Fig. 9.

CaM-kinase II and PKC regulate the delayed, sustained rise of [Ca²⁺]_i.a, Inhibition of CaM-kinase II (KN-62) blocks LN-induced rises in [Ca²⁺]_i. The distribution of [Ca²⁺]_i of a population of growth cones is plotted against [Ca²⁺]_i. Open squaresillustrate the distribution of resting [Ca²⁺]_i in growth cones advancing on FN. After the addition of soluble LN, a large number of growth cones respond with rises of [Ca²⁺]_i, and the distribution of [Ca²⁺]_i shifts to higher [Ca²⁺]_i (open circles). A presence of 2 μm KN-62 negates the shift in the distribution of [Ca²⁺]_iexpected on the addition of soluble LN (filled triangles). The distribution of resting [Ca²⁺]_i is unaffected by KN-62 (filled circles). b, In the presence of 10 nm bisindolylmaleimide (BIS), a specific PKC inhibitor, the distribution of resting [Ca²⁺]_i (filled circles) is identical to that under control conditions (open squares). However, BIS blocks the expected change in the distribution of [Ca²⁺]_i in growth cones on the addition of soluble LN (closed triangles).c, The change in [Ca²⁺]_i induced by soluble LN is shown as a function of the inhibitors that are present. Inhibition of both CaM-kinase II [KN-62 (KN)] and PKC [bisindolylmaleimide (BIS)] negates LN-induced rises in [Ca²⁺]_i. Con, Control conditions.