Up-regulation of PSD-95 in the Rat Hippocampal Formation after Chronic Renal Failure.
- Author:
Yong Wook JUNG
1
;
Il Soo MOON
;
Dai Hai CHOI
;
Bok Hyun KO
Author Information
1. Department of Anatomy, College of Medicine, Dongguk University,Kyungju 780-714, Korea. jungyw@dongguk.ac.kr
- Publication Type:Original Article
- Keywords:
Chronic renal failure;
PSD-95;
NF200;
Hippocampus;
Rat
- MeSH:
alpha-Amino-3-hydroxy-5-methyl-4-isoxazolepropionic Acid;
Animals;
Axons;
Calcium;
Central Nervous System;
Hippocampus*;
Intermediate Filaments;
Kidney Failure, Chronic*;
Memory;
N-Methylaspartate;
Neurons;
Rats*;
Receptors, AMPA;
Up-Regulation*;
Uremia
- From:Korean Journal of Anatomy
2006;39(4):289-295
- CountryRepublic of Korea
- Language:English
-
Abstract:
The mechanism of central nervous system (CNS) dysfunction in uremia are multifactorial and only partially characterized. Studies using hippocampal formation (HF) evaluate the relationship between the uremia and memory impairment. Immunoblots with calcium permeable NMDA (N-methyl-D-aspartate) and AMPA (2-amino-3-hydroxy-5-methylisoxazole-4-propinoic acid) receptors and their associated PSD-95 proteins after chronic renal failure (CRF) provided significant new informations. CRF rats induced by 5/6 nephrectomized had significant effects on up-regulation of PSD-95 protein rather than those of calcium permeable NMDA and AMPA receptor subunits. Up-regulation of PSD-95 after CRF might be associated with the enhanced activity of NMDA and/or AMPA receptors, thereby leads to the intracellular Ca2+ accumulation and functional neuronal cell damage subsequently. Degradation of intermediate filament 200 (NF200) in the axon after CRF may induce an impairment of intracellular transport and eventual cellular dysfunction through destruction of the neuronal cytoarchitecture. These data suggest that up-regulation of PSD-95 in CRF may increase the functional derangement between the nerve cells and ultimately lead to memory impairment.
