Kindling and long-term potentiation (LTP) are two common paradigms of synaptic plasticity. Initially proposed as a model of learning of memory, kindling is considered as a model of epilepsy, with LTP filling in its role as a model of learning and memory. This review suggests that LTP is not critical for kindling-induced epileptiform activity such as spontaneous interictal spikes. Repeated theta-frequency primed burst stimulations (PBs) and repeated ADs (kindling) of the hippocampal commissures were compared in their ability to induce potentiation and to disrupt spatial behavior. Repeated PBs and kindling both induced large potentiation of the CA1 basal dendritic synapse, but only hippocampal kindling disrupted the retention of spatial task on the radial arm maze. While there was evidence that transynaptic potentiation was more persistent after hippocampal kindling than repeated PBs, disruption of inhibition rather than enhancement of excitation may more readily explain the disruption of spatial behavior by kindling. In conclusion, there is little evidence that LTP is essential for the epileptiform activity or the disruption of spatial behavior after hippocampal kindling.