We used tunicamycin, an inhibitor of protein fatty acylation, to exami
ne the possibility that there is a cycle of acylation and deacylation
of cysteine string proteins at nerve terminals. Using both physiologic
al and immunoblot approaches, we obtained no evidence for a cycle of a
cylation and deacylation that affects these proteins. These data sugge
st that this lipid modification of cysteine string proteins is relativ
ely more stable than that observed for other nerve ending proteins, li
ke SNAP-25.