Analysis of Neuronal Nitric Oxide Synthase Expression and Increasing Astrogliosis in the Brain of Senescence-Accelerated-Prone 8 Mice

• Published in: International journal of neuroscience Vol. 120; no. 9; pp. 602 - 608
• Main Authors: Han, Shu, Rudd, John A., Hu, Zhi Ying, Zhang, Lihong, Yew, David T., Fang, Marong
• Format: Journal Article
• Language: English
• Published: England Informa Healthcare 01.08.2010; Taylor & Francis
• Subjects: age-related astrogliosis; Aging - genetics; Aging - metabolism; Animals; Brain - metabolism; Cerebral Cortex - metabolism; Glial Fibrillary Acidic Protein - metabolism; Gliosis - metabolism; Hippocampus - metabolism; learning and memory deficits; Male; Memory; Mice; Mice, Mutant Strains; Nitric Oxide - metabolism; Nitric Oxide Synthase Type I - biosynthesis; Nitric Oxide Synthase Type I - genetics; nNOS; senescence accelerated mouse
• ISSN: 0020-7454; 1563-5279; 1543-5245
• DOI: 10.3109/00207454.2010.503911

ABSTRACT The senescence-accelerated mouse (SAM) is an autogenic senile murine model characterized by early cognitive impairment and age-related deterioration of learning and memory. The present study investigated the alternations of neuronal nitric oxide synthase (nNOS) expression in frontal cortex and hippocampus in the aging process of SAM-prone 8 (SAMP8) and SAM-resistant 1 (SAMR1) mice. The results demonstrated that the expression of nNOS was upregulated in the frontal cortex, but downregulated in the hippocampus in SAMP8. Further, age-related increases of astrogliosis were seen in the cortex and hippocampi of aged SAMP8 and SAMR1, as revealed by the expression of the astrocyte specific marker, glial fibrillary acidic protein (GFAP). Indeed, astrogliosis in aged SAMP8 was significantly greater than that of aged SAMR1. Our results suggest the possibility of a correlation between the downregulation of nitric oxide (NO) in the hippocampus and reported learning and memory deficits in SAMP8. However, the toxic effects of NO and age-related increases of astrogliosis, may have contributed to abnormal alterations in metabolism and neurochemical mechanisms in aged SAMP8.