Glial scar shown to stimulate growth-inhibitory proteoglycans by astrocytes. Experimental reduction of TGFβ-1 and TGFβ-2 has been shown to partially reduce glial scarring. Interleukins are another potential family of scar-inducing cellular messengers. Particularly, interleukin-1, a protein produced by mononuclear phagocytes, helps to initiate the inflammatory response in astrocytes, leading to reactive astrogliosis and the formation of the glial scar. The cytokine family of glial scar inducers include interferon-γ (IFNγ) and fibroblast growth factor 2 (FGF2). IFNγ has been shown to induce astrocyte proliferation and increase the extent of glial scarring in injured brain models. Further, FGF2 production increases after injury to the
Perisynaptic schwann cells These proteins are seen in other glial cells such as Myelinating Schwann cells and Neural Crest cells. While the lineage of non-Myelinating Schwann cells is known from neural crest cells, the exact development of PSCs from non-Myelinating Schwann cells is not fully understood. Synaptogenesis is the formation of a synapse and in this case the Neuromuscular Junction is of interest. In this section, the focus is on the development of the NMJ from the outgrowth of axons during development. As mentioned in the development section, Schwann cell precursors accompany growing axons as they reach their associated muscles. It is now