Hippocampal ERK1/ERK2 activation after memory reconsolidation modulation by α7 nicotinic acetylcholine receptor

KRAWCZYK M; FELD M; BLAKE MG; BARATTI CM; BOCCIA MM

Congreso; Reunión de la Sociedad Argentina de Investigación en Neurociencias; 2012

Sociedad Argentina de Investigación en Neurociencias

Previously we reported that hippocampal alpha7 nicotinic acetylcholine receptors (nAChRs) play a critical role in reconsolidation of an inhibitory avoidance response. Extracellular signal-regulated kinases (ERK) were demonstrated to be involved in downstream signaling after alpha7-nAchRs activation. CF-1 male mice were trained in an inhibitory avoidance task using either a mild or a strong footshock. A retention/reactivation test was given 48 hours later. Immediately after it, mice were given intra-dorsal hippocampal infusions of choline, an alpha7-nAchRs agonist (Ch, dosis), or methylcaconitine, an alpha7-nAchRs antagonist (MLA, dosis). Fifteen minutes after infusion, the hippocampi were dissected and ERK1/ERK2 activation was determined either in the nuclear or the cytosolic fractions. ERK1/ERK2 is activated differentially, depending on the training conditions (mild or strong footshock), after memory reactivation. Ch or MLA, given immediately after memory reactivation, modified ERK1/ERK2 patterns of activation. Altogether our results suggest for the first time a specific pattern of differential activation of a molecular pathway that correlates with memory reconsolidation modulation (enhancement or impairment).