Skip to main content

Lund University Publications

LUND UNIVERSITY LIBRARIES

Extracellular levels of quinolinic acid are moderately increased in rat neostriatum following severe insulin-induced hypoglycaemia

Westerberg, E. ; Magnusson, K. ; Wieloch, T. LU ; Ungerstedt, U. ; Speciale, C. and Schwarcz, R. (1990) In Acta Physiologica Scandinavica 138(3). p.417-422
Abstract

Extracellular concentrations of the brain metabolite quinolinic acid, an endogenous excitotoxin, were monitored by microdialysis in rat neostriatum and hippocampus/cortex during and following a 30-min period of insulin-induced hypoglycaemia. During hypoglycaemia-induced isoelectricity, extracellular levels of quinolinic acid in the striatum (basal value, 1.1 ± 0.3 pmol per 30-μl fraction) were elevated 1.7 times as compared to the control period. Thirty to ninety minutes following hypoglycaemia a significant increase in extracellular quinolinic acid to 2.2 times basal level was noted. After 2 h recovery, the beginning of neuronal necrosis was observed in the dorsolateral striatum. Implantation of the dialysis probe did not influence the... (More)

Extracellular concentrations of the brain metabolite quinolinic acid, an endogenous excitotoxin, were monitored by microdialysis in rat neostriatum and hippocampus/cortex during and following a 30-min period of insulin-induced hypoglycaemia. During hypoglycaemia-induced isoelectricity, extracellular levels of quinolinic acid in the striatum (basal value, 1.1 ± 0.3 pmol per 30-μl fraction) were elevated 1.7 times as compared to the control period. Thirty to ninety minutes following hypoglycaemia a significant increase in extracellular quinolinic acid to 2.2 times basal level was noted. After 2 h recovery, the beginning of neuronal necrosis was observed in the dorsolateral striatum. Implantation of the dialysis probe did not influence the extent of neuronal damage. No changes in extracellular quinolinic acid levels were observed in the hippocampus/cortex. The data indicate the following a severe hypoglycaemic insult vulnerable striatal cells are exposed to hyperphysiological extracellular quinolinic acid concentrations over an extended period of time. Considering the pronounced susceptibility of rat striatal neurons to the toxin, the small but prolonged elevation in the extracellular levels of quinolinic acid could be of significance for the development of delayed neuronal death in hypoglycaemia.

(Less)
Please use this url to cite or link to this publication:
author
; ; ; ; and
organization
publishing date
type
Contribution to journal
publication status
published
subject
keywords
Excitotoxins, Hypoglycaemia, Microdialysis, Neuronal death, Quinolinic acid
in
Acta Physiologica Scandinavica
volume
138
issue
3
pages
6 pages
publisher
Wiley-Blackwell
external identifiers
  • scopus:0025216768
  • pmid:2139298
ISSN
0001-6772
DOI
10.1111/j.1748-1716.1990.tb08865.x
language
English
LU publication?
yes
id
99cdeac0-ba69-4d88-b5ca-b05fa69dcda3
date added to LUP
2019-06-13 16:38:28
date last changed
2024-01-01 10:23:02
@article{99cdeac0-ba69-4d88-b5ca-b05fa69dcda3,
  abstract     = {{<p>Extracellular concentrations of the brain metabolite quinolinic acid, an endogenous excitotoxin, were monitored by microdialysis in rat neostriatum and hippocampus/cortex during and following a 30-min period of insulin-induced hypoglycaemia. During hypoglycaemia-induced isoelectricity, extracellular levels of quinolinic acid in the striatum (basal value, 1.1 ± 0.3 pmol per 30-μl fraction) were elevated 1.7 times as compared to the control period. Thirty to ninety minutes following hypoglycaemia a significant increase in extracellular quinolinic acid to 2.2 times basal level was noted. After 2 h recovery, the beginning of neuronal necrosis was observed in the dorsolateral striatum. Implantation of the dialysis probe did not influence the extent of neuronal damage. No changes in extracellular quinolinic acid levels were observed in the hippocampus/cortex. The data indicate the following a severe hypoglycaemic insult vulnerable striatal cells are exposed to hyperphysiological extracellular quinolinic acid concentrations over an extended period of time. Considering the pronounced susceptibility of rat striatal neurons to the toxin, the small but prolonged elevation in the extracellular levels of quinolinic acid could be of significance for the development of delayed neuronal death in hypoglycaemia.</p>}},
  author       = {{Westerberg, E. and Magnusson, K. and Wieloch, T. and Ungerstedt, U. and Speciale, C. and Schwarcz, R.}},
  issn         = {{0001-6772}},
  keywords     = {{Excitotoxins; Hypoglycaemia; Microdialysis; Neuronal death; Quinolinic acid}},
  language     = {{eng}},
  month        = {{01}},
  number       = {{3}},
  pages        = {{417--422}},
  publisher    = {{Wiley-Blackwell}},
  series       = {{Acta Physiologica Scandinavica}},
  title        = {{Extracellular levels of quinolinic acid are moderately increased in rat neostriatum following severe insulin-induced hypoglycaemia}},
  url          = {{http://dx.doi.org/10.1111/j.1748-1716.1990.tb08865.x}},
  doi          = {{10.1111/j.1748-1716.1990.tb08865.x}},
  volume       = {{138}},
  year         = {{1990}},
}