title: Changes of pyridoxal kinase expression and activity in the gerbil hippocampus following transient forebrain ischemia.
abstract: In the previous study, we observed chronological alterations of glutamic acid decarboxylase (GAD), which is the enzyme converting glutamate into GABA. GAD isoforms (GAD65 and GAD67) differ substantially in their interactions with cofactor pyridoxal 5'-phosphate, which is catalyzed by pyridoxal kinase (PLK). In the present study, we examined the chronological changes of PLK expression and activity in the hippocampus after 5 min transient forebrain ischemia in gerbils. PLK immunoreactivity in the sham-operated group was detected weakly in the hippocampus. Ischemia-related change of PLK immunoreactivity in the hippocampus was significant in the hippocampal cornu ammonis (CA1)region, not in the hippocampal CA2/3 region and dentate gyrus. PLK immunoreactivity was observed in non-pyramidal GABAergic neurons at 30 min to 3 h after ischemic insult. At 12 h after ischemic insult, PLK immunoreactivity was shown in many CA1 pyramidal cells as well as some non-pyramidal cells. At this time point, PLK immunoreactivity and protein content was highest after ischemia. Thereafter, PLK immunoreactivity and protein content is decreased time-dependently by 4 days after ischemic insult. Four days after ischemia, some astrocytes expressed PLK in the CA1 region. The specific PLK activity was not altered following ischemic insult up to 2 days after ischemic insult. Thereafter, the specific PLK activity decreased time-dependently. However, total activity of PLK was significantly increased 12-24 h after ischemic insult, and thereafter total activity of PLK decreased. Therefore, we suggest that the over-expression of PLK in the CA1 pyramidal cells at 12 h after ischemia may induce increase of GAD in the CA1 pyramidal cells, which plays an important role in delayed neuronal death via the increase of GABA or enhancement of GABA shunt pathway.
authors.affiliation: Department of Anatomy, College of Medicine, Hallym University, Chunchon 200-702, South Korea.
authors.forename: I K
authors.initials: IK
authors.lastname: Hwang
authors.forename: K-Y
authors.initials: KY
authors.lastname: Yoo
authors.forename: D S
authors.initials: DS
authors.lastname: Kim
authors.forename: W S
authors.initials: WS
authors.lastname: Eum
authors.forename: J-K
authors.initials: JK
authors.lastname: Park
authors.forename: J
authors.initials: J
authors.lastname: Park
authors.forename: O-S
authors.initials: OS
authors.lastname: Kwon
authors.forename: T-C
authors.initials: TC
authors.lastname: Kang
authors.forename: S Y
authors.initials: SY
authors.lastname: Choi
authors.forename: M H
authors.initials: MH
authors.lastname: Won
mesh_terms: D000818:Animals; D001253:Astrocytes / Q000201:enzymology; D004195:Disease Models, Animal; D015536:Down-Regulation / Q000502:physiology; D005849:Gerbillinae; D005968:Glutamate Decarboxylase / Q000378:metabolism; D006624:Hippocampus / Q000201:enzymology* / Q000503:physiopathology; D007150:Immunohistochemistry; D007395:Interneurons / Q000201:enzymology; D002546:Ischemic Attack, Transient / Q000201:enzymology* / Q000503:physiopathology; D008297:Male; D009410:Nerve Degeneration / Q000201:enzymology* / Q000209:etiology / Q000503:physiopathology; D016548:Prosencephalon / Q000098:blood supply / Q000201:enzymology* / Q000503:physiopathology; D017966:Pyramidal Cells / Q000201:enzymology; D011731:Pyridoxal Kinase / Q000378:metabolism*; D013997:Time Factors; D015854:Up-Regulation / Q000502:physiology; D005680:gamma-Aminobutyric Acid / Q000096:biosynthesis*
chemical_list: D005680:gamma-Aminobutyric Acid; D011731:Pyridoxal Kinase; D005968:Glutamate Decarboxylase