Activation of the complement system has been reported in a variety of infla
mmatory diseases and neurodegenerative processes of the CNS. Recent evidenc
e indicates that complement proteins and receptors are synthesized on or by
glial cells and, surprisingly, neurons. Among these proteins are the recep
tors for the chemotactic and anaphylactic peptides, C5a and C3a,which are t
he most-potent mediators of complement inflammatory functions. The function
s of glial-cell C3a and C5a receptors (C3aR and C5aR) appear to be similar
to immune-cell C3aRs and C5aRs. However, little is known about the roles th
ese receptors might have on neurons. Indeed, when compared with glial cells
, neurons display a distinct pattern of C3aR and C5aR expression, in either
the normal or the inflamed CNS. These findings suggest unique functions fo
r these receptors on neurons.