Increased neuroinflammatory reaction is frequently observed
during normal brain aging. However, a direct link between
neuroinflammation and neurodegeneration during aging has not
yet been clearly shown. Here, we have characterized the agerelated hippocampal inflammatory processes and the potential
relation with hippocampal neurodegeneration. The mRNA
expression of the pro-inflammatory cytokines IL-1b and tumor
necrosis factor-a (TNF-a), and the iNOs enzyme was significantly increased in aged hippocampus. Accordingly, numerous
activated microglial cells were observed in aged rats. These
cells were differentially distributed along the hippocampus,
being more frequently located in the hilus and the CA3 area. The
mRNA expression of somatostatin, a neuropeptide expressed
by some GABAergic interneurons, and the number of somatostatin-immunopositive cells decreased in aged rats. However,
the number of hippocampal parvalbumin-containing GABAergic
interneurons was preserved. Interestingly, in aged rats, the
mRNA expression of somatostatin and IL-1b was inversely
correlated and, the decrease in the number of somatostatinimmunopositive cells was higher in the hilus of dentate gyrus
than in the CA1 region. Finally, intraperitoneal chronic lipopolysaccharide (LPS) injection in young animals mimicked the agerelated hippocampal inflammation as well as the decrease of
somatostatin mRNA expression. Present results strongly support the neuroinflammation as a potential factor involved in the
age-related degeneration of somatostatin GABAergic cells.
