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D1 dopamine receptors distribution following photothrombotic stroke in rat cerebral cortex

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Rogozinska K., Skangiel-Kramska J.
Acta Neurobiologiae Experimentalis
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2005
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vol. 65
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issue 2
167-172
EN
The effect of focal photothrombotic stroke on the distribution of D1 dopamine receptor (D1R) sites was examined in different cortical areas of rat brain with quantitative receptor autoradiography using [3H]SCH23390 as a ligand. Unilateral cortical stroke was located in the primary somatosensory cortex. After different survival times (1, 7 and 28 days) D1R binding levels were determined in the lesion core, penumbra, frontoparietal motor (FrPaM) and somatosensory (FrPaSS) areas as well as in homotopic regions in the contralateral hemisphere. One day after stroke, D1R density decreased by 36% (P<0.01) in the lesion core relative to sham-operated controls. At 7th day binding density was further reduced by 56% (P<0.002). Twenty-eight days after infarction, D1R binding returned to control level. No alterations in D1R binding levels were found in penumbra and other investigated regions. We suggest that the return of D1R binding to control level in the area initially corresponding to the infarct results from the shrinkage of the lesion volume.
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Spatiotemporal dynamics of astroglial and microglial responses after photothrombotic stroke in the rat brain

71%
Nowicka D., Rogozinska K., Aleksy M., Witte O. W., Skangiel-Kramska J.
Acta Neurobiologiae Experimentalis
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2008
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vol. 68
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issue 2
155-168
EN
The effects of photothrombotic stroke in primary somatosensory cortex on astroglial and microglial activation in various regions of lesioned brain were examined at different time points, using immunohistochemistry and lectin binding. The increase in GFAP expression was observed exclusively in the ipsilateral hemisphere, both in the perilesional area and cortical regions distant from the infarct. This remote increase was detectable up to sixty days after the infarct. Transient GFAP elevation was also found in the hippocampus one day after photothrombosis, whereas it was more prolonged in amygdala, as demonstrated at four days after lesion. In contrast to a widespread astrocytic activation, the microglial response was shortlasting and local, confined to lesion and perilesional area. Widespread and prolonged activation of astrocytes after stroke may provide factors promoting slowly developing recovery processes in the whole brain, while microglial response seems to be involved in local repair and removal of cellular debris.
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