Animal models of
scopolamine-induced
amnesia are widely used to study underlying mechanisms and treatment of
cognitive impairment in
neurodegenerative diseases such as
Alzheimer's disease (AD). Previous studies have identified that
melatonin improves
cognitive dysfunction in animal models. In this study, using a mouse model of
scopolamine-induced
amnesia, we assessed spatial and short-term memory functions for 4 weeks, investigated the expression of
myelin-basic protein (MBP) in the dentate gyrus, and examined whether
melatonin and
scopolamine cotreatment could keep cognitive function and MBP expression. In addition, to study functions of
melatonin for keeping cognitive function and MBP expression, we examined expressions of
brain-derived neurotrophic factor (
BDNF) and tropomycin receptor
kinase B (TrkB) in the mouse dentate gyrus.
Scopolamine (1 mg/kg) and
melatonin (10 mg/kg) were intraperitoneally treated for 2 and 4 weeks. Two and 4 weeks after
scopolamine treatment, mice showed significant
cognitive impairment; however,
melatonin and
scopolamine cotreatment recovered
cognitive impairment. Two and 4 weeks of
scopolamine treatment, the density of MBP immunoreactive myelinated nerve fibers was significantly decreased in the dentate gyrus; however,
scopolamine and
melatonin cotreatment significantly increased the
scopolamine-induced reduction of MBP expression in the dentate gyrus. Furthermore, the cotreatment of
scopolamine and
melatonin significantly increased the
scopolamine-induced decrease of
BDNF and TrKB immunoreactivity in the dentate gyrus. Taken together, our results indicate that
melatonin treatment exerts anti-amnesic effect and restores the
scopolamine-induced reduction of MBP expression through increasing
BDNF and TrkB expressions in the mouse dentate gyrus.