RESEARCH Chronic brain inflammatio

voltage-dependent calcium channel dependent-LTP and Gwangjin-gu, Seoul 143-701, Republic of Korea Full list of author information is available at the end of the articleBackground Neuroinflammation plays a key role in the initiation and progression of neurodegeneration in Alzheimer’s disease (AD) [1-5]. In vivo measurement of activated microglia using brain imaging suggests that inflammation is an early event in the pathogenesis of the disease [6,7]. A series of animal experiments with chronic lipopolysaccharide (LPS) infusion into the brain has demonstrated that inflammation leads to cognitive deficits, which are the most common symptom of AD [8,9]. It has also been demonstrated that brain inflammation leads to a decrease in the number of GluN1 N-methyl-D-aspartate receptors (NMDARs) within the dentate gyrus (DG) and cornu ammonis 3 (CA3) hippocampal areas, without any loss of neurons [10]. On the basis of the asso-ciation of GluN1 and synaptic plasticity [11], electro-physiological studies were performed to examine the effects of chronic LPS infusion on long-term potentiation (LTP) and long-term depression (LTD) in the hippocam-pus [12-14]. LPS infusion has been shown to impair LT