In the present study, we investigated ischemia-induced changes of pyridoxal 5′-phosphate synthesizing enzyme and degrading enzyme and neuroprotective effects and roles of pyridoxal 5′-phosphate against ischemic damage in the gerbil hippocampal CA1 region. Pyridoxal 5′-phosphate oxidase and pyridoxal phosphate phosphatase immunoreactivities were changed in neurons up to 2 days after ischemia, while 4 days after ischemia their immunoreactivities were expressed in astrocytes. Pyridoxal 5′-phosphate oxidase immunoreactivity and its protein level were highest 12 h after ischemia, while those in pyridoxal phosphate phosphatase were highest 2 days after ischemia. Total activities of these enzymes were changed after ischemia, but specific activities of the enzymes were not altered. Treatment with pyridoxal 5′-phosphate into brains (4 μg/5 μl, i.c.v.) at 30 min before transient ischemia protected about 80% of CA1 pyramidal cells 4 days after ischemia and induced elevation of glutamic acid decarboxylase 67 immunoreactivity in the CA1 region. However, pyridoxal 5′-phosphate treatment into ischemic brains decreased GABA transaminase immunoreactivity in the CA1 region after ischemia. These results indicate that pyridoxal 5′-phosphate may be associated with the inhibitory discharge of GABA in the hippocampal CA1 neurons, and the increased level of GABA may protect hippocampal CA1 pyramidal cells from ischemic damage.
Bibliographical noteFunding Information:
The authors would like to thank Mr. Seok Han, Mr. Seung Uk Lee, and Ms. Hyun Sook Kim for their technical help for this study. This study was supported by a grant of the Korean Health 21 R&D Project, Ministry of Health and Welfare, Republic of Korea (A030079).
All Science Journal Classification (ASJC) codes
- Developmental Neuroscience