【摘 要】
：
Melatonin, an indole hormone secreted by the pineal gland, has been reported to have strong neuropeotective effects.However, whether melatonin could protect hippocampal synaptic plasticity and neurona
【机 构】
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Department of Physiology,Key Laboratory for Cellular Physiology of Ministry of Education,Shanxi Medi
【出 处】
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International Conference for Physiological Sciences 2012(201
论文部分内容阅读
Melatonin, an indole hormone secreted by the pineal gland, has been reported to have strong neuropeotective effects.However, whether melatonin could protect hippocampal synaptic plasticity and neuronal firing against amyloid beta protein (Aβ)-induced impairments remains little reported.The present study is designed to explore the influence of melatonin on hippocampal long-term potentiation (LTP), spontaneous neuronal discharge and local field potential (LFP) in the Alzheimers disease (AD) related animal model.SD rats were pretreated by bilateral intrahippocampal injection of Aβ31-35 to make animal model, followed by intraperitoneal injection of melatonin for ten days.Hippocampal LTP and neuron activity in CA1 region were then recorded in vivo.The results showed that: (1) compared with control, the level of LTP in Aβ31-35 alone group was significantly decreased.While treatment with melatonin for 10 days effectively prevented against the depression of LTP induced by Aβ31-35 in a dose-dependent manner;(2) the firing frequencies of neurons in Aβ31-35 alone group were markedly reduced compared to control group.But, the firing frequency after melatonin treatment for ten days did not show any significant decrease;in addition, (3) Aβ31-35 disrupted the power of theta rhythm in CA1 region, while melatonin dose-dependently reversed the disruption.These results indicates that melatonin could protect against Aβ-induced impairments of synaptic plasticity and neuronal activity, suggesting that melatonin application in AD may be useful for the alleviation of cognition deficits.
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