Decrease of protein phosphatase 2A subunit B by glutamate exposure in the cerebral cortex of neonatal rats
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Kang et al. Laboratory Animal Research (2020) 36:34 https://doi.org/10.1186/s42826-020-00064-y
RESEARCH
Open Access
Decrease of protein phosphatase 2A subunit B by glutamate exposure in the cerebral cortex of neonatal rats Ju-Bin Kang†, Dong-Ju Park†, Hyun-Kyoung Son and Phil-Ok Koh*
Abstract Glutamate induces neurotoxicity during brain development, causing nerve damage. Protein phosphatase 2A (PP2A) is a type of serine/threonine phosphatase that regulates various biological functions. Among the PP2A subunit types, subunit B is abundant in brain tissue and plays an essential role in the nervous system. This study investigated changes in PP2A subunit B expression through glutamate exposure in the cerebral cortex of newborn rats. Sprague-Dawley rat pups (7 days after birth) were injected intraperitoneally with vehicle or glutamate (10 mg/ kg). After 4 h of drug treatment, the brain tissue was isolated and fixed for morphological study. In addition, the cerebral cortex was collected for RNA and protein works. We observed severe histopathological changes including swollen neuron and atrophied dendrite in the glutamate exposed cerebral cortex. Glutamate exposure leads to a decrease in PP2A subunit B. Reverse-transcription PCR and Western blot analyses confirmed that glutamate induces a decrease of PP2A subunit B in the cerebral cortex of newborn rats. Moreover, immunohistochemical study showed a decrease in PP2A subunit B positive cells. The reduction of PP2A subunit B expression is considered an indicator of neurodegenerative damage. These results suggest that glutamate exposure causes neuronal damage in the cerebral cortex of new born rats through a decrease in PP2A subunit B. Keywords: Cerebral cortex, Glutamate, Neonate, PP2A
Introduction Glutamate is a excitatory neurotransmitter in the central nervous system [1]. It plays an essential role in learning and memory, synaptic plasticity, and cytoskeleton formation [2, 3]. It also contributes to regulation of synaptic development during brain development. Glutamate transporters are located in neuronal and glial cell membranes and remove glutamate from the extracellular space. However, in brain injury or disease, glutamate transporters often reverse their activity and cause accumulation of glutamate in the extracellular space. * Correspondence: [email protected] † Ju-Bin Kang and Dong-Ju Park contributed equally to this work. Department of Anatomy, College of Veterinary Medicine, Research Institute of Life Science, Gyeongsang National University, 501 Jinju-daero, Jinju 52828, South Korea
Excessive glutamate accumulation causes calcium influx into the intracellular matrix through the N-methyl-d-aspartate (NMDA) receptor channel. Calcium ion concentration is an important factor for regulation of mitochondrial function [4, 5]. High calcium ion concentration increases intracellular nitric oxide (NO) concentration and oxidative stress [6]. This leads to downregulates anti-apoptosis genes and induces apoptosis cell death [7]. In addition, excessive glutamate induces excit
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