Long-term potentiation (LTP) was first discovered at the perforant path-dentate granule cell synapse. However, this form of synaptic plasticity has not been extensively studied in this pathway in the mouse. LTP is a striking form of synaptic plasticity that is believed to underlie the expression of learning and memory (Bliss and Lomo, 1973). Understanding the basic features and mechanisms underlying the induction and expression of these forms of synaptic plasticity in wild type mice will be essential in understanding any pathological changes in disorders such as Alzheimer’s disease. Following decapitation, acute transverse hippocampal slices were prepared from 21-29 day old male C57Bl/6j mice. Extracellular stimulation was applied to either the medial or lateral perforant pathway to evoke dendritic field potentials recorded from the dentate gyrus. Pairs of stimuli were applied 50 ms apart to confirm correct electrode placement, as the interaction between the two field excitatory postsynaptic potentials is different in the two pathways. Paired-pulse facilitation characterised the lateral perforant pathway, while paired-pulse depression was evident in the medial perforant path. Two different conditioning paradigms were then applied to induce LTP (referred to here for simplicity as tetanus (TET): single train of 40 pulses at 100 Hz; or high-frequency stimulation (HFS): 8 trains of 8 pulses each at 200 Hz, inter-train interval 1.5 s). In the lateral perforant pathway TET, but not HFS, induced significant potentiation at 51-60 minutes compared to baseline (114±4%, n=9 and 102±6%, n=6 mice, respectively). In contrast, in the medial perforant path, LTP was induced only using the HFS conditioning (111±5%, n=12 mice), while TET failed to induce significant potentiation (100±4%, n=10 mice). Paired-pulse ratio was monitored throughout the recordings to assess locus of expression of LTP. There was no correlation between the change in paired-pulse ratio following induction and the magnitude of LTP in the medial perforant pathway (r2=0.15, p>0.05), suggesting a postsynaptic locus of expression at these synapses. In the lateral perforant pathway, paired-pulse ratio changes correlated with the magnitude of LTP (r2=0.55, p<0.05), indicating a presynaptic component to the expression of LTP. Treatment with D-2-amino-5-phosphonopentanoate (D-AP5, 25 mM) blocked the induction of LTP (100±6%; n=5 mice) in the medial perforant path. While an NMDA-dependent mechanism of LTP induction was shown in the medial perforant path, our results suggest the presence of a significant presynaptic component in the expression of LTP in the lateral perforant pathway. We demonstrate here that the conditioning protocols contribute to different forms of LTP expressed in these pathways in the mouse and may represent different functions of the pathways.