Acute Effects of Alcohol on Encoding and Consolidation of Memory for Emotional Stimuli

Abstract

ABSTRACT. Objective: Acute doses of alcohol impair memory when administered before encoding of emotionally neutral stimuli but enhance memory when administered immediately after encoding, potentially by affecting memory consolidation. Here, we examined whether alcohol produces similar biphasic effects on memory for positive or negative emotional stimuli. Method: The current study examined memory for emotional stimuli after alcohol (0.8 g/kg) was administered either before stimulus viewing (encoding group; n = 20) or immediately following stimulus viewing (consolidation group; n = 20). A third group received placebo both before and after stimulus viewing (control group; n = 19). Participants viewed the stimuli on one day, and their retrieval was assessed exactly 48 hours later, when they performed a surprise cued recollection and recognition test of the stimuli in a drug-free state. Results: As in previous studies, alcohol administered before encoding impaired memory accuracy, whereas alcohol administered after encoding enhanced memory accuracy. Critically, alcohol effects on cued recollection depended on the valence of the emotional stimuli: Its memory-impairing effects during encoding were greatest for emotional stimuli, whereas its memory-enhancing effects during consolidation were greatest for emotionally neutral stimuli. Effects of alcohol on recognition were not related to stimulus valence. Conclusions: This study extends previous findings with memory for neutral stimuli, showing that alcohol differentially affects the encoding and consolidation of memory for emotional stimuli. These effects of alcohol on memory for emotionally salient material may contribute to the development of alcohol-related problems, perhaps by dampening memory for adverse consequences of alcohol consumption. (J. Stud. Alcohol Drugs, 77, 86-94, 2016)

Alcohol and pharmacologically similar sedatives impair encoding and facilitate consolidation of both recollection and familiarity in episodic memory

“…Considering Wixted’s account that retrograde facilitation involves preventing retroactive interference in the hippocampus, post-encoding GABA A PAMs should enhance hippocampally-dependent recollection. This account is also consistent with past work that has used tasks thought to tap into recollection (e.g., Mednick et al, 2013; Weafer et al, 2016a). Nevertheless, it is less clear if or how familiarity would be impacted.…”

“…It is worth noting, however, that every study in Table 1 implemented minimal delays between encoding and retrieval, thereby opening up the possibility that the GABA A PAM manipulations also impacted memory retrieval. When drug effects have been isolated to either encoding or retrieval by implementing delays between these phases, encoding manipulations modulate hit rates (e.g., Ballard, Gallo, & de Wit, 2013; Becker et al, 2017; Weafer et al, 2016a), whereas retrieval manipulations increase false alarm rates (Ballard, Gallo, & de Wit, 2014; Doss, Weafer, Gallo, & de Wit, 2018a, 2018b). Indeed, increases in false alarm rates were observed in the drug conditions of some of the studies in Table 1.…”

“…A recent study by Weafer et al (2016a) tested the effects of alcohol on either the encoding or consolidation of memories for emotional and neutral pictures. They reported that alcohol administered prior to encoding disproportionately impaired memory for emotional over neutral pictures, consistent with other studies of GABA A PAMs during encoding (Brignell, Rosenthal, & Curran, 2007; Buchanan, Karafin, & Adolphs, 2003; Kamboj & Curran, 2006).…”

“…It is well established that alcohol and other GABA A positive allosteric modulators (PAMs; i.e., sedating drugs such as benzodiazepines and hypnotics that facilitate activity at the GABA A receptor) can have paradoxical effects on episodic memory. When administered prior to encoding, these drugs impair memory for the to-be-remembered information (e.g., Kamboj & Curran, 2006; Weafer, Gallo, & de Wit, 2016a), but when they are administered immediately post-encoding, they enhance memory for this same information (known as ‘retrograde facilitation’; Mednick et al, 2013; Weafer et al, 2016a). To explain these opposing drug effects during different stages of memory, Wixted (2004) argued that GABA A PAMs disrupt the encoding of new information in the hippocampus (i.e., by preventing new long-term potentiation or LTP) while at the same time sparing the hippocampally-based consolidation of previously encoded information (i.e., by sparing the stabilization of pre-drug LTP).…”

“…However, the dual-process signal detection (DPSD) model is another method of estimating recollection and familiarity from confidence data (Yonelinas, 2002). Therefore, to address the second question, we conducted a DPSD analysis on the confidence data from a recent study that examined the impact of either pre- or post-encoding alcohol on emotional and neutral memory (Weafer et al 2016a).…”