Cinnarizine against excitotoxicity in rat hippocampus induced dementia monoamine neurotransmitter.docVIP

 PAGE \* MERGEFORMAT 14 Cinnarizine against excitotoxicity in rat hippocampus induced dementia monoamine neurotransmitter [Abstract] Objective cinnarizine (Cin) on the excitotoxicity induced Alzheimer’s disease (AD) model for the improvement of learning and memory and hippocampal monoamine neurotransmitter. Methods microinjection method, quinoline acid (QA) injected into rat hippocampus CA1, learning and memory in rat model of AD was observed Cin on rat behavior, morphology and neural pathology and biochemistry-related index. Results Cin can be reduced rats in the Morris water maze to find the average latency and platform in the shuttle box experiment to avoid latency, and significantly reduce the pathological damage of brain tissue; dose-dependent increase in rat hippocampus in tyrosine hydroxylase (TH) , tryptophan hydroxylase (TPH) the number of positive cells, away norepinephrine (NA), dopamine (DA) and 5 - hydroxytryptamine (5-HT) levels also increased significantly. Conclusions Cin increase in single-pass Neurotransmitter content to improve learning and memory in rats AD. [Keywords:] Cinnarizine; excitotoxicity; monoamine neurotransmitters Excitotoxic injury in the central nervous system diseases and injury of neuronal degeneration and necrosis of one of the mechanisms (1). Quinolinic acid (QA) is a potential endogenous toxins, a study area in the hippocampal CA1 injection of QA, Using the selective destruction of glutamate (Glu) neurons characteristic of Glu prepared to damage the learning and memory impairment model (2). cinnarizine (Cin) as a calcium channel blocker, on cerebral ischemia injury good efficacy (3,4), but Cin on QA induced neuronal injury protective effects have not been reported. In this study, method of excitotoxicity in rat Alzheimer’s disease (AD) model, Cin on learning and memory in animal models of AD and its effects on monoamine neurotransmitters protection, provide the theoretical basis for its prevention and treatment.