Basolateral amygdala complex plays an essential role in the generationof an emotional state caused by an aversive experience. Insulin growth factorlike I (IGF-I) could modulate hippocampal circuits modifying cognitivefunctions, and possibly, the molecular mechanisms involved in somepsychopathologies related to traumatic memories. Objectives: 1)To promote andevaluate the expression of a memory trace through IGF-I gene therapy; 2)Toevaluate if structural plastic changes in dorsal hippocampus, are responsiblefor the expression of this memory trace. M&M: Adult male Wistar rats  were bilaterally infused into BLA withRAd-DS-Red, as a control virus and RAd-IGF-I, as therapeutic virus. 7 dayslater we performed a weak fear conditioning protocol (WFCP). Freezing behavior(FB) was assessed as a measure of retrieval and memory retention. At day 15 we performed hot plate test to evaluatesensitivity damage. Rats were perfused and the brain fixed for dendritic spineanalysis. Results: A significantly increase in FB in the RAd-IGF-1 group wasobserved after 7 days and maintained for 14 days post injection. There was notsensitivity damage in both groups. Preliminary results for dendritic spineanalysis indicate no significant differences in spine density. Conclusions:IGF-I gene therapy induces a significant expression of FB in a WFCP, with apossible promotor effect on the formation of a fear memory trace which promptus to further studies under this experimental model.