▁morph ology ▁and ▁functional ▁properties ▁of ▁central ▁nerv ous ▁system ▁neur ons ▁are ▁highly ▁complex , ▁for ▁this ▁reason ▁a ▁neur on ▁function ally ▁identical ▁cannot ▁be ▁replaced ▁by ▁one ▁of ▁another ▁type ▁( L lin ás ' ▁law ). ▁ ▁In hib ition ▁of ▁ax onal ▁reg row th ▁▁ ▁Gli al ▁cell ▁scar ▁formation ▁is ▁induced ▁following ▁damage ▁to ▁the ▁nerv ous ▁system . ▁In ▁the ▁central ▁nerv ous ▁system , ▁this ▁gli al ▁scar ▁formation ▁significantly ▁in hib its ▁n erve ▁reg ener ation , ▁which ▁leads ▁to ▁a ▁loss ▁of ▁function . ▁Several ▁families ▁of ▁mole cules ▁are ▁released ▁that ▁promote ▁and ▁drive ▁gli al ▁scar ▁formation . ▁For ▁instance , ▁transform ing ▁growth ▁factors ▁B - 1 ▁and ▁- 2 , ▁inter le uk ins , ▁and ▁cy tok ines ▁play ▁a ▁role ▁in ▁the ▁init iation ▁of ▁scar ▁formation . ▁The ▁accum ulation ▁of ▁re active ▁ast ro cy tes ▁at ▁the ▁site ▁of ▁injury ▁and ▁the ▁up ▁reg ulation ▁of ▁mole cules ▁that ▁are ▁in hib itory ▁for ▁neur ite ▁out g row th ▁contribute ▁to ▁the ▁failure ▁of ▁neur or eg ener ation . ▁The ▁up - reg ulated ▁mole cules ▁alter ▁the ▁composition ▁of ▁the ▁ext rac ell ular ▁matrix ▁in ▁a ▁way ▁that ▁has ▁been ▁shown ▁to ▁in hib it ▁neur ite ▁out g row th ▁extension . ▁This ▁scar ▁formation ▁involves ▁several ▁cell ▁types ▁and ▁families ▁of ▁mole cules . ▁ ▁Ch ond roit in ▁sul f ate ▁prote og ly can