Abstract
Previous neuroimaging studies support a role for the medial temporal lobes in maintaining novel stimuli over brief working memory (WM) delays, and suggest delay period activity predicts subsequent memory. Additionally, slice recording studies have demonstrated neuronal persistent spiking in entorhinal cortex, perirhinal cortex (PrC), and hippocampus (CA1, CA3, subiculum). These data have led to computational models that suggest persistent spiking in parahippocampal regions could sustain neuronal representations of sensory information over many seconds. This mechanism may support both WM maintenance and encoding of information into long term episodic memory. The goal of the current study was to use high-resolution fMRI to elucidate the contributions of the MTL cortices and hippocampal subfields to WM maintenance as it relates to later episodic recognition memory. We scanned participants while they performed a delayed match to sample task with novel scene stimuli, and assessed their memory for these scenes post-scan. We hypothesized stimulus-driven activation that persists into the delay period—a putative correlate of persistent spiking—would predict later recognition memory. Our results suggest sample and delay period activation in the parahippocampal cortex (PHC), PrC, and subiculum (extending into DG/CA3 and CA1) was linearly related to increases in subsequent memory strength. These data extend previous neuroimaging studies that have constrained their analysis to either the sample or delay period by modeling these together as one continuous ongoing encoding process, and support computational frameworks that predict persistent activity underlies both WM and episodic encoding.
Highlights
Converging evidence from human neuroimaging (Fernández et al, 1999; Kirchhoff et al, 2000; Preston et al, 2010) and animal studies (Zola-Morgan and Squire, 1986; Beason-Held et al, 1999; for review see: Eichenbaum, 2000; Squire et al, 2004) have implicated the hippocampus (HC), parahippocampal cortex (PHC), entorhinal cortex (EC), and perirhinal cortex (PrC) as critical for Hippocampal subfields, medial temporal lobe (MTL), and ongoing encoding long-term episodic encoding
We predicted the magnitude of this sustained activation would be related to subsequent episodic memory strength, lending indirect support to our hypothesis that continued activity reflects ongoing encoding
The present study demonstrated that the PHC and PrC as well as hippocampal subregions subiculum, CA1, and CA3/dentate gyrus (DG) exhibited activation during the delayed matchto-sample (DMS) sample period that persisted into the delay period in the absence of continued stimulus input
Summary
Converging evidence from human neuroimaging (Fernández et al, 1999; Kