MMP-2, VCAM-1 and NCAM-1 expression in the brain of rats with experimental autoimmune encephalomyelitis as a trigger mechanism for synaptic plasticity and pathology.

The neural cell adhesion molecules (NCAMs), and vascular cell adhesion molecules (VCAMs) that regulate cell-to-extracellular matrix adhesion, and matrix metalloproteinases (MMPs), modulating the extracellular matrix (ECM), are considered to play an important role in the pathogenesis of experimental autoimmune encephalomyelitis (EAE). Clinical signs appearance and significant increases of MMP-2 expression in CA1 and CA3 subdomains of the hippocampus and around the central canal of the cervical spinal cord, with the clusters of VCAM-1(+) immunoreactive cells localized in the choroid plexus epithelium and hypothalamo-hypophyses portal vessel system indicate an inflammation in acute EAE. Decreased NCAM-1 expression in CA1 and CA3 fields of the hippocampus, and in a lesser degree in the basal ganglia, limbic structure and cervical spinal cord, support the concept that the demyelinating neuroinflammatory damage in an autoimmune brain affect synaptic organization of the brain, altering the balance between extracellular proteases and cell adhesion molecules which appears to be critical for both the brain plasticity and autoimmune processes.