Topic: cuprizone

Synchronization of neural activity is a fundamental component of information processing in the nervous system. Precise axonal conduction is required for correlated spiking activity between pairs of neurons at the millisecond timescale. Previous studies report that myelin loss results in deficient action potential propagation and a loss of population synchronization in the gamma band. Loss of myelination in demyelinating diseases like multiple sclerosis (MS) results in impaired motor function in patients with MS. However, a deeper understanding of how demyelination alters the timing, synchrony

Adenosine A1 receptor (A1AR) signaling exerts important functions in the central nervous system (CNS). Among all CNS cell types, oligodendrocyte (OL) lineage cells possess the highest A1AR expression levels. However, in vivo data regarding the functions of A1ARs in OL lineage cells remain elusive. Here, we first generated NG2-CreERT2xA1ARfl/fl conditional knockout (cKO) mice to specifically delete A1ARs from oligodendrocyte precursor cells (OPCs) upon tamoxifen administration. Immunohistochemical analysis for OL lineage markers PDGFRα, APC CC1, as well as BrdU incorporation detected unaltered

Multiple sclerosis (MS) is an autoimmune and neurodegenerative disorder of the central nervous system (CNS), a heterogeneous disease that courses with both demyelination and inflammation. We used two different animal models to recapitulate different aspects of this disease, experimental autoimmune encephalomyelitis (EAE) and cuprizone (CPZ) induced demyelination. To study the differential response of the CNS, we compared the proteomic profile of EAE mice (at peak disease) and CPZ mice (in the acute phase) in two different CNS regions: somatosensorial cortex (Cx) and spinal cord (SC). Our resul