interested in the factors that might underlie this difference. In both the Canning and Leung and Liu and Bilkey studies, it was shown that single-pulse stimulation of the perirhinal cortex (PRC) evoked field potentials in the hippocampus in urethane-anaesthetised rats. Similarly, in both studies, when the PRC and the lateral perforant path (LPP) were stimulated separately, the depth/amplitude profiles obtained from a roving recording electrode located within the hippocampus resembled each other. When a current source density (CSD) analysis was conducted, the sink/source patterns were generally similar across studies, with a current sink detected in the outer molecular layer of the dentate gyrus [note: a current sink in the stratum lacunosum-moleculare of CA1 was observed in Liu and Bilkey (1997), but not in Canning and Leung (1997)]. These data can be interpreted either as evidence of a PRC-hippocampal projection, or as evidence that PRC stimulation activates fibers projecting to the hippocampus but originating from neighbouring regions (e.g., entorhinal cortex). Our findings that electrolytic lesions of the perirhinal cortex produced a significant decrease in the amplitude of LPP-hippocampal potentials, and that both electrolytic and ibotenic acid lesions of the perirhinal cortex resulted in a major decrease in the amplitude of LPP-elicited potentials and a corresponding reduction across the whole sink/source CSD pattern, indicated to us that neurons located within the perirhinal cortex project directly to the CA1 and DG of the dorsal hippocampus via the LPP. By comparison, Canning and Leung (1997) found that a stimulating electrode located in the ibotenic acid lesioned perirhinal cortex evoked responses that were not significantly different from those in normal rats, suggesting to these authors that the ''PRC'' potential was actually generated by activation of fibers located outside this region.
We see two possible explanations for this difference. First, the hippocampal recording electrode in the Canning and Leung (1997) study was located in a more posterior position (AP ฯช4.52 to ฯช5.2 mm) than ours (AP ฯช3.8 mm). Since there is evidence that the connections between the entorhinal/ perirhinal cortices and hippocampus are topographically organized along the longitudinal axis of the hippocampal formation (e.g., Ruth et al.,