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Role of c - Jun - N - terminal kinase in beta amyloid mediated impairment of long - term potentiation


, : Role of c - Jun - N - terminal kinase in beta amyloid mediated impairment of long - term potentiation. Society for Neuroscience Abstract Viewer & Itinerary Planner : Abstract No 690 8

Beta-amyloid (Abeta) is a 40-42 amino acid peptide, which forms neuritic plaques in brains of Alzheimer's disease (AD) patients. Abeta causes neuronal loss, with sequence 25-35 deemed to be the most neurotoxic fragment. Abeta expression is associated with enhanced c-Jun N-terminal kinase (JNK) activation, which mediates cell death. We have reported previously that soluble Abeta impairs hippocampal long-term potentiation (LTP). Here we investigated effect of an inhibitor of JNK phosphorylation on synaptic transmission and the Abeta(25-35)-mediated impairment of LTP. Experiments were performed on hippocampal slices from male Wistar rats. Field excitatory postsynaptic potentials were recorded in the CA1 and LTP was induced by trains of high frequency stimuli (HFS, 200Hz). In controls, HFS produced a post-tetanic potentiation (PTP) of 186+-7% (mean %EPSP slope +- SEM, n=9), measured 5min post-HFS and 169+-7% LTP (n=9), 60min post-HFS. Abeta(25-35) at 200nM, for 60min prior to HFS had no effect on baseline, however PTP and LTP were attenuated significantly (154+-8%, n=6, p<0.05 and 137+-6%, n=6, p<0.05). The JNK inhibitor, SP600125 (SP; 20muM), significantly enhanced synaptic transmission 30min following application (120+-4%, n=12, p<0.05), which persisted at 90min (113+-5%, n=8, p<0.05), and reduced paired-pulse facilitation (inter-pulse interval 50ms) significantly (1.26+-0.06, n=6, p<0.05) compared to controls (1.42+-0.03, n=6). SP treatment for 30min prior to HFS did not alter LTP significantly (166+-7%, n=6) when measured from pre-drug baseline, and when applied for 30min following control LTP, had no significant effect (161+-6%, n=6). SP added for 30min prior to Abeta significantly reversed the PTP and LTP attenuation observed in Abeta treated slices (226+-11% and 174+-14%, n=6, p<0.05, respectively). This suggests that JNK activation mediates the Abeta-induced impairment of LTP and may also play a role in neurotransmitter release and LTP.

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