Advanced

Hypoglycemic brain injury. II. Electron-microscopic findings in rat cerebral cortical neurons during profound insulin-induced hypoglycemia and in the recovery period following glucose administration

Kalimo, H; Agardh, Carl-David LU ; Olsson, Y and Siesjö, Bo LU (1980) In Acta Neuropathologica 50(1). p.43-52
Abstract
Severe hypoglycemia was induced in rats by insulin. The brain was fixed in situ by perfusion after the spontaneous EEG had disappeared for 30 or 60 min or after recovery had been induced for 30 or 180 min by glucose injection. Samples from the cerebral cortex from the area corresponding to the previous metabolic studies were processed for electron microscopy. The light-microscopic finding of two different types of nerve cell injury, reported in a preceding communication (Agardh et al. 1980), was also verified at the ultrastructural level. The type I injury was characterized by cellular shrinkage, condensation of the cell sap and nuclei, and perineuronal astrocytic swelling. No swelling of mitochondria occurred. The slightly swollen type II... (More)
Severe hypoglycemia was induced in rats by insulin. The brain was fixed in situ by perfusion after the spontaneous EEG had disappeared for 30 or 60 min or after recovery had been induced for 30 or 180 min by glucose injection. Samples from the cerebral cortex from the area corresponding to the previous metabolic studies were processed for electron microscopy. The light-microscopic finding of two different types of nerve cell injury, reported in a preceding communication (Agardh et al. 1980), was also verified at the ultrastructural level. The type I injury was characterized by cellular shrinkage, condensation of the cell sap and nuclei, and perineuronal astrocytic swelling. No swelling of mitochondria occurred. The slightly swollen type II injured neurons showed contraction of mitochondria, disintegration of ribosomes, loss of RER, and appearance of membrane whorls, while their nuclear chromatin remained evenly distributed. No transition from one type to the other was observed. Neither type of nerve cell injury in hypoglycemia was like that commonly seen in anoxic-ischemic insults indicating a different pathogenesis in these states despite the common final pathway of energy failure. The loss of endoplasmic membranes and disintegration of ribosomes suggests that these structures might be sacrificed for energy production in the absence of normal substrates. During recovery, though, the number of type I injured neurons decreased while some of the remaining ones appeared even more severely affected, suggesting irreversible damage. Type II injured neurons were no longer seen indicating reversibility of these changes. (Less)
Please use this url to cite or link to this publication:
author
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Hypoglycemia, Nerve cell injury, Electron microscopy, Rat cerebral cortex
in
Acta Neuropathologica
volume
50
issue
1
pages
43 - 52
publisher
Springer
external identifiers
  • pmid:6990680
  • scopus:0018877338
ISSN
1432-0533
DOI
10.1007/BF00688533
language
English
LU publication?
yes
id
ab7f3d42-c86b-414c-9017-866fdb7a9c4c (old id 1102756)
date added to LUP
2008-08-14 08:57:54
date last changed
2017-08-20 04:22:42
@article{ab7f3d42-c86b-414c-9017-866fdb7a9c4c,
  abstract     = {Severe hypoglycemia was induced in rats by insulin. The brain was fixed in situ by perfusion after the spontaneous EEG had disappeared for 30 or 60 min or after recovery had been induced for 30 or 180 min by glucose injection. Samples from the cerebral cortex from the area corresponding to the previous metabolic studies were processed for electron microscopy. The light-microscopic finding of two different types of nerve cell injury, reported in a preceding communication (Agardh et al. 1980), was also verified at the ultrastructural level. The type I injury was characterized by cellular shrinkage, condensation of the cell sap and nuclei, and perineuronal astrocytic swelling. No swelling of mitochondria occurred. The slightly swollen type II injured neurons showed contraction of mitochondria, disintegration of ribosomes, loss of RER, and appearance of membrane whorls, while their nuclear chromatin remained evenly distributed. No transition from one type to the other was observed. Neither type of nerve cell injury in hypoglycemia was like that commonly seen in anoxic-ischemic insults indicating a different pathogenesis in these states despite the common final pathway of energy failure. The loss of endoplasmic membranes and disintegration of ribosomes suggests that these structures might be sacrificed for energy production in the absence of normal substrates. During recovery, though, the number of type I injured neurons decreased while some of the remaining ones appeared even more severely affected, suggesting irreversible damage. Type II injured neurons were no longer seen indicating reversibility of these changes.},
  author       = {Kalimo, H and Agardh, Carl-David and Olsson, Y and Siesjö, Bo},
  issn         = {1432-0533},
  keyword      = {Hypoglycemia,Nerve cell injury,Electron microscopy,Rat cerebral cortex},
  language     = {eng},
  number       = {1},
  pages        = {43--52},
  publisher    = {Springer},
  series       = {Acta Neuropathologica},
  title        = {Hypoglycemic brain injury. II. Electron-microscopic findings in rat cerebral cortical neurons during profound insulin-induced hypoglycemia and in the recovery period following glucose administration},
  url          = {http://dx.doi.org/10.1007/BF00688533},
  volume       = {50},
  year         = {1980},
}