Abstract |
The effects of indeloxazine on the ischemia-induced death of hippocampal CA1 pyramidal cells following transient cerebral ischemia were examined in the mongolian gerbil. Increased survival of CA1 pyramidal cells was demonstrated in animals pre- and post-treated with indeloxazine. Increased survival of CA1 pyramidal cells was, however, not demonstrated in animals post-treated but not pre-treated with indeloxazine. A previous study has demonstrated that indeloxazine increases the glucose and adenosine triphosphate ( ATP) contents in the brain probably through an enhanced capability of oxidative phosphorylation. It has been reported that increases in the glucose and ATP contents in the brain before ischemia delay the onset of massive ionic fluxes during ischemia. The delay in onset of this ionic event may help to protect these cells from death. The present data suggest that energy state before ischemia may play an important role in the protective effect of indeloxazine.
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Authors | T Kano, Y Katayama, S Miyazaki, K Kinoshita, T Kawamata, T Tsubokawa |
Journal | Neuropharmacology
(Neuropharmacology)
Vol. 32
Issue 3
Pg. 307-10
(Mar 1993)
ISSN: 0028-3908 [Print] England |
PMID | 8474628
(Publication Type: Journal Article)
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Chemical References |
- Antidepressive Agents
- Morpholines
- indeloxazine
- Adenosine Triphosphate
- Glucose
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Topics |
- Adenosine Triphosphate
(metabolism)
- Animals
- Antidepressive Agents
(therapeutic use)
- Cell Death
(drug effects)
- Gerbillinae
- Glucose
(metabolism)
- Hippocampus
(metabolism, pathology)
- Ischemic Attack, Transient
(drug therapy, metabolism, pathology)
- Male
- Morpholines
(therapeutic use)
- Oxidative Phosphorylation
(drug effects)
- Pyramidal Tracts
(metabolism, pathology)
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