H. M. arose most probably from damage to the hippocampus and cortical structures immediately surrounding the medial temporal lobe [14]. Follow up studies by Anderson and Lomo reported that a single, short test shock, following an initial period of conditioning test shocks to the perforant path in the hippocampus, elicited a potentiated response in the dentate gyrus region of the hippocampus [15]. Furthermore, Lynch et al reported that a tetanic stimulation of one pathway in the CA1 region of the hippocampus depresses the effectiveness of the other synapses in the hippocampus [16]. They called this phenomenon a heterosynaptic long-term depression (LTD) which can be observed in the dentate gyrus and in the CA1 region of the hippocampus in vitro. In support of this phenomena, Dudek and Bear reported that several hundred stimuli delivered at low frequency (1–3 Hz) produced a sustained depression of a modest, but significant amplitude. This phenomenon is known as homosynaptic LTD, and is much harder to demonstrate in vivo compared with heterosynaptic LTD [17].
