A visual danger stimulus (VDS) elicits an escape response in the crab Chasmagnathus that declines after a few iterative presentations. Long-lasting retention of such decrement, termed context-signal memory (CSM), is mediated by an association between danger stimulus and environmental cues, cycloheximide sensitive, correlated with PKA activity and NFkappa-B activation, positively modulated by angiotensins, and selectively regulated by a muscarinic-cholinergic mechanism. The present research was aimed at studying the possible involvement of NMDA-like receptors in CSM, given the role attributed to these receptors in vertebrate memory and their occurrence in invertebrates including crustaceans. Vertebrate antagonists (+/-)-2-amino-5-phosphonopentanoic acid (AP5) and (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine (MK-801) were used. Memory retention impairment was shown with MK-801 10(-3) M (1 microg/g) injected immediately before training or after training, or delayed 1 or 4 h, but not 6 h, posttraining. An AP5 10(-3) M dose (0.6 microg/g) impairs retention when given before but not after training. Neither antagonist produced retrieval deficit. A memory process similar to CSM but nonassociative in nature and induced by massed training (termed signal memory, SM), proved entirely insensitive to AP5 or MK-801, confirming the view that distinct mechanisms subserve these different types of memory in the crab.