It is now well established that the glial fibrillary acidic protein (GFAP)
is the principal 8-9 nm intermediate filament in mature astrocytes of the c
entral nervous system (CNS). Over a decade ago, the value of GFAP as a prot
otype antigen in nervous tissue identification and as a standard marker for
fundamental and applied research at an interdisciplinary level was recogni
zed (Raine, 135). As a member of the cytoskeletal protein family, GFAP is t
hought to be important in modulating astrocyte motility and shape by provid
ing structural stability to astrocytic processes. In the CNS of higher vert
ebrates, following injury, either as a result of trauma, disease, genetic d
isorders, or chemical insult, astrocytes become reactive and respond in a t
ypical manner, termed astrogliosis. Astrogliosis is characterized by rapid
synthesis of GFAP and is demonstrated by increase in protein content or by
immunostaining with GFAP antibody. In addition to the major application of
GFAP antisera for routine use in astrocyte identification in the CNS, the m
olecular cloning of the mouse gene in 1985 has opened a new and rich realm
for GFAP studies. These include antisense, null mice, and numerous promoter
studies. Studies showing that mice lacking GFAP are hypersensitive to cerv
ical spinal cord injury caused by sudden acceleration of the head have prov
ided more direct evidence for a structural role of GFAP. While the structur
al function of GFAP has become more acceptable, the use of GFAP antibodies
and promoters continue to be valuable in studying CNS injury, disease, and
development.