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
(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:
https://lup.lub.lu.se/record/1102756
- author
- Kalimo, H ; Agardh, Carl-David LU ; Olsson, Y and Siesjö, Bo LU
- organization
- publishing date
- 1980
- 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
- additional info
- The information about affiliations in this record was updated in December 2015. The record was previously connected to the following departments: Unit on Vascular Diabetic Complications (013241510), Neurology, Lund (013027000)
- id
- ab7f3d42-c86b-414c-9017-866fdb7a9c4c (old id 1102756)
- date added to LUP
- 2016-04-01 16:09:59
- date last changed
- 2021-01-03 11:28:22
@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}}, keywords = {{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}}, doi = {{10.1007/BF00688533}}, volume = {{50}}, year = {{1980}}, }