The involvement of thalamic midline nuclei in early stage of Alzheimer’s disease and in diancephalic amnesia has recently drawn attention to the connectivity between the Reuniens nucleus (RE) and structures of limbic system. RE is a major source of thalamic afferents to the hippocampal CA1 area, which is supposed to be involved in learning and memory processes. So far, few studies have been done about the role of this nucleus on synaptic plasticity in the CA1 area. Therefore, a series of experiments have been designed to address this question. The field excitatory post synaptic potential (fEPSP) was recorded from CA1 following stimulation of Schaffer collateral pathway in urethane anesthetized rats. To induce long term potentation (LTP) theta pattern primed-bursts (PBs) and for short term plasticity, paired-pulse paradigm were used. RE inactivation was performed by intra RE injection of 0.5μl tetracaine 2% through an implanted guide cannula. Saline or tetracaine had no effect on the baseline slope of fEPSP. RE inactivation impaired LTP induction but had no effect on LTP maintenance. Also, inactivation of RE increased paired pulse inhibition in interpulse intervals of 10 and 20ms. It seems that RE normal activity has an excitatory role in long term and short term synaptic plasticity in CA1 region.