Hippocamppal structural plasticity associated to the f ear memory destabilization/reconsolidation process

RAMIRO GABRIEL COMAS MUTIS; IRENE DELIA MARTIJENA; VICTOR ALEJANDRO MOLINA; GASTÓN DIEGO CALFA

Congreso; XXXIV Annual Meeting of the Argentine Society for Research in Neuroscience; 2019

A consolidated memory can enter a transient labile state when presented with areminder, requiring a protein synthesis dependent re stabilization process termedreconsolidation. It is known that the basolat eral amygdala (BLA) and the DorsalHippocampus (DH) pl ay a key role in processing emotional information and thecontextual representation of fear memories respectively. In the pr esent study, weassessed the modulating role of BLA on the hippocampal structu ral plasticityassociated with the labilization/recons olidation of a contextual fear memory. Weused Ifenprodil (IFEN), a selective NR2B subunit of the NMDA receptor antagonist,infused intra BLA in male wistar rats, in order to prevent the labilization. R ats weresacrificed 60 minutes and 24 hours after the retrieval session to evaluate thestructural plasticity of the CA1 region of DH.Our results show that rats infused with IF EN present a high number of spines atboth 60 minutes and 24 hours post retrie val, while rats infused with saline solution(SAL) sho w a decrease in dendritic spines 60 minutes after retrieval, consistentwith the dynamic changes in dendritic spines observe d in our previous work.Altogether, our findings seem to indicate that labiliz ation impairment preventsstructural changes in the CA 1 region of DH, thus supporting our hypothesis of themodulating role of BLA on the hippocampal structural plasticity and th e idea thatchanges in dendritic spines density are required for a memory to b e updated.