Nicotinic cholinergic mechanisms on memory reconsolidation of an inhibitory avoidance response in mice

KRAWCZYK MC; BOCCIA MM; CASAL MJ; BLAKE MG; BARATTI CM

Córdoba, Argentina

Congreso; IRCN First Joint Meeting of the Argentine Society for Neuroscience (SAN) and the Argentine Workshop in Neurosciences (TAN); 2009

Sociedad Argentina de Neurociencias

When a well-consolidated memory is recalled it becomes transiently sensitive to disruptionto the same treatments that affect consolidation. This new window of susceptibility isreferred as memory reconsolidation. Previously, we reported that icv infusions of HC-3, aspecific inhibitor of the high affinity choline uptake by brain cholinergic neurons, impairedretention performance of a one-trial step-through inhibitory avoidance response (IAR) inmice (Boccia et al., 2004). In addition, HC-3 produced a deleterious effect on retention onlywhen given immediately after memory reactivation, but not if memory is not reactivated.The memory vulnerability to HC-3 change as a function of the time elapsing betweenoriginal learning and retrieval. Also, we did not observe spontaneous recovery 21 daysafter training (Boccia et al., 2006). Thus for the first time, we suggested a participation ofcentral cholinergic mechanisms in memory reconsolidation of an IAR in mice.Here we investigate the effect of nicotinic receptor (nAchR) ligands infused bilaterally in thedorsal hippocampus after memory reactivation of the IAR in mice. The nAchR antagonistswere mecamylamine (M, α3β4, 1-30 ug/side), dihydro-β-eritroidine (DHβE, α4β2 , 3–30ug/side) and methyllycaconitine (MLA, α7,1-30 ug/side).