Ischemia-induced glutamate release in the dentate gyrus. A microdialysis study in the gerbil.

Abstract

The levels of extracellular glutamate were measured in the dentate gyrus by using an in vivo brain microdialysis method to determine whether the ischemia-induced glutamate release might be correlated with the neuronal vulnerability to ischemia. A microdialysis membrane was placed in CA4 (vulnerable to ischemia) and the molecular and granule cell layers of the dentate gyrus (resistant to ischemia) of gerbils. A significant increase in glutamate levels was induced in the normal dentate gyrus during 10-min ischemia. The increase was completely suppressed during the first 5 min of ischemia when CA4 neurons were eliminated. Thus, it was indicated that during the first 5 min of ischemia glutamate was released mostly from CA4 neurons but not from granule cells of the dentate gyrus. During the second half of 10-min ischemia, a significant increase in glutamate release was induced even in the dentate gyrus where CA4 neurons were eliminated; this increase was significantly suppressed by inhibiting proliferation of astrocytes. A large part of glutamate that was released during the second half of 10-min ischemia was considered to be attributable to glutamate release from astrocytes.

• Authors: Y Cui, L Zhang, K Utsunomiya, H Yanase, A Mitani, K Kataoka
• Journal: Neuroscience letters (Neurosci Lett) Vol. 271 Issue 3 Pg. 191-4 (Aug 27 1999) ISSN: 0304-3940 [Print] Ireland
• PMID: 10507701 (Publication Type: Journal Article)

Chemical References

• Glial Fibrillary Acidic Protein
• Glutamic Acid

Topics

• Animals
• Astrocytes (chemistry, metabolism)
• Dentate Gyrus (blood supply, cytology, metabolism)
• Gerbillinae
• Glial Fibrillary Acidic Protein (analysis)
• Glutamic Acid (metabolism)
• Ischemic Attack, Transient (metabolism)
• Male
• Microdialysis
• Neurons (metabolism)