Literature DB >> 426476

Selective chromatolysis of neurons in the gerbil brain: a possible consequence of "epileptic" activity produced by common carotid artery occlusion.

A W Brown, D E Levy, M Kublik, J Harrow, F Plum, J B Brierley.   

Abstract

Unilateral (50 to 118 minutes) and bilateral (2 to 33 minutes) carotid artery occlusion in gerbils resulted in two distinct types of neuronal alteration: ischemic cell change (ICC) in selectively vulnerable brain regions, and selective chromatolysis (SC) confined to the deeper layers of the cortex, the Sommer sector of zone h-1, and the paramedian region (PM) of the hippocampus. In typical SC the nucleus was eccentric and the Nissl substance was lost in the central eosinophilic cytoplasm. In electron micrographs this area of cytoplasm showed disruption of smooth and rough endoplasmic reticulum with disaggregation of polyribosomes and accumulation of mitochrondria and various dense bodies. SC was identified at 2 to 3 hours and was still recognizable at five days. When bilateral carotid artery occlusion lasted 5 to 6 minutes, SC was seen in the hippocampal Sommer sector and cerebral cortex, while ICC was restricted to the endfolium (h3-5). Unlike ICC, the frequency of SC was not related to the duration of ischemia but probably to the epileptic seizures (overt and subclinical) initiated by ischemia in the gerbil. These changes must be considered when the gerbil is employed as a model of experimental stroke.

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Year:  1979        PMID: 426476     DOI: 10.1002/ana.410050206

Source DB:  PubMed          Journal:  Ann Neurol        ISSN: 0364-5134            Impact factor:   10.422


  14 in total

1.  Determinants of survival after forebrain ischemia in Mongolian gerbils.

Authors:  K Weber; A Baethmann; O Kempski
Journal:  Metab Brain Dis       Date:  1988-12       Impact factor: 3.584

2.  NMDA receptor antagonism does not inhibit induction of ischemic tolerance in gerbil brain in vivo.

Authors:  M Duszczyk; R Gadamski; A Ziembowicz; W Danysz; J W Lazarewicz
Journal:  Neurotox Res       Date:  2005       Impact factor: 3.911

3.  Dynamic alterations in hippocampal morphology following intra-ventricular kainic acid.

Authors:  J E Franck
Journal:  Acta Neuropathol       Date:  1984       Impact factor: 17.088

4.  Morphological studies on cerebral cortical lesions induced by transient ischemia in Mongolian gerbil--diffuse and peripheral pallor of the neuronal perikarya.

Authors:  Y Nishikawa; T Takahashi; A Shimoda
Journal:  Acta Neuropathol       Date:  1989       Impact factor: 17.088

5.  Pathogenesis of brain lesions caused by experimental epilepsy. Light- and electron-microscopic changes in the rat cerebral cortex following bicuculline-induced status epilepticus.

Authors:  B Söderfeldt; H Kalimo; Y Olsson; B Siesjö
Journal:  Acta Neuropathol       Date:  1981       Impact factor: 17.088

6.  The behavioral and neuropathologic sequelae of intoxication by trimethyltin compounds in the rat.

Authors:  A W Brown; W N Aldridge; B W Street; R D Verschoyle
Journal:  Am J Pathol       Date:  1979-10       Impact factor: 4.307

7.  Neuroprotective activity of chlormethiazole following transient forebrain ischaemia in the gerbil.

Authors:  A J Cross; J A Jones; H A Baldwin; A R Green
Journal:  Br J Pharmacol       Date:  1991-10       Impact factor: 8.739

8.  Selective vulnerability in the gerbil hippocampus following transient ischemia.

Authors:  T Kirino; K Sano
Journal:  Acta Neuropathol       Date:  1984       Impact factor: 17.088

9.  Fine structural nature of delayed neuronal death following ischemia in the gerbil hippocampus.

Authors:  T Kirino; K Sano
Journal:  Acta Neuropathol       Date:  1984       Impact factor: 17.088

10.  Ultrastructural changes in the hippocampal CA1 region following transient cerebral ischemia: evidence against programmed cell death.

Authors:  J Deshpande; K Bergstedt; T Lindén; H Kalimo; T Wieloch
Journal:  Exp Brain Res       Date:  1992       Impact factor: 1.972

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