the dorsolateral group of cells coincided with low level of cholineacetyltransferase-po-sitive neurons. The data presented suggest that in the AF64A-dependent model of neurodegeneration NO may play a neuroprotective function. |
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Keywords: | cholinergic deficit AF64A NADPH-diaphorase neurodegeneration nitric oxide |
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