<P> The development of the long astrocyte cellular processes that are integral to the glia limitans structure has been linked to the presence of meningeal cells in the pia mater . Meningeal cells are specialized fibroblast - like cells that surround the CNS and major blood vessels . They have been found to co-operate with astrocytes in the initial formation of the glia limitans during development and participate in its continued maintenance throughout life . Artificially induced destruction of meningeal cells during CNS development have been found to result in the alteration of subpial extracellular matrix and a disruption of the glia limitans . </P> <P> The glia limitans has also proven to be important in the recovery of the CNS after injuries . When lesions are made on the brain surface, meningeal cells will divide and migrate into the lesion, eventually lining the entire injury cavity . If the injury has significantly reduced the density of astrocytes and created space within the tissue, the meningeal cells will invade even more diffusely . As invading meningeal cells make contact with astrocytes, they can induce the formation of a new, functional glia limitans . The new glia limitans formed after CNS injury usually presents itself as a barrier to regenerating axons . </P> <P> There are a number of diseases associated with problems or abnormalities with the glia limitans . Many diseases can arise from a breach to the glia limitans in which it will no longer be able to fulfill its functional role as a barrier . Two of the more common diseases resulting from a breach to the glia limitans are described below . </P> <P> Breaches in the glia limitans - basal lamina complex have been associated with Fukuyama - type congenital muscular dystrophy (FCMD), which is thought to be the result of micropolygyri, or small protrusions of nervous tissue . Although the underlying mechanism for the formation of these breaches is largely unknown, recent research has indicated that the protein fukutin is directly linked to the developing lesions . Mutations in the fukutin protein lead to a depressed level of its expression in the brain and spinal cord of neonatal subjects, which in turn has been found to contribute to the weakening of the structural integrity of the glia limitans . Neuronal and glial cells migrate through the weakened barrier resulting in the accumulation of neural tissue in the subarachnoid space . This abnormal migration, known as cortical dysplasia, is theorized to be one of the primary causes for FCMD . </P>

Neuroglial cells most directly associated with the formation of csf