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The D 3  dopamine receptor (D 3 R) is selectively and transiently expressed in the barrel neurons of the somatosensory cortex (SI) between the first and second postnatal weeks. The D 3 R 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 D 3 R mRNA concentration in the lesioned SI 7 days after the lesion, whereas the D 3 R binding is little affected. Fourteen days after the neonatal thalamic lesion, the D 3 R binding and mRNA are drastically reduced and the barrel-like pattern of the D 3 R is absent. Elevation of the D 3  binding normally seen between the first and second postnatal weeks does not occur. Thalamic lesion on P6 differentially affects the D 3 R expression. One day after the lesion, the D 3  binding and mRNA are down-regulated, but the effect is transient. Five days after the lesion the concentration of D 3  mRNA in the lesioned hemisphere returns to the control level. The typical barrel-like pattern of D 3 R expression is evident in the lesioned SI, although TCAs are completely absent. Quantitative analysis demonstrated elevated cellular levels of the D 3  mRNA in barrel neurons 5 days after the lesion. These higher levels are needed, perhaps, to support the increased production of the D 3 R protein appropriate for this age. Age-related dynamics of the D 3 R binding is retained in the lesioned SI, although the concentration of D 3 R sites remains reduced. These data demonstrate that intact thalamic input is essential for the formation of mechanisms responsible for developmental regulation of the D 3 R expression in the SI.

Thalamo-cortical Afferents Control Transient Expression of the Dopamine D 3 Receptor in the Rat Somatosensory Cortex