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Current source density analysis does not reveal a direct projection from the perirhinal cortex to septal part of hippocampal CA1 or dentate gyrus

✍ Scribed by Kevin J. Canning; L. Stan Leung


Publisher
John Wiley and Sons
Year
1999
Tongue
English
Weight
335 KB
Volume
9
Category
Article
ISSN
1050-9631

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✦ Synopsis


In a recent letter to the editor, Liu and Bilkey (1998) discussed the differences between their results (Liu and Bilkey, 1997) and ours (Canning and Leung, 1997). In both studies, the perirhinal cortex (PRh) was stimulated at a similar location and the evoked field potentials in the hippocampus were studied using current source density (CSD) analysis. We concluded that PRh ''does not have a major direct projection to the dentate gyrus or CA1. '' In contrast, Liu and Bilkey (1997) claimed that that their CSD results supported their earlier conclusion based on field potentials only (Liu and Bilkey, 1996) that ''the perirhinal cortex projects to both the dentate gyrus and CA1 regions of the hippocampus.'' While we agree with Liu and Bilkey that the projection of the PRh to CA1 may be restricted in its septotemporal extent, we disagree with them that PRh projects to the septal part of CA1 at P3.8. Liu and Bilkey suggested that their recording location (P3.8), which was more anterior or septally located than ours (P4.5 to P 5.6), may account for their finding of a dendritic sink in CA1. Although not stated in our 1997 report, we had also mapped the hippocampus, now totalling 18 rats, at a location of P3.6 to P4.3 following PRh stimulation. In all these tracks, we found no evidence of a dendritic sink in CA1 following PRh stimulation. However, when we mapped at the CA1/subiculum border at P5.6 to P6, we (Canning and Leung, 1996) and others (Naber et al., 1997, in press) have found a distal dendritic sink following PRh stimulation. The PRh-activated distal dendritic sink at the CA1/subiculum border was accompanied by proximal sources in CA1/subiculum but no sink or source in the dentate gyrus. This distal dendritic sink is probably mainly generated by subicular neurons, although the contribution of CA1 neurons near the subiculum cannot be excluded. The PRh activation of the subiculum/CA1 at a midseptotemporal level is consistent with anterograde tracer studies using tritiated amino acids and Phaseolus vulgaris leucoagglutinin. Kosel et al. (1983) andMcIntyre et al. (1996) showed unambiguously that the PRh projects substantially to the subiculum, much less to the apical dendrites of CA1, and not at all to the dentate gyrus (see, e.g., fig. 4 of McInytre et al., 1996). The PRh does not project to CA1 at P3.8 where the subiculum is not present.

There are differences in the CSD techniques and results between the two studies. First, Liu and Bilkey (1997) used a Teflon-coated 75-m diameter wire for mapping potentials. In our opinion, this recording