Thalamo-cortical afferents control transient expression of the dopamine D-3 receptor in the rat somatosensory cortex

Citation
Ev. Gurevich et al., Thalamo-cortical afferents control transient expression of the dopamine D-3 receptor in the rat somatosensory cortex, CEREB CORT, 11(8), 2001, pp. 691-701
Citations number
41
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Neurosciences & Behavoir
Journal title
CEREBRAL CORTEX
ISSN journal
1047-3211 → ACNP
Volume
11
Issue
8
Year of publication
2001
Pages
691 - 701
Database
ISI
SICI code
1047-3211(200108)11:8<691:TACTEO>2.0.ZU;2-1
Abstract
The D-3 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 ingrowt h of thalamocortical afferents (TCAs) into the barrel cortex and could be i nduced or controlled by them. We show that unilateral electrolytic lesion o f the thalamic ventrobasal complex immediately after birth leads to a decre ase in the D3R mRNA concentration in the lesioned SI 7 days after the lesio n, whereas the D3R binding is little affected, Fourteen days after the neon atal thalamic lesion, the D3R binding and mRNA are drastically reduced and the barrel-like pattern of the D3R 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 D3R expression. One day af ter 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-li ke pattern of D3R expression is evident in the lesioned S1, although TCAs a re completely absent. Quantitative analysis demonstrated elevated cellular levels of the D-3 mRNA in barrel neurons 5 days after the lesion. These hig her levels are needed, perhaps, to support the increased production of the D3R protein appropriate for this age, Age-related dynamics of the D3R bindi ng is retained in the lesioned S1, although the concentration of D3R sites remains reduced. These data demonstrate that intact thalamic input is essen tial for the formation of mechanisms responsible for developmental regulati on of the D3R expression in the SI.