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Long-term potentiation (LTP) and depression (LTD) are activity-dependent changes in synaptic strength that model how the brain might store memories. The mechanisms of LTP and LTD have been studied extensively in the hippocampus because the hippocampus is critical for memory storage. The neocortex is also believed to be critical for the long-term storage of memories, but less work on LTP and LTD has been done in the neocortex. Furthermore, the majority of neocortical LTP and LTD studies have been carried out in artifical brain-slice preparations. The experiments presented in this thesis test some mechanisms of LTP and LTD in the neocortex of the awake, freely behaving rat. In the hippocampus and anesthetized neocortex, simultaneous stimulation of a 'strong' and a 'weak' input pathway can induce LTP in the weak pathway (even though stimulation of the weak pathway alone does not induce LTP). However, the results presented here show that in the neocortex of awake, freely behaving animals, simultaneous activation of strong and weak input pathways does not induce LTP in the weak pathway. In fact, under these conditions, an LTD is induced in the weak pathway. However, under these conditions, LTP induction was facilitated in the strong pathway. Associative LTD has also been shown in the hippocampus following anticorrelated activity delivered to two input pathways. The associative LTD in the hippocampus is larger than either homosynaptic or heterosynaptic LTD. The results presented here