Structural and chemical changes in glial cells in the rat neocortex induced by constant occlusion of the middle cerebral artery

Калиниченко, С. Г.; Korobtsov, A. V.; Matveeva, N. Yu.; Pushchin, Igor

doi:10.1016/j.acthis.2020.151573

Cited by 6 publications

(1 citation statement)

References 32 publications

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“…BBB leakage can result in disturbance of ionic homeostasis and thus can lead to neuronal dysregulation. Vascular pathology can lead to increased S100β expression ( 69 ). Furthermore, stress can also lead to increased S100β expression ( 70 ).…”

Section: Discussionmentioning

confidence: 99%

In utero exposure to maternal anti–aquaporin-4 antibodies alters brain vasculature and neural dynamics in male mouse offspring

Mader

Brimberg

et al. 2022

Sci. Transl. Med.

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The fetal brain is constantly exposed to maternal IgG before the formation of an effective blood-brain barrier (BBB). Here, we studied the consequences of fetal brain exposure to an antibody to the astrocytic protein aquaporin-4 (AQP4-IgG) in mice. AQP4-IgG was cloned from a patient with neuromyelitis optica spectrum disorder (NMOSD), an autoimmune disease that can affect women of childbearing age. We found that embryonic radial glia cells in neocortex express AQP4. These cells are critical for blood vessel and BBB formation through modulation of the WNT signaling pathway. Male fetuses exposed to AQP4-IgG had abnormal cortical vasculature and lower expression of WNT signaling molecules Wnt 5a and Wnt 7a. Positron emission tomography of adult male mice exposed in utero to AQP4-IgG revealed increased blood flow and BBB leakiness in the entorhinal cortex. Adult male mice exposed in utero to AQP4-IgG had abnormal cortical vessels, fewer dendritic spines in pyramidal and stellate neurons, and more S100β + astrocytes in the entorhinal cortex. Behaviorally, they showed impairments in the object-place memory task. Neural recordings indicated that their grid cell system, within the medial entorhinal cortex, did not map the local environment appropriately. Collectively, these data implicate in utero binding of AQP4-IgG to radial glia cells as a mechanism for alterations of the developing male brain and adds NMOSD to the conditions in which maternal IgG may cause persistent brain dysfunction in offspring.

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Section: Discussionmentioning

confidence: 99%