Alterations of AQP4 and Cx43 protein levels in subpial astrocytes (glia limitans superficialis) of the medial prefrontal cortex in reaction to experimental neuropathic pain
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| Year of publication | 2023 |
| Type | Appeared in Conference without Proceedings |
| MU Faculty or unit | |
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| Description | Subpial astrocytes (SAs) are a specific type of astrocytes covering the CNS surface, including the cortex, forming the glia limitans superficialis (GLS). These astrocytes send cytoplasmic processes into cortical layer I and form an interface between the cortical parenchyma and subpial cerebrospinal fluid (CSF). Therefore, the GLS is considered to be a superficial CSF-brain barrier. The dynamic of AQP4 and Cx43 protein levels in the SAs was investigated in coronal sections of the medial prefrontal cortex (mPFC) from rats and mice in response to sham operation and sciatic nerve compression (SNC) or spinal cord injury (SCI) after different periods of survival. Indirect immunofluorescence staining was performed with primary antibodies against glial fibrillary acidic protein (GFAP), aquaporin-4 (AQP4), and connexin-43 (Cx43). Immunofluorescence (IF) intensities in the SAs were measured by image analysis and compared between naive control and operated groups. Our results revealed progressive sending of cytoplasmic processes of the SAs into layer-I of mPFC after both sham operation and SNC or SCI. The SAs displayed distinct immunostaining for AQP4, the intensities of which were reduced in both sham- and SNC- or SCI-operated animals. Simultaneously, increased Cx43-IF intensities were found in both sham- and SNC- or SCI-operated rats and mice over all periods of survival. In summary, we detected the reactivity of the SAs in response to both sham operation and traumatic injury of a peripheral nerve or spinal cord used as neuropathic pain models. The decreased levels of AQP4 in the reactive SAs may indicate impaired bidirectional transport of water and solutes between the cortical parenchyma and subpial CSF through the GLS. In addition, the elevation of Cx43 protein reflects an increased amount of gap junction channels between SA bodies and their cytoplasmic processes, leading to enhanced communication between these astrocytes. These parallel processes are probably associated with changes in ion balance associated with mPFC activity, which plays an important role in the control of anxiety-depressive components of neuropathic pain. |
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