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J Neurophysiol 82: 1303-1310, 1999;
0022-3077/99 $5.00
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The Journal of Neurophysiology Vol. 82 No. 3 September 1999, pp. 1303-1310
Copyright ©1999 by the American Physiological Society

Loss of IA Expression and Increased Excitability in Postnatal Rat Cajal-Retzius Cells

Jean-Marc Mienville,1 Irina Maric,2 Dragan Maric,2 and John R. Clay2

 1The Psychiatric Institute, Department of Psychiatry, The University of Illinois at Chicago, Chicago, Illinois 60612; and  2Laboratory of Neurophysiology, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland 20892

Mienville, Jean-Marc, Irina Maric, Dragan Maric, and John R. Clay. Loss of IA Expression and Increased Excitability in Postnatal Rat Cajal-Retzius Cells. J. Neurophysiol. 82: 1303-1310, 1999. Although an important secretory function of Cajal-Retzius (CR) cells has been discovered recently, the precise electrical status of these cells among other layer I neurons in particular and in cortical function in general is still unclear. In this paper, early postnatal CR cells from rat neocortex were found to express an inactivating K current whose molecular substrate is likely to be the Kv1.4 channel. Both electrophysiological and immunocytochemical experiments revealed that expression of this A-type current is down-regulated in vivo and virtually disappears by the end of the second postnatal week. At this time, CR cells have become capable of evoked repetitive firing, and their action potentials are larger and faster, yet these electrical properties still appear incompatible with a role in cortical network function, as inferred from comparisons with other cortical neurons. Also at this time, a large proportion of CR cells display spontaneous spiking activity, which suggests the possibility of additional roles for these cells. We conclude that the loss of A channels along with an increase in Na channel density shape the changes in excitability of postnatal CR cells, in terms of both the patterns of evoked firing and the emergence of spontaneous spiking.




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