A MODIFIED TECHNIQUE OF HISTOCHEMICAL DEMONSTRATION FOR N-Acetyl-Β-Hexosaminidase

Katayama, Yoshiho; Kobatake, Hiroshi; Shida, H

doi:10.1267/ahc.9.111

Cited by 4 publications

(2 citation statements)

References 14 publications

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“…The histochemical method for β‐hexosaminidase was performed as previously described 23. Briefly, sections were washed in distilled water and then incubated for 1 hour at 37°C in fast red violet salt solution (0.63M ethylene glycol monomethyl ether, 1% polyvinyl pyrrolidone, 0.1M citric acid‐citrate buffer pH 4.4, 1.6M sodium chloride, 2.7mM fast red violet LB salt [Sigma]), using 0.5mM naphthol‐AS‐BI‐N‐acetyl‐β‐D‐glucosaminide (Sigma) as the substrate.…”

Section: Methodsmentioning

confidence: 99%

Postischemic treatment of neonatal cerebral ischemia should target autophagy

Puyal

Vaslin

Mottier

et al. 2009

Annals of Neurology

242

222

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Section: Methodsmentioning

confidence: 99%

Postischemic treatment of neonatal cerebral ischemia should target autophagy

Puyal

Vaslin

Mottier

et al. 2009

Annals of Neurology

242

222

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“…The procedure of Katayama et al 23 was used. Briefly, sections were washed in distilled water and then incubated for 1 hour at 37°C in Fast red violet salt solution (0.63mol/L ethylene glycol monomethyl ether, 1% polyvinyl pyrrolidone, 0.1 mol/L citric acid-citrate buffer (pH 4.4), 1.6 mol/L sodium chloride, 2.7 mmol/L 5-chloro-4-benzamido-2-methylbenzene-diazonium chloride (Fast red violet LB salt) (Sigma-Aldrich) using 0.5mmol/L naphthol-AS-BI-N-acetyl-␤-D-glucosaminide (Sigma-Aldrich) as the substrate.…”

Section: ␤-N-acetylhexosaminidase Histochemistrymentioning

confidence: 99%

Enhancement of Autophagic Flux after Neonatal Cerebral Hypoxia-Ischemia and Its Region-Specific Relationship to Apoptotic Mechanisms

Ginet

Puyal

Clarke

et al. 2009

The American Journal of Pathology

141

152

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The multiplicity of cell death mechanisms induced by neonatal hypoxia-ischemia makes neuroprotective treatment against neonatal asphyxia more difficult to achieve. Whereas the roles of apoptosis and necrosis in such conditions have been studied intensively, the implication of autophagic cell death has only recently been considered. Here, we used the most clinically relevant rodent model of perinatal asphyxia to investigate the involvement of autophagy in hypoxic-ischemic brain injury. Seven-day-old rats underwent permanent ligation of the right common carotid artery, followed by 2 hours of hypoxia. This condition not only increased autophagosomal abundance (increase in microtubule-associated protein 1 light chain 3-11 level and punctuate labeling) but also lysosomal activities (cathepsin D, acid phosphatase, and ␤-Nacetylhexosaminidase) in cortical and hippocampal CA3-damaged neurons at 6 and 24 hours, demonstrating an increase in the autophagic flux. In the cortex, this enhanced autophagy may be related to apoptosis since some neurons presenting a high level of autophagy also expressed apoptotic features, including cleaved caspase-3. On the other hand, enhanced autophagy in CA3 was associated with a more purely autophagic cell death phenotype. In striking contrast to CA3 neurons, those in CA1 presented only a minimal increase in autophagy but strong apoptotic characteristics. These results suggest a role of enhanced autophagy in delayed neuronal death after severe hypoxia-ischemia that is differentially linked to apoptosis according to the cerebral region. (Am J Pathol 2009,

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Combined effects of deafferentation and de-efferentation on isthmo-optic neurons during the period of their naturally occurring cell death

Clarke

Egloff

1988

Anat Embryol

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We have studied the effects on the chick embryo's isthmo-optic nucleus of de-efferentation alone or in combination with deafferentation. De-efferentation was achieved by pharmacological destruction of the axonal target cells in the retina at E13, or by colchicine-blockade of axoplasmic transport in the intraocular parts of the isthmo-optic axons at E13; deafferentation was by a tectal lesion at E11 or E12. De-efferentation alone causes all the isthmo-optic neurons to die, and mostly by the "endocytic-autophagic" mode of cell death, which is characterized by pronounced endocytosis (of an intravascularly injected label) and by intense, clumped activity of two lysosomal enzymes (acid phosphatase and N-acetyl-beta-glucosaminidase). Deafferentation plus de-efferentation caused there to be less endocytic-autophagic dying cells in the isthmo-optic nucleus than after de-efferentation alone, but all the neurons still died. Our interpretation is that deafferentation switched many of the isthmo-optic neurons to a completely different (nonendocytic, nonautophagic) mode of cell death.

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A MODIFIED TECHNIQUE OF HISTOCHEMICAL DEMONSTRATION FOR N-Acetyl-Β-Hexosaminidase

Cited by 4 publications

References 14 publications

Postischemic treatment of neonatal cerebral ischemia should target autophagy

Postischemic treatment of neonatal cerebral ischemia should target autophagy

Enhancement of Autophagic Flux after Neonatal Cerebral Hypoxia-Ischemia and Its Region-Specific Relationship to Apoptotic Mechanisms

Combined effects of deafferentation and de-efferentation on isthmo-optic neurons during the period of their naturally occurring cell death

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