Abstract: An anti-GAP43 antibody which is capable of distinguishing a non-phosphorylated threonine residue at position 89 (T89) from a phosphorylated threonine residue at position 89 (pT89) of mouse GAP43 set forth in SEQ ID NO: 13, and which is capable of specifically detecting a growth cone; an anti-GAP43 antibody which is capable of distinguishing a non-phosphorylated serine residue at position 96 (S96) from a phosphorylated serine residue at position 96 (pS96) of mouse GAP43, and which is capable of specifically detecting a growth cone; an anti-GAP43 antibody which is capable of distinguishing a non-phosphorylated threonine residue at position 172 (T172) from a phosphorylated threonine residue at position 172 (pT172) of mouse GAP43, and which is capable of specifically detecting a growth cone; and an immunological analysis method using these anti-GAP43 antibodies.

Abstract: An anti-GAP43 antibody which is capable of distinguishing a non-phosphorylated threonine residue at position 89 (T89) from a phosphorylated threonine residue at position 89 (pT89) of mouse GAP43 set forth in SEQ ID NO: 13, and which is capable of specifically detecting a growth cone; an anti-GAP43 antibody which is capable of distinguishing a non-phosphorylated serine residue at position 96 (S96) from a phosphorylated serine residue at position 96 (pS96) of mouse GAP43, and which is capable of specifically detecting a growth cone; an anti-GAP43 antibody which is capable of distinguishing a non-phosphorylated threonine residue at position 172 (T172) from a phosphorylated threonine residue at position 172 (pT172) of mouse GAP43, and which is capable of specifically detecting a growth cone; and an immunological analysis method using these anti-GAP43 antibodies.

Abstract: Inhibition of nerve growth normally helps to prevent aberrant pathway or target selection, but also prevents needed regeneration in the mammalian central nervous system. The responsible inhibitory ligands are unknown, but pertussis toxin-sensitive G proteins, which are enriched in growth cones, appear to be involved in causing the responding growth cones to collapse. GAP-43 is an intracellular protein that can amplify the response to the stimulation of G protein-coupled receptors. We have attempted to modify the sensitivity of nerves to inhibitory signals by the use of GAP-43 peptides. The peptide corresponding to the native amino terminus sequence stimulates G.sub.o and enhances the growth cone collapse induced by inhibitory ligands. Modification of two critical cysteines generates peptides which inhibit G.sub.o and which markedly reduce the degree of inhibitor-mediated growth cone collapse.