Suppressive Effects of Melatonin on Amyloid-β-induced Glial Activation in Rat Hippocampus

Background g evidence indicates that activated glia, as a result of chronic inflammation, are associated with amyloid-β peptide (Aβ) deposits in the brain of Alzheimerʹs disease (AD) patients. The purpose of the present study was to investigate, in vivo, the effects of melatonin on glia activation, which may contribute to improved learning and memory in amnesic rats induced by amyloid-β peptide 25–35 (Aβ25–35). s mined cognitive function using the Morris water maze test. Expression of interleukin 1α (IL-1α) or complement 1q (C1q) in rat hippocampal tissue was determined by immunohistochemistry. s found that Aβ25–35 injected into rat hippocampus induced an impairment in learning and memory and a marked increase of positive glial cells expressing IL-1α and C1q in hippocampus, compared with the controls. This suggests that glial activation triggered by Aβ25–35 parallels the dysfunction of learning and memory. Melatonin, at doses of 0.01, 0.1, and 1 mg/kg (i.g. for 10 days), improved learning and memory of rats treated with Aβ25–35. Cells expressing IL-1α and C1q were significantly decreased in hippocampus by pretreatment with melatonin at doses of 0.1 mg/kg and 1 mg/kg, but not at the dose of 0.01 mg/kg. sions ta indicate that melatonin inhibited expressions of proinflammatory factors, which may contribute to improvement of learning and memory function in AD.