Differential expression of Zif268 and c-Fos in the primary visual cortex and lateral geniculate nucleus of normal Cebus monkeys and after monocular lesions
The transcription factors c‐Fos and Zif268 have been used as markers of neuronal activity, and they also have been implicated in neuronal plasticity. In this study, we investigated the expression of c‐Fos and Zif268 proteins in the lateral geniculate nucleus (LGN) and in the cortical primary visual...
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Veröffentlicht in: | Journal of comparative neurology (1911) 2005-02, Vol.482 (2), p.166-175 |
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Zusammenfassung: | The transcription factors c‐Fos and Zif268 have been used as markers of neuronal activity, and they also have been implicated in neuronal plasticity. In this study, we investigated the expression of c‐Fos and Zif268 proteins in the lateral geniculate nucleus (LGN) and in the cortical primary visual area (V1) of normal adult Cebus apella monkeys and in animals with monocular lesions. In the LGN, the reaction for c‐Fos showed immunopositive cells in both magnocellular (M) and parvocellular (P) layers; however, the label was heavier in P layers. In animals that suffered monocular lesions, the immunocytochemistry for c‐Fos showed more labeling in layers related to the normal eye compared with those of the lesioned eye. No specific label was observed after the reaction for Zif268 in the LGN. In V1, the reaction for both Zif268 and c‐Fos showed a pattern of lamination in which heavier labeling was found in layers 2/3, 4A, 4C, and 6. After monocular lesions, we observed a clear pattern of ocular dominance columns in V1 for both c‐Fos and Zif268, in which the columns related to the normal eye are more heavily labeled than those related to the lesioned eye. This pattern is more evident in layer 4C after c‐Fos reaction, whereas, after Zif268, it is more clearly observed in layers 2/3. These results suggest that, in addition to be regulated by functional activity, these transcription factors are involved in different processes during cortical reorganization. J. Comp. Neurol. 482:166–175, 2005. © 2004 Wiley‐Liss, Inc. |
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ISSN: | 0021-9967 1096-9861 |
DOI: | 10.1002/cne.20361 |