Nature Publishing Group, publisher of Nature, and other science journals and reference works
Nature
my account e-alerts subscribe register
SEARCH JOURNAL     advanced search
Journal Home
Current Issue
AOP
Archive
Download PDF
References
Export citation
Export references
Send to a friend
More articles like this

Letters to Nature
Nature 366, 464 - 466 (02 December 1993); doi:10.1038/366464a0

Modulation of the cell cycle contributes to the parcellation of the primate visual cortex

Colette Dehay, Pascale Giroud, Michel Berland*, Iain Smart & Henry Kennedy

INSERM U371, Cerveau et Vision, 18 Avenue Doyen Lépine, 69500 Bron, France
*Faculté de Medécine Lyon-Nord, Hopital Claude Bernard, Service de Gynécologic et Obstétrique, Oullins 69600, France
Department of Anatomy and Physiology, University of Dundee, Dundee DD1 4HN, UK
To whom correspondence should be addressed.

AN as-yet unresolved issue in developmental neurobiology is whether the discrete areas that form the mammalian cortex emerge from a uniform cortical plate or whether they are already specified in the germinal zone1,2. A feature of the primate striate cortex is that the number of neurons per unit area is twice that of anywhere else in the cerebral cortex3. Here we take advantage of this unique structural feature to investigate whether the extra striate cortical cells are due to increased neuron production during neurogenesis. We labelled precursors undergoing terminal cell division with 3H-thymidine and allowed them to migrate to the cortical plate. Cell counts revealed that their rate of production in the germinal zone of striate cortex is higher than in that giving rise to extrastriate cortex. Also, we used 3H-thymidine pulse injections to investigate cell cycle dynamics and found that this phase of increased production of striate cortical cells is associated with changes in the parameters of the cell cycle. These results show that cortical area identity is at least partially determined at the level of the ventricular zone.

------------------

References
1. O'Leary, D. D. M. Trends Neurosci. 12, 400−406 (1989).
2. Rakic, P. Science 241, 170−176 (1988).
3. Rockel, A. J., Hiorns, R. W. & Powell, T. P. S. Brain 103, 221−244 (1980).
4. Bisconte, J. C. & Marty, R. Expl Brain Res. 22, 37−56 (1975).
5. Angevine, J. B. & Sidman, R. L. Nature 192, 766−768 (1961).
6. Rakic, P. Expl Brain Res. Suppl. 1 439−450 (1976).
7. Rakic, P. Science 183, 425−427 (1974).
8. Waechter, R. V. & Jaensch, B. Brain Res. 46, 235−250 (1972).
9. Schultze, B. & Korr, H. Cell Tissue Kinet. 14, 309−325 (1981).
10. Takahashi, T., Nowakowski, R. S. & Caviness, V. S. J. Neurosci. 13, 820−833 (1993).
11. Korr, H. Adv. Anat. Embryol. Cell Biol. 61, 1−70 (1980).
12. Laskey, R. A., Fairman, M. P. & Blow, J. J. Science 246, 609−613 (1989).
13. Pardee, A. B. Science 246, 603−608 (1989).
14. Mac Auley, A., Werb, Z. & Mirkes, P. E. Development 117, 873−883 (1993).
15. Finlay, B. L. & Slattery, M. Science 219, 1349−1351 (1983).
16. Williams, R. W., Ryder, K. & Rakic, P. Soc. Neurosci. Abstr. 13, 1044 (1987).
17. O'Leary, D. D. M. & Stanfield, B. B. J. Neurosci. 9, 2230−2246 (1989).
18. Schlaggar, B. L. & O'Leary D. D. M. Science 252, 1556−1560 (1991).
19. Barbe, M. F. & Levitt, P. J. Neurosci. 11, 519−533 (1991).
20. Ferri, R. T. & Levitt, P. Cereb. Cortex 3, 187−198 (1993).
21. Arimatsu, Y. et al. Proc. natn. Acad. Sci. U.S.A. 89, 8879−8883 (1992).
22. Cohen-Tannoudji, M. thesis, Paris Univ. (1992).
23. Johnston, J. G. & Van Der Kooy, D. Proc. natn. Acad. Sci. U.S.A. 86, 1066−1070 (1989).
24. Dehay, C., Horsburgh, G., Berland, M., Killackey, H. & Kennedy, H. Nature 337, 265−267 (1989).
25. Kennedy, H. & Dehay, C. Cereb. Cort. 3, 171−186 (1993).
26. Kostovic, I. & Rakic, P. J. Neurosci. 4, 25−42 (1984).



© 1993 Nature Publishing Group
Privacy Policy