Abstract
Alzheimer’s disease (AD) is associated with cognitive deficits of varying degrees and with impairment of the synaptic transmission-related tasks. Pathologically, AD is highlighted with accumulation of extracellular β-amyloid plaques and of neurofibrillary tangles. Glutamate-mediated neurotoxicity plays a pivotal role in the pathogenesis of AD. Deficits of long-term potentiation (LTP) and neuronal synaptic plasticity as an essential mechanism of the learning and memory disorders in AD has been ascribed to over-activation of glutamate receptors. We examined the effect of riluzole, a glutamate release inhibitor, on LTP impairment in the dentate gyrus (DG) in a rat model of AD provided by bilateral intrahippocampal amyloid β (Aβ 25-35) injections; riluzole was administered at a dose of 10 mg/kg. The LTP in perforant path-DG synapses was evaluated using measurements of the field excitatory postsynaptic potential (fEPSP) slope and population spike (PS) amplitude. We found that Aβ (25–34) significantly decreased the fEPSP slope and PS amplitude, as compared to those in the sham group; riluzole pretreatment in the Aβ-microinjected group significantly increased these parameters. Taken together, it is concluded that riluzole could noticeably improve synaptic plasticity and enhan ce LTP in the rat model of AD.
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