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Cerebral Cortex, Vol. 11, No. 8, 691-701, August 2001
© 2001 Oxford University Press

Thalamo-cortical Afferents Control Transient Expression of the Dopamine D3 Receptor in the Rat Somatosensory Cortex

Eugenia V. Gurevich, Richard T. Robertson1, and Jeffrey N. Joyce

Christopher Center for Parkinson's Disease Research, Sun Health Research Institute, Sun City, AZ 85351 and , 1 Department of Anatomy and Neurobiology, College of Medicine, University of California, Irvine, CA 92697-1289, USA

The D3 dopamine receptor (D3R) is selectively and transiently expressed in the barrel neurons of the somatosensory cortex (SI) between the first and second postnatal weeks. The D3R expression starts after the initial ingrowth of thalamocortical afferents (TCAs) into the barrel cortex and could be induced or controlled by them. We show that unilateral electrolytic lesion of the thalamic ventrobasal complex immediately after birth leads to a decrease in the D3R mRNA concentration in the lesioned SI 7 days after the lesion, whereas the D3R binding is little affected. Fourteen days after the neonatal thalamic lesion, the D3R binding and mRNA are drastically reduced and the barrel-like pattern of the D3R is absent. Elevation of the D3 binding normally seen between the first and second postnatal weeks does not occur. Thalamic lesion on P6 differentially affects the D3R expression. One day after the lesion, the D3 binding and mRNA are down-regulated, but the effect is transient. Five days after the lesion the concentration of D3 mRNA in the lesioned hemisphere returns to the control level. The typical barrel-like pattern of D3R expression is evident in the lesioned SI, although TCAs are completely absent. Quantitative analysis demonstrated elevated cellular levels of the D3 mRNA in barrel neurons 5 days after the lesion. These higher levels are needed, perhaps, to support the increased production of the D3R protein appropriate for this age. Age-related dynamics of the D3R binding is retained in the lesioned SI, although the concentration of D3R sites remains reduced. These data demonstrate that intact thalamic input is essential for the formation of mechanisms responsible for developmental regulation of the D3R expression in the SI.


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