RESUMEN
PURPOSE: The goal was to evaluate whether implicit talker familiarization via an interactive computer game, designed for this study, could improve children's word recognition in classroom noise. It was hypothesized that, regardless of age, children would perform better when recognizing words spoken by the talker who was heard during the game they played. METHOD: Using a one-group pretest-posttest experimental design, this study examined the impact of short-term implicit voice exposure on children's word recognition in classroom noise. Implicit voice familiarization occurred via an interactive computer game, played at home for 10 min a day for 5 days. In the game, children (8-12 years) heard one voice, intended to become the "familiar talker." Pre- and postfamiliarization, children identified words in prerecorded classroom noise. Four conditions were tested to evaluate talker familiarity and generalization effects. RESULTS: Results demonstrated an 11% improvement when recognizing words spoken by the voice heard in the game ("familiar talker"). This was observed only for words that were heard in the game and did not generalize to unfamiliarized words. Before familiarization, younger children had poorer recognition than older children in all conditions; however, after familiarization, there was no effect of age on performance for familiarized stimuli. CONCLUSIONS: Implicit short-term exposure to a talker has the potential to improve children's speech recognition. Therefore, leveraging talker familiarity through gameplay shows promise as a viable method for improving children's speech-in-noise recognition. However, given that improvements did not generalize to unfamiliarized words, careful consideration of exposure stimuli is necessary to optimize this approach.
RESUMEN
Drug craving triggered by cues that were once associated with drug intoxication is a major contributor to continued drug-seeking behaviors. Addictive drugs engage molecular pathways of associative learning and memory. Reactivated memories are vulnerable to disruption by interference with the process of reconsolidation, hence targeting reconsolidation could be a strategy to reduce cue-induced drug craving and relapse. Here we examined the circuitry of cocaine contextual memory reconsolidation and explored neuroplasticity following memory reactivation. Mice underwent chemogenetic inhibition of either nucleus accumbens (NA) neurons or the glutamatergic projection neurons from the ventral hippocampus (vHPC) to NA using inhibitory designer receptors exclusively activated by designer drugs (iDREADD). Mice underwent cocaine conditioned place preference followed by reactivation of the cocaine contextual memory. Clozapine-N-oxide (CNO) was administered after memory reactivation to inhibit either NA neurons or the accumbens-projecting vHPC neurons during the reconsolidation period. When retested 3 days later, a significant reduction in the previously established preference for the cocaine context was found in both conditions. FosTRAP2-Ai14 mice were used to identify neurons activated by cocaine memory recall and to evaluate plasticity in NA medium spiny neurons (MSNs) and vHPC pyramidal neurons upon recall of cocaine memories. Results indicate a significant increase in dendritic spine density in NA MSNs activated by cocaine memory recall, particularly of the thin spine type. Sholl analysis indicated longer dendritic length and more branching of NA MSNs after cocaine memory recall than without memory reactivation. vHPC neurons showed increased spine density, with the most robust change in stubby spines. These results implicate a circuit involving glutamatergic projections from the vHPC onto NA neurons which is necessary for the reconsolidation of cocaine memories. Interruption of cocaine memory reconsolidation reduced drug-seeking behavior.