Life-time expression of the proteins peroxiredoxin, beta-synuclein, PARK7/DJ-1, and stathmin in the primary visual and primary somatosensory cortices in rats.

Michael R R Böhm

doi:10.3389/fnana.2015.00016

Abstract

Four distinct proteins are regulated in the aging neuroretina and may be regulated in the cerebral cortex, too: peroxiredoxin, beta-synuclein, PARK[Parkinson disease(autosomal recessive, early onset)]7/DJ-1, and Stathmin. Thus, we performed a comparative analysis of these proteins in the the primary somatosensory cortex (S1) and primary visual cortex (V1) in rats, in order to detect putative common development-, maturation- and age-related changes. The expressions of peroxiredoxin, beta-synuclein, PARK[Parkinson disease (autosomal recessive, early onset)]7/DJ-1, and Stathmin were compared in the newborn, juvenile, adult, and aged S1 and V1. Western blot (WB), quantitative reverse-transcription polymerase chain reaction (qRT-PCR), and immunohistochemistry (IHC) analyses were employed to determine whether the changes identified by proteomics were verifiable at the cellular and molecular levels. All of the proteins were detected in both of the investigated cortical areas. Changes in the expressions of the four proteins were found throughout the life-time of the rats. Peroxiredoxin expression remained unchanged over life-time. Beta-Synuclein expression was massively increased up to the adult stage of life in both the S1 and V1. PARK[Parkinson disease (autosomal recessive, early onset)]7/DJ-1 exhibited a massive up-regulation in both the S1 and V1 at all ages. Stathmin expression was massively down regulated after the neonatal period in both the S1 and V1. The detected protein alterations were analogous to their retinal profiles. This study is the first to provide evidence that peroxiredoxin, beta-synuclein, PARK[Parkinson disease (autosomal recessive, early onset)]7/DJ-1, and Stathmin are associated with postnatal maturation and aging in both the S1 and V1 of rats. These changes may indicate their involvement in key functional pathways and may account for the onset or progression of age-related pathologies.

Highlights

Cerebral maturation and aging is characterized by stereotypical structural and neurophysiological changes that result in marked variations in the dendritic morphology of pyramidal neurons in different cortical areas (Elston, 2002; Jacobs and Scheibel, 2002)
In a previous comparative proteomic analysis of the neuroretinas of marmosets and rats, we found that peroxiredoxin (Prx), beta-synuclein (SNCB), Parkinson’s disease (PD; autosomal recessive, early onset) 7/DJ-1 (DJ-1), and stathmin (STMN) were regulated in an age-related fashion in both species (Böhm et al, 2013)
First, the expressions of Prx, SNCB, DJ-1, and STMN in the S1 and V1 were verified at the protein and gene level using Western blot (WB) and quantitative reverse-transcription polymerase chain reaction (qRT-polymerase chain reaction (PCR))

Summary

Introduction

Cerebral maturation and aging is characterized by stereotypical structural and neurophysiological changes that result in marked variations in the dendritic morphology of pyramidal neurons in different cortical areas (Elston, 2002; Jacobs and Scheibel, 2002). There is a significant loss of synapses in the post-exhuberant postnatal cortex (Huttenlocher, 1990; Bourgeois and Rakic, 1993; Rakic et al, 1994; Huttenlocher and Dabholkar, 1997) These regional differences in pyramidal cell structure and synaptic density patterns may be the determinants of cortical function and may be associated with the functional and physiological aspects of learning processes for each cortical region (Elston, 2003; Spruston, 2008). Neuroglia plays important roles in synapse formation during development, as well as in multiple forms of synaptic plasticity (Liu et al, 1994; Prewitt et al, 1997; Rochefort et al, 2002; López-Hidalgo and Schummers, 2014), whereas dynamic physical and molecular interactions between astrocytes and neurons control the morphology and structural plasticity of the dendritic spines. Once the appropriate synaptic connections are formed during the critical period of maturation and refinement, the function of astrocytes is likely modulated (Stevens, 2008)

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