Neurology
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
Right arrow Correspondence:
Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when Correspondence are posted
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Tecoma, E. S.
Right arrow Articles by Choi, D. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tecoma, E. S.
Right arrow Articles by Choi, D. W.
NEUROLOGY 1989;39:676
© 1989 American Academy of Neurology

GABAergic neocortical neurons are resistant to NMDA receptor-mediated injury

Evelyn S. Tecoma, MD, PhD and Dennis W. Choi, MD, PhD

Department of Neurology, Stanford University Medical Center, Stanford, CA.

N-methyl-D-aspartate (NMDA) receptors are thought to mediate much of the central neuronal loss produced by certain neurologic insults, including hypoxia-ischemia, hypoglycemia, and trauma. Therefore, the specific vulnerability of GABAergic inhibitory neurons to NMDA receptor-mediated toxicity might be an important determinant of the potential for epileptogenesis following these insults. We have examined the fate of GABAergic cortical neurons in mouse cell cultures exposed to toxic levels of NMDA. GABAergic cells (about 10% of the cultured neuronal population) were identified either by immunoreactivity with antisera to GABA or by autoradiography following high-affinity uptake of 3H-GABA. Cultures exposed for 5 min to 20 to 750 µM NMDA showed NMDA concentration-dependent, widespread neuronal loss. However, GABAergic neurons were relatively spared, and thus represented an enhanced fraction of neuronal survivors. These observations suggest that GABAergic cortical neurons may possess some intrinsic resistance to NMDA receptor-mediated neurotoxicity, a property which might convey an anticonvulsant "inhibitory safety factor" to neocortex against certain forms of injury.

Address correspondence and reprint requests to Dr. Choi, Department of Neurology, Stanford University Medical Center. Stanford, CA 94305.

Supported by NIH grants NS12151 and NS26907.

Received September 28.1988. Accepted for publication in final form November 30, 1988.




This article has been cited by other articles:


Home page
 Clin Med ResHome page
K. Madden, W. Clark, and N. Lessov
Failure of Ischemic Neuroprotection by Potentiators of Gamma-aminobutyric Acid
Clin. Med. Res., April 1, 2003; 1(2): 119 - 124.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Pathol.Home page
Y. Konishi, K. Lindholm, L.-B. Yang, R. Li, and Y. Shen
Isolation of Living Neurons from Human Elderly Brains Using the Immunomagnetic Sorting DNA-Linker System
Am. J. Pathol., November 1, 2002; 161(5): 1567 - 1576.
[Abstract] [Full Text] [PDF]

Home page
 StrokeHome page
D. A. Sun, S. Sombati, and R. J. DeLorenzo
Glutamate Injury-Induced Epileptogenesis in Hippocampal Neurons: An In Vitro Model of Stroke-Induced "Epilepsy"
Stroke, October 1, 2001; 32(10): 2344 - 2350.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
Q. Cheng, J. C. Kulli, and J. Yang
Suppression of Neuronal Hyperexcitability and Associated Delayed Neuronal Death by Adenoviral Expression of GABAC Receptors
J. Neurosci., May 15, 2001; 21(10): 3419 - 3428.
[Abstract] [Full Text] [PDF]

Home page
 NeuroscientistHome page
M. D. Ginsberg
Review : Neuroprotection in Brain Ischemia: An Update (Part II
Neuroscientist, May 1, 1995; 1(3): 164 - 175.
[Abstract] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Copyright © 1989 by AAN Enterprises, Inc.