scholarly journals Decision-making increases episodic memory via post-encoding consolidation

2018 ◽  
Author(s):  
Vishnu P. Murty ◽  
Sarah DuBrow ◽  
Lila Davachi

AbstractThe ability for individuals to actively make decisions engages regions within the mesolimbic system and enhances memory for chosen items. In other behavioral contexts, mesolimbic engagement has been shown to enhance episodic memory by supporting consolidation. However, research has yet to investigate how consolidation may support interactions between decision-making and episodic memory. Across two studies, participants encoded items that were occluded by cover screens and could either actively decide which of two items to uncover or were pre-selected by the experimenter. In Study 1, we show that active decision-making reduces forgetting rates across an immediate and 24-hour memory test, a behavioral marker of consolidation. In Study 2, we use functional neuroimaging to characterize putative neural markers of memory consolidation by measuring post-encoding interactions between the hippocampus and perirhinal cortex (PRC). We show that choice-related striatal engagement is associated with increased post-encoding hippocampal-PRC interactions. Finally, we show that a previous reported relationship between choice-related striatal engagement and long-term memory is accounted for by post-encoding hippocampal-PRC interactions. Together these findings support a model by which actively deciding to encode information enhances subsequent consolidation mechanisms to preserve episodic memory for outcomes.

2019 ◽  
Vol 31 (9) ◽  
pp. 1308-1317 ◽  
Author(s):  
Vishnu P. Murty ◽  
Sarah DuBrow ◽  
Lila Davachi

The ability for individuals to actively make decisions engages regions within the mesolimbic system and enhances memory for chosen items. In other behavioral contexts, mesolimbic engagement has been shown to enhance episodic memory by supporting consolidation. However, research has yet to investigate how consolidation may support interactions between decision-making and episodic memory. Across two studies, participants encoded items that were covered by occluder screens and could either actively decide which of two items to uncover or an item was preselected by the experimenter. In Study 1, we show that active decision-making reduces forgetting rates across an immediate and 24-hr memory test, a behavioral marker of consolidation. In Study 2, we use functional neuroimaging to characterize putative neural markers of memory consolidation by measuring interactions between the hippocampus and perirhinal cortex (PRC) during a postencoding period that reexposed participants to elements of the decision-making context without exposing them to memoranda. We show that choice-related striatal engagement is associated with increased postencoding hippocampal–PRC interactions. Finally, we show that a previous reported relationship between choice-related striatal engagement and long-term memory is accounted for by these postencoding hippocampal–PRC interactions. Together, these findings support a model by which actively deciding to encode information enhances memory consolidation to preserve episodic memory for outcomes, a process that may be facilitated by reexposure to the original decision-making context.


2018 ◽  
Author(s):  
James W. A. Strachan ◽  
Anna á Váli Guttesen ◽  
Anika Smith ◽  
M. Gareth Gaskell ◽  
Steven Tipper ◽  
...  

People make inferences about the trustworthiness of others based on their observed gaze behaviour. Faces that consistently look towards a target location are rated as more trustworthy than those that look away from the target. Representations of trust are important for future interactions; yet little is known about how they are consolidated in long-term memory. Sleep facilitates memory consolidation for incidentally-learned information and may therefore support the retention of trust representations. We investigated the consolidation of trust inferences across periods of sleep or wakefulness. In addition, we employed a memory cueing procedure (targeted memory reactivation, TMR) in a bid to strengthen certain trust memories over others. We observed no difference in the retention of trust inferences following delays of sleep or wakefulness, and there was no effect of TMR in either condition. Interestingly, trust inferences remained stable one week after learning, irrespective of the initial post-learning delay. A second experiment showed that this implicit learning occurs despite participants’ being unable to explicitly recall the gaze behaviour of specific faces immediately after encoding. Together, these results suggest that gist-like, social inferences are formed at the time of learning without retaining the original episodic memory and thus do not benefit from offline consolidation through replay. We discuss our findings in the context of a novel framework whereby trust judgements reflect an efficient, powerful, and adaptable storage device for social information.


