Ricerc@Sapienza

Trauma patients treated with ketamine during emergency care present aggravated early post- traumatic stress reaction which is highly predictive of post-traumatic stress disorder (PTSD) development and severity. The use of ketamine in the acute trauma phase may directly or indirectly interfere with neural processes of memory consolidation of the traumatic event, thus leading to the formation of maladaptive memories, a hallmark symptom of PTSD.

The endocannabinoid system is a key modulator of memory consolidation for aversive experiences. We recently found that the fatty acid amide hydrolase (FAAH) inhibitor URB597, which increases anandamide levels by inhibiting its hydrolysis, facilitates memory consolidation through a concurrent activation of both cannabinoid receptor type 1 (CB1) and 2 (CB2). Here, we investigated the role played on memory consolidation by the other major endocannabinoid, 2-arachidonoylglycerol (2-AG).

The effects induced by exogenous manipulation of endocannabinoid neurotransmission on emotion and memory are often contradictory. Among the different factors involved, of particular interest is the binding affinity of endocannabinoids, and their analogs, for other receptor families beyond cannabinoid receptors, such as the peroxisome proliferator-activated receptors (PPARs), and the transient receptor potential cation channel subfamily V member 1 (TRPV1).