The effects of post-learning alcohol ingestion on human motor memory consolidation

Abstract

The neurochemical mechanisms underlying motor memory consolidation remain largely unknown. Based on converging work showing that ethyl alcohol retrogradely enhances declarative memory consolidation, this work tested the hypothesis that post-learning alcohol ingestion would enhance motor memory consolidation. In a within-subject and fully counterbalanced design, participants (n = 24; 12M; 12F) adapted to a gradually introduced visual deviation and ingested, immediately after adaptation, a placebo (PBO), a medium (MED) or high (HIGH) dose of alcohol. The alcohol doses were bodyweight- and gender-controlled to yield peak breath alcohol concentrations of 0.00% in the PBO, ~0.05% in the MED and ~0.095% in the HIGH condition. Retention was evaluated 24 h later through reach aftereffects when participants were sober. The results revealed that retention levels were neither significantly nor meaningfully different in both the MED and HIGH conditions as compared to PBO (all absolute Cohen's d_z values < ~0.2; small to negligible effects), indicating that post-learning alcohol ingestion did not alter motor memory consolidation. Given alcohol's known pharmacological GABAergic agonist and NMDA antagonist properties, one possibility is that these neurochemical mechanisms do not decisively contribute to motor memory consolidation. As converging work demonstrated alcohol's retrograde enhancement of declarative memory, the present results suggest that distinct neurochemical mechanisms underlie declarative and motor memory consolidation. Elucidating the neurochemical mechanisms underlying the consolidation of different memory systems may yield insights into the effects of over-the-counter drugs on everyday learning and memory but also inform the development of pharmacological interventions seeking to alter human memory consolidation.

Keywords: alcohol; consolidation; motor learning; motor memory; visuomotor adaptation.

FIGURE 1

Overview of the within‐subject placebo‐controlled procedures. (a) Timeline of the experimental acquisition and retention visits (separated by 24 h). Condition order was fully counterbalanced across participants. Participants arrived drug‐free and on an empty stomach. Breathalyser measurements were taken at several time points to ensure sobriety and measure BrACs. Immediately following dominant hand acquisition, participants ingested their placebo or alcohol‐containing beverage. Memory consolidation of the dominant hand acquisition block was evaluated 24 h later. (b) Dominant hand acquisition block. Participants reached visual targets while adapting to a gradually introduced visual deviation in an alcohol‐free state. The beverage was ingested immediately after this block. (c) Non‐dominant hand session. To evaluate the effects of alcohol on learning, participants used their non‐dominant hand to reach visual targets while adapting to a visual deviation introduced in a stepwise manner. Immediately after adaptation, reach aftereffects without corrective visual feedback were evaluated (50 NoVision trials). This block occurred 60 min after the complete beverage ingestion. (d) Procedures of the dominant hand retention block. In an alcohol‐free state, memory consolidation of the dominant hand acquisition was evaluated 24 h later through reach aftereffects first without (50 NoVision trials) and then with corrective visual feedback (50 Washout trials). (e) Bodyweight‐ and gender‐controlled alcohol dosages. Females ingested 15% less alcohol than their male counterparts in both the MED and HIGH conditions.

FIGURE 2

BrAC and hand direction at PV results. (a) BrAC results. All participants were sober during acquisition (Day 1) and retention (Day 2) when using their dominant hand. The ingestion of alcohol elevated BrAC values in a dose‐dependent manner, confirming that participants were under the influence of alcohol in the MED and HIGH conditions. The average and individual data of each condition are shown. (b) dominant hand acquisition. Top panel: the time‐course of hand direction at PV is shown. Bottom panel: The average and individual data of each condition for each phase are shown. (c) Non‐dominant hand session. Top panel: The time‐course of hand direction at PV is shown. Bottom panel: The average and individual data of each condition for each phase are shown. Note the lack of difference in hand direction at PV despite the greatly differing BrAC values. (d) Dominant hand retention. Top panel: The time‐course of hand direction at PV is shown. Bottom panel: The average and individual data of each condition for each phase are shown. Post‐learning alcohol ingestion did not enhance memory consolidation as compared to placebo. Asterisks (*) indicate significant differences, and ‘n.s.’ means ‘non‐significant’. The data represent the mean ± 1 SD (middle row only). For each depicted condition, n = 24.