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2014 ; 289
(44
): 30279-30288
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Sustained down-regulation of ?-dystroglycan and associated dysfunctions of
astrocytic endfeet in epileptic cerebral cortex
#MMPMID25228692
Gondo A
; Shinotsuka T
; Morita A
; Abe Y
; Yasui M
; Nuriya M
J Biol Chem
2014[Oct]; 289
(44
): 30279-30288
PMID25228692
show ga
Epilepsy is characterized by the abnormal activation of neurons in the cerebral
cortex, but the molecular and cellular mechanisms contributing to the development
of recurrent seizures are largely unknown. Recently, the critical involvement of
astrocytes in the pathophysiology of epilepsy has been proposed. However, the
nature of plastic modulations of astrocytic proteins in the epileptic cortex
remains poorly understood. In this study, we utilized the zero magnesium in vitro
model of epilepsy and examined the potential molecular changes of cortical
astrocytes, focusing specifically on endfeet, where specialized biochemical
compartments exist. We find that the continuous epileptic activation of neurons
for 1 h decreases the expression level of ?-dystroglycan (?DG) in acute cortical
brain slices prepared from mice. This change is completely abolished by the
pharmacological blockade of NMDA-type glutamate receptors as well as by matrix
metalloproteinase inhibitors. Consistent with the highly specialized localization
of ?DG at astrocytic endfeet, where it plays a pivotal role in anchoring
endfeet-enriched proteins in astrocytes, the down-regulation of ?DG is
accompanied by a decrease in the expression of AQP4 but not laminin. Importantly,
this down-regulation of ?DG persists for at least 1 h, even after the apparent
recovery of neuronal activation. Finally, we show that the down-regulation of ?DG
is associated with the dysfunction of the endfeet at the blood-brain interface as
a diffusion barrier. These results suggest that the sustained down-regulation of
?DG leads to dysfunctions of astrocytic endfeet in the epileptic cerebral cortex
and may contribute to the pathogenesis of epilepsy.
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