1999 ◽  
Vol 22 (3) ◽  
pp. 452-453
Author(s):  
Kim S. Graham ◽  
John R. Hodges

Aggleton & Brown (A&B) propose that the hippocampal-anterior thalamic and perirhinal-medial dorsal thalamic systems play independent roles in episodic memory, with the hippocampus supporting recollection-based memory and the perirhinal cortex, recognition memory. In this commentary we discuss whether there is experimental support for the A&B model from studies of long-term memory in semantic dementia.


2007 ◽  
Vol 88 (3) ◽  
pp. 342-351 ◽  
Author(s):  
Lisa Conboy ◽  
Claire M. Seymour ◽  
Marco P. Monopoli ◽  
Niamh C. O’Sullivan ◽  
Keith J. Murphy ◽  
...  

2019 ◽  
Vol 122 (3) ◽  
pp. 1123-1135 ◽  
Author(s):  
C. J. Scavuzzo ◽  
M. J. LeBlancq ◽  
F. Nargang ◽  
H. Lemieux ◽  
T. J. Hamilton ◽  
...  

The nearly axiomatic idea that de novo protein synthesis is necessary for long-term memory consolidation is based heavily on behavioral studies using translational inhibitors such as anisomycin. Although inhibiting protein synthesis has been shown to disrupt the expression of memory, translational inhibitors also have been found to profoundly disrupt basic neurobiological functions, including the suppression of ongoing neural activity in vivo. In the present study, using transverse hippocampal brain slices, we monitored the passive and active membrane properties of hippocampal CA1 pyramidal neurons using intracellular whole cell recordings during a brief ~30-min exposure to fast-bath-perfused anisomycin. Anisomycin suppressed protein synthesis to 46% of control levels as measured using incorporation of radiolabeled amino acids and autoradiography. During its application, anisomycin caused a significant depolarization of the membrane potential, without any changes in apparent input resistance or membrane time constant. Anisomycin-treated neurons also showed significant decreases in firing frequencies and spike amplitudes, and showed increases in spike width across spike trains, without changes in spike threshold. Because these changes indicated a loss of cellular energetics contributing to maintenance of ionic gradients across the membrane, we confirmed that anisomycin impaired mitochondrial function by reduced staining with 2,3,5-triphenyltetrazolium chloride and also impaired cytochrome c oxidase (complex IV) activity as indicated through high-resolution respirometry. These findings emphasize that anisomycin-induced alterations in neural activity and metabolism are a likely consequence of cell-wide translational inhibition. Critical reevaluation of studies using translational inhibitors to promote the protein synthesis dependent idea of long-term memory is absolutely necessary. NEW & NOTEWORTHY Memory consolidation is thought to be dependent on the synthesis of new proteins because translational inhibitors produce amnesia when administered just after learning. However, these agents also disrupt basic neurobiological functions. We show that blocking protein synthesis disrupts basic membrane properties of hippocampal neurons that correspond to induced disruptions of mitochondrial function. It is likely that translational inhibitors cause amnesia through their disruption of neural activity as a result of dysfunction of intracellular energetics.


Cortex ◽  
2015 ◽  
Vol 63 ◽  
pp. 68-78 ◽  
Author(s):  
Monika Schönauer ◽  
Melanie Grätsch ◽  
Steffen Gais

2015 ◽  
Vol 22 (10) ◽  
pp. 527-531 ◽  
Author(s):  
Jan-Willem Thielen ◽  
Atsuko Takashima ◽  
Femke Rutters ◽  
Indira Tendolkar ◽  
Guillén Fernández

2015 ◽  
Vol 1627 ◽  
pp. 109-118 ◽  
Author(s):  
Jian Zheng ◽  
Fei Luo ◽  
Nan-nan Guo ◽  
Zong-yue Cheng ◽  
Bao-ming Li

Sign in / Sign up

Export Citation Format

Share Document