ArticleNeurochemical research2008
Differential changes in pyridoxine 5'-phosphate oxidase immunoreactivity and protein levels in the somatosensory cortex and striatum of the ischemic gerbil brain.
Article in Neurochemical research, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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3 citing papers in PubMed, 10 citations in OpenAlex.
- High fat diet accelerates and exacerbates microgliosis and neuronal damage/death in the somatosensory cortex after transient forebrain ischemia in gerbils.Laboratory animal research · 2020Article
- Brain ischemic preconditioning protects against moderate, not severe, transient global cerebral ischemic injury.Metabolic brain disease · 2018Article
- Chronic effects of pyridoxine in the gerbil hippocampal CA1 region after transient forebrain ischemia.Neurochemical research · 2012Article
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8 authors at 3 institutions in 1 country.
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Abstract
Pyridoxal 5'-phosphate (PLP) is an important cofactor in a wide range of biochemical reactions, such as the metabolism of various amino acids, including GABA. PLP is synthesized by the oxidation of pyridoxine 5'-phosphate (PNP), which is catalyzed by PNP oxidase (PNPO). We observed the changes in cresyl violet-positive neurons, PNPO immunoreactivity and PNPO protein levels in the somatosensory cortex and striatum in gerbils after 5 min of transient forebrain ischemia. Cresyl violet-positive neurons showed condensed cytoplasm in the somatosensory cortex and lateral part of the striatum at 2 days after ischemia/reperfusion. PNPO immunoreactivity began to increase in neurons in layers III and V at 3 h after ischemia/reperfusion and this immunoreactivity was significantly increased at 12 h after ischemia/reperfusion. Thereafter, PNPO immunoreactivity decreased with time after ischemia/reperfusion. PNPO-immunoreactive neurons were only slightly detected in the lateral part of the striatum at 12 h after ischemia/reperfusion. In addition, the PNPO protein levels in both the somatosensory cortex and striatum homogenates peaked at 12 h after ischemia/reperfusion. These results indicate that PNPO is significantly increased in the ischemic somatosensory cortex and lateral part of the striatum, and this change in the level of PNPO may be associated with the neuronal damage induced by ischemia.
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