Intense stress can cause a long-lasting impairment of learning and memory. This impairment may be due to activation of the endocannabinoid system. Here we determined in Lymnaea stagnalis whether traumatic stress altered both learning and long-term memory (LTM) formation of aerial respiratory behaviour and its neural correlates. Snails received repeated mechanical traumatic stress and we tested the ability of snails to form LTM 2, 4, and 7 days later. Learning and memory were impaired on day 2 and 4, and was fully recovered by day 7. Thus, the intense stress caused a lasting yet reversible impairment. Next, we examined if the actions of endocannabinoids mediate this deficit. Injection of WIN55212-2 (WIN55), a selective agonist for the endocannabinoid receptor 1 (CB1R), in the absence of stress, mimicked the stress-induced memory impairment. Conversely, administration of AM251, a selective CB1R antagonist, prior to the intense stressor significantly mitigated LTM impairment. Next, we hypothesized that robust CB1R activation during the intense stress caused receptor desentization and a long lasting loss of CB1R functioning, which is required for LTM formation. To test this hypothesis, we examined the effect of WIN55 on the neuronal activity of Right Pedal Dorsal 1 (RPeD1) a neuron necessary for LTM formation. In RPeD1 in naïve snails, WIN55 decreased neuronal activity. In contrast, WIN55 had no effect on RPeD1 neuronal activity in stressed animals (examined on day 4), consistent with our hypothesis that stress caused a loss of CB1R function. Consistent with behavioral data, in vivo administration of AM251 prior to stress prevented stress induced changes in RPeD1; while WIN55 injection mimicked the effects of stress. Together the data suggest that stress induced changes in learning and memory formation abilities are the result of changes in the activation of endocannabinoid system.