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Astrocyte reactivity in the glia limitans superficialis of the rat medial prefrontal cortex following sciatic nerve injury

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BRETOVÁ Karolína SVOBODOVÁ Viktorie DUBOVÝ Petr

Rok publikování 2023
Druh Článek v odborném periodiku
Časopis / Zdroj Histochemistry and Cell Biology
Fakulta / Pracoviště MU

Lékařská fakulta

Citace
www https://link.springer.com/10.1007/s00418-022-02161-6
Doi http://dx.doi.org/10.1007/s00418-022-02161-6
Klíčová slova Peripheral nerve lesion; Reactive astrocytes; Glial fibrillary acidic protein; Glutamine synthetase; NF kappa B; p65
Přiložené soubory
Popis The glia limitans superficialis (GLS) on the rodent cortical surface consists of astrocyte bodies intermingled with their cytoplasmic processes. Many studies have observed astrocyte reactivity in the medial prefrontal cortex (mPFC) parenchyma induced by a peripheral nerve injury, while the response of GLS astrocytes is still not fully understood. The aim of our study was to identify the reactivity of rat GLS astrocytes in response to sciatic nerve compression (SNC) over different time periods. The alteration of GLS astrocyte reactivity was monitored using immunofluorescence (IF) intensities of glial fibrillary acidic protein (GFAP), glutamine synthetase (GS), and NF?Bp65. Our results demonstrated that SNC induced GLS astrocyte reactivity seen as increased intensities of GFAP-IF, and longer extensions of cytoplasmic processes into lamina I. First significant increase of GFAP-IF was observed on post-operation day 7 (POD7) after SNC with further increases on POD14 and POD21. In contrast, dynamic alteration of the extension of cytoplasmic processes into lamina I was detected as early as POD1 and continued throughout the monitored survival periods of both sham and SNC operations. The reactivity of GLS astrocytes was not associated with their proliferation. In addition, GLS astrocytes also displayed a significant decrease in GS immunofluorescence (GS-IF) and NF?B immunofluorescence (NF?B-IF) in response to sham and SNC operation compared with naive control rats. These results suggest that damaged peripheral tissues (following sham operation as well as peripheral nerve lesions) may induce significant changes in GLS astrocyte reactivity. The signaling mechanism from injured peripheral tissue and nerve remains to be elucidated.
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