Abstract
Aversive memories help us to deal with similar, future threatening situations. Understanding the neural and molecular bases of the learning and memory process provides insights into the physiopathology of memory-related conditions, including posttraumatic stress disorder (PTSD). PTSD patients often present neurochemical dysfunctions, such as noradrenergic hyperactivation, increased glucocorticoid sensitivity, and low endocannabinoid tonus. The individual role of these stress-related neurotransmitters during fear memory formation and maintenance is well documented, but addressing their potential interplay may pave the way for more effective therapeutic approaches. This chapter reviews and discusses animal studies investigating the abovementioned aspect. There is a complex endocannabinoid-noradrenergic-glucocorticoid interplay in fear memory consolidation, reconsolidation, and extinction. Both antagonistic and synergic actions are possible. The outcome depends on neurotransmitter systems targeted by the interventions tested, the brain region considered, and the memory phase studied. Further research will examine still-open questions, such as potential sex-dependent differences.
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