The influence of learning history on anterograde interference.

Classically interpreted as a competition between opposite memories (A vs B), anterograde interference (AI) also emerges in the absence of competing memories (A vs A), suggesting that mechanisms other than those involved in memory competition contribute to AI. To investigate this, we tested the hypothesis that extending motor practice would enhance a first memory, but come at the cost of reduced learning capabilities when subsequently exposed to a second learning session of the same task. Based on converging biological evidence, AI was expected to depend upon the degree of extended practice of the initial exposure. During a first Session, four conditions were carried out where participants (n = 24) adapted to a gradually introduced -20° visual deviation while the extent of the initial exposure was manipulated by varying the duration or type of the performance asymptote. Specifically, the performance asymptote at -20° was either Short (40 trials), Moderate (160 trials), Long (320 trials), or absent due to continuously changing perturbations around the mean of -20° (Jagged; 160 trials). After a 2-min interval, participants re-adapted to the same (-20°) visual deviation, which was meant to probe the effect of extended practice in the first Session on the learning capabilities of a second identical memory (A vs A). The results first confirmed that the duration of exposure in the first Session enhanced immediate aftereffects in the Moderate, Long, and Jagged conditions as compared to the Short condition, suggesting that extended practice enhanced retention of the first memory. When comparing the second Session to the first one, results revealed a different pattern of re-adaptation depending on the duration of initial exposure: in the Short condition, there was evidence for facilitated re-adaptation and similar aftereffects. However, in the Moderate, Long and Jagged conditions, re-adaptation was similar and aftereffects were impaired, suggestive of AI. This suggests that extended practice initially enhances memory formation, but comes at the cost of reduced subsequent learning capabilities. One possibility is that AI occurs because extended practice induces the emergence of network-specific homeostatic constraints, which limit subsequent neuroplastic and learning capabilities in the same neural network.

Punishments and rewards both modestly impair visuomotor memory retention.

While the effects of rewards on memory appear well documented, the effects of punishments remain uncertain. Based on neuroimaging data, this study tested the hypothesis that, as compared to a neutral condition, a context allowing successful punishment avoidance would enhance memory to a similar extent as rewards. In a fully within-subject and counter-balanced design, participants (n = 18) took part in 3 distinct learning sessions during which the delivery of performance-contingent monetary punishments and rewards was manipulated. Specifically, participants had to reach towards visual targets while compensating for a gradually introduced visual deviation. Accuracy at achieving targets was either punished (Hit: "+0$"; Miss: "-0.5$), rewarded (Hit: "+0.5$"; Miss: "-0$"), or associated with neutral binary feedback (Hit: "Hit"; Miss: "Miss"). Retention was assessed through reach aftereffects both immediately and 24 h after initial acquisition. The results disconfirmed the hypothesis by showing that the punishment and reward learning sessions both impaired retention as compared to the neutral session, suggesting that both types of incentives similarly impaired memory formation and consolidation. Two alternative but complementary interpretations are discussed. One interpretation is that the presence of punishments and rewards induced a negative learning context, which - based on neurobiological data - could have been sufficient to interfere with memory formation and consolidation. Another interpretation is that punishments and rewards emphasized the disrupting effects of target hits on implicit learning processes, therefore yielding retention impairments. Altogether, these results suggest that incentives can have counter-productive effects on memory.

Learning the same motor task twice impairs its retention in a time- and dose-dependent manner.

Anterograde interference emerges when two differing tasks are learned in close temporal proximity, an effect repeatedly attributed to a competition between differing task memories. However, recent development alternatively suggests that initial learning may trigger a refractory period that occludes neuroplasticity and impairs subsequent learning, consequently mediating interference independently of memory competition. Accordingly, this study tested the hypothesis that interference can emerge when the same motor task is being learned twice, that is when competition between memories is prevented. In a first experiment, the inter-session interval (ISI) between two identical motor learning sessions was manipulated to be 2 min, 1 h or 24 h. Results revealed that retention of the second session was impaired as compared to the first one when the ISI was 2 min but not when it was 1 h or 24 h, indicating a time-dependent process. Results from a second experiment replicated those of the first one and revealed that adding a third motor learning session with a 2 min ISI further impaired retention, indicating a dose-dependent process. Results from a third experiment revealed that the retention impairments did not take place when a learning session was preceded by simple rehearsal of the motor task without concurrent learning, thus ruling out fatigue and confirming that retention is impaired specifically when preceded by a learning session. Altogether, the present results suggest that competing memories is not the sole mechanism mediating anterograde interference and introduce the possibility that a time- and dose-dependent refractory period-independent of fatigue-also contributes to its emergence. One possibility is that learning transiently perturbs the homeostasis of learning-related neuronal substrates. Introducing additional learning when homeostasis is still perturbed may not only impair performance improvements, but also memory formation.