Glial gene expression during aging in rat striatum and in long-term responses to 6-OHDA lesions
β Scribed by Giulio M. Pasinetti; Mike Hassler; David Stone; Caleb E. Finch
- Publisher
- John Wiley and Sons
- Year
- 1999
- Tongue
- English
- Weight
- 130 KB
- Volume
- 31
- Category
- Article
- ISSN
- 0887-4476
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β¦ Synopsis
The male rat striatum was examined for age-related changes in mRNAs expressed in astrocytes and microglia in two rat genotypes that differ by 35% in mean and maximum life spans: F344 and the longer-lived F 1 (BN Ο« F344) hybrid. The findings extend the established age-related increases in GFAP (glial fibrillary acidic protein) to other glial mRNAs: two lipoprotein mRNAs that are predominantly expressed in striatal astrocytes, apoE (apolipoprotein E) and apoJ (apolipoprotein J, clusterin, CLI, or SGP-2), and two mRNAs expressed in striatal microglia, TGF-β€1 and complement C1qB. By Northern blot hybridization, both genotypes showed progressive increases of GFAP mRNA to ΟΎ2.5-fold by the lifespan. Although the rat strains differed 35% in life span, the slope of the GFAP mRNA regression on age did not differ. Relative to GFAP, the increases of apoE, apoJ, C1q, and TGF-β€1 mRNAs were smaller, Υ 1.5-fold. Because prior studies showed that acute damage to striatal afferents induced astrocyte gene expression increases resembling those that also occur during aging, we examined long-term effects of damage to substantia nigra neurons on striatal astrocyte changes during aging. Young F344 rats were given 6-OHDA lesions that cause striatal dopamine deficits and induce GFAP. When examined 15 months later at age 18 months, there was no effect during prior lesions on the age-related elevation of GFAP mRNA. We conclude that aging changes in striatal GFAP mRNAs do not interact with loss of dopaminergic output to the striatum from 6-OHDA lesions and may be independent of the relatively modest dopaminergic losses during normal aging.
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