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Glial gene expression during aging in rat striatum and in long‐term responses to 6‐OHDA lesions
Author(s) -
Pasinetti Giulio M.,
Hassler Mike,
Stone David,
Finch Caleb E.
Publication year - 1999
Publication title -
synapse
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.809
H-Index - 106
eISSN - 1098-2396
pISSN - 0887-4476
DOI - 10.1002/(sici)1098-2396(19990315)31:4<278::aid-syn5>3.0.co;2-0
Subject(s) - glial fibrillary acidic protein , astrocyte , striatum , biology , substantia nigra , endocrinology , medicine , microglia , dopaminergic , apolipoprotein e , gene expression , dopamine , central nervous system , immunohistochemistry , immunology , gene , inflammation , biochemistry , disease
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 × 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‐β1 and complement C1qB. By Northern blot hybridization, both genotypes showed progressive increases of GFAP mRNA to >2.5‐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‐β1 mRNAs were smaller, ≤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. Synapse 31:278–284, 1999. © 1999 Wiley‐Liss, Inc.