The Status of Vitamin B₆ Metabolism in Brains of Genetically Epilepsy‐Prone Rats

Abstract

The status of vitamin B6 in brains of genetically epilepsy-prone and epilepsy-resistant rats was ascertained by measuring the concentrations of pyridoxal phosphate and the activities of pyridoxal kinase in the hippocampus, basal ganglia, cerebellum, and cerebral cortex, as well as in the entire brain. The concentrations of pyridoxal phosphate in whole brain of control rats and seizure-prone rats did not vary significantly from each other and were 1.2 +/- 0.02 and 1.2 +/- 0.03 microgram/g, respectively. Similarly, the activities of pyridoxal kinase in brains of the two groups were uniform and had values of 3.6 +/- 0.1 and 3.5 +/- 0.06 microgram pyridoxal phosphate formed/mg protein/15 min, respectively. Unlike in the whole brain, the concentration of pyridoxal phosphate in the cerebral cortex of seizure-prone rats was lower (1.24 +/- 0.026 microgram/g) than that of seizure-resistant rats (1.47 +/- 0.23 microgram/g). The opposite was noted in the cerebellum. The concentrations of pyridoxal phosphate in the hippocampus and in the basal ganglion of seizure-prone and seizure-resistant rats were identical. The activities of pyridoxal kinase in the basal ganglion (3.84 +/- 0.23 vs. 4.99 +/- 0.11 microgram pyridoxal phosphate/mg protein/15 min) and in the cerebral cortex (3.40 +/- 0.06 vs. 3.70 +/- 0.04 microgram pyridoxal phosphate/mg protein/15 min) were lower in seizure-prone rats than in seizure-resistant rats. The reverse took place in the hippocampus and in the cerebellum. No uniform associations among the concentration of pyridoxal phosphate, the activity of pyridoxal kinase, and the susceptibility or lack of susceptibility to seizure could be demonstrated.(ABSTRACT TRUNCATED AT 250 WORDS)

MicroRNA339 Targeting PDXK Improves Motor Dysfunction and Promotes Neurite Growth in the Remote Cortex Subjected to Spinal Cord Transection

“…By thoroughly investigating the molecules involved in functional remodeling of the spinal cord in remote cortexes, we discovered that PDXK is substantially upregulated in the motor cortex after SCT. It has been reported that the function of PDXK is prominently enhanced in the whole brain tissue of humans, embryos, and fetuses ( Bukin Iu and Ivanova, 1976 ; Shin et al, 2004 ), as well as in the whole brain of in epilepsy-prone and epilepsy-resistant rats ( Ebadi et al, 1985 ). Additionally, PDXK is expressed in the porcine brain cortex ( Gao et al, 1998 ).…”