Tumor necrosis factor-alpha (TNF-α) is a cytokine involved in a variety of neurobiological activities including changing behavior and regulation of both neurotrophin and neuropeptide levels. In this study we used two lines of transgenic mice overexpressing brain TNF-α characterized by neurological deficits (line Tg6074) or phenotypically normal (line TgK3). We analyzed whether or not impairments in learning and memory processes due to TNF-α overexpression were associated with changes in endogenous brain NGF, NPY and β-amyloid. The results indicate that full TNF-α transgene expression disrupted the learning capabilities of transgenic mice (both Tg6074 and TgK3). NGF decreased in the hippocampus of both transgenic mice whereas hippocampal NPY slightly potentiated in Tg6074. The decrease in NGF is correlated with deficits in spatial learning and memory whereas inflammation in the brain of Tg6074 could be responsible of the hippocampal increase in NPY. As a whole, these results show that transgenic mice overexpressing TNF-α in the brain represent a useful model for studying neuronal degeneration and brain inflammatory processes.
|Number of pages||11|
|Journal||Behavioural Brain Research|
|Publication status||Published - 2000|
- Water maze
ASJC Scopus subject areas
- Behavioral Neuroscience