Architectonic analysis of the human retrosplenial cortex

The architecture of the macaque retrosplenial cortex, including its posteroventral extension around and below the splenium of the corpus callosum, was recently characterized (Morris et al. [1999a] Eur. J. Neurosci. 11:2506–2518.). This analysis was made possible by sectioning the posterior cingulate...

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Veröffentlicht in:Journal of comparative neurology (1911) 2000-05, Vol.421 (1), p.14-28
Hauptverfasser: Morris, Renée, Paxinos, George, Petrides, Michael
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Sprache:eng
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Zusammenfassung:The architecture of the macaque retrosplenial cortex, including its posteroventral extension around and below the splenium of the corpus callosum, was recently characterized (Morris et al. [1999a] Eur. J. Neurosci. 11:2506–2518.). This analysis was made possible by sectioning the posterior cingulate gyrus radially, i.e., in planes that were orthogonal to its line of curvature and that, therefore, preserved the laminar organization of this region. The aim of the present study was to examine the architecture and the limits of the human retrosplenial cortex. Cross sections through the entire posterior cingulate gyrus were obtained by applying the sectioning technique developed in the monkey, so that an explicit comparison could be made between the architecture of the human and the monkey retrosplenial cortex. The present analysis revealed that, as is the case in the macaque brain, the human retrosplenial cortex is composed of granular areas 29a–c and d, and dysgranular/agranular area 30. The human retrosplenial cortex, like that of the macaque monkey, runs, as an arch, around the splenium of the corpus callosum. In the macaque brain, the retrosplenial cortex remains buried within the callosal sulcus throughout its entire course around the splenium. In the human brain, however, the posteroventral segment of the retrosplenial cortex extends on the medial wall of the cerebral hemisphere to encompass most of the cortical region commonly referred to as the “isthmus of the cingulate gyrus.” J. Comp. Neurol. 421:14–28, 2000. © 2000 Wiley‐Liss, Inc.
ISSN:0021-9967
1096-9861
DOI:10.1002/(SICI)1096-9861(20000522)421:1<14::AID-CNE2>3.0.CO;2-S