The entorhinal cortex is a major structure linking neocortical areas with the hippocampal formation, and is thought to contribute to the integration and encoding of sensory information. The superficial layers of the entorhinal cortex receive a large projection from the piriform (primary olfactory) cortex, and synaptic plasticity within this input pathway may affect olfactory information processing. In addition, the mesocortical dopamine system provides a substantial input to layer II of the lateral entorhinal cortex and dopamine may therefore play an important role in modulating sensory processing in the entorhinal cortex. Recently, we have shown that systemic administration of the dopamine reuptake inhibitor GBR12909, which elevates extracellular dopamine levels in the lateral entorhinal cortex, also inhibits the induction of both long-term potentiation (LTP) and long-term depression (LTD) in the entorhinal cortex of the awake rat. In the present study, we have used field potential recordings from slices of entorhinal cortex maintained in vitro to assess the effects of dopamine on the induction of LTP in synaptic inputs to layer II. Acute brain slices (400 μm thick) were obtained using a vibratome and were maintained in a gas-fluid interface recording chamber at a temperature of 32 ºC. Stimulation pulses (0.1 ms duration) were delivered to layer I using a concentric bipolar electrode, and field excitatory postsynaptic potentials were obtained in layer I close to the cells of layer II using glass pipettes filled with ACSF (in mM, 124 NaCl, 5 KCl, 1.25 NaH2PO4, 2 MgSO4, 2 CaCl2, 26 NaHCO3, 10 dextrose, ascorbic acid; 2-4 MΩ). Following a 10 min baseline period, dopamine (10 μM) was bath-applied for a period of 15 min prior to induction of LTP using three 1-sec duration trains of pulses delivered at 100 Hz. Control cells received tetanisation in the absence of dopamine, or dopamine alone. As demonstrated previously, results of initial experiments show that application of 10 μM dopamine causes a reversible enhancement of the amplitude of fEPSPs. However, dopamine did not cause a significant change in the amount of LTP observed, and both control slices exposed to normal ACSF, and slices that underwent 15 min pre-exposure to dopamine, showed similar levels of LTP 60 min post-tetanization. The present findings therefore suggest that 10 uM dopamine does not result in a marked modulation of the induction of LTP as tested here using strong tetanizing stimuli in vitro.