BDNF and its receptors are expressed in brain areas exhibiting high degree of neuronal plasticity such as the cerebral cortex and hippocampus. In this study we investigated BDNF effect on basal synaptic transmission and long–term synaptic plasticity in entorhinal cortex (EC). Extracellular field potential (FPs) were evoked and recorded in cortical layers II–III of EC slices and long-term potentiation (LTP) was elicited by high frequency stimulation (HFS). We verified the effects of nanomolar concentrations (40-1 ng/mL) of BDNF on synaptic transmission. We found that BDNF does not interfere with basal synaptic transmission and it does not affect LTP induction and maintenance in cortical layer II–III. Next step was to know whether BDNF exerts a neuroprotective role in Alzheimer's disease (AD). It is well known that EC is involved in learning and memory and its early impairment contributes to cardinal symptoms of AD. Notably, BDNF expression is reduced in EC of AD patients. At first, we showed that BDNF at different concentrations (10–50 ng/ml) prevents Ab neurotoxicity in mouse primary cortical cell culture. In addition oligomeric soluble Ab(1-42) was able to inhibit LTP in EC slices. On-going experiments are clarifying whether BDNF is capable of preventing synaptic dysfunction caused by oligomeric soluble Ab(1-42). We are interested on this issue as BDNF represents a key molecule that regulates synaptic plasticity and related cognitive functions.