Abstract: The transection of nerve fibers evokes a characteristic reaction in
the injured neurons, the so-called cell body response (CBR), which com-prises
aspects of developmental re-differentiation with parallel loss of the
transmittory phenotype, efforts or achievement of axonal elongation and
re-construction of effective synapses. Neither the signals underlying the onset
of CBR nor the programs underlying regeneration are suffi-ciently elucidated.
Here we review the putative role of two subfamilies of the MAP kinases, the
JNKs (c-Jun N-terminal kinases) and the p38 kinases in the CBR. Following nerve
injury with subsequent CBR, JNKs are rapidly activated and this activation
persists for weeks until neu-ronal cell death or successful regeneration. The
various functions render JNKs to perfect candidate molecules for the
realization of the CBR including axonal transport, activation of c-Jun,
modulation of cytoskeletal functions, detection of cytoskeletal alterations, or
signal transduc-tion of adhesion molecules in the axon and growth cone. On the
other hand, the rapid but transient activation of p38 might interfere with the
mitotic arrest, a putative feature of the CBR.
Keywords: cell body response, c-Jun, JNKs, p38, regeneration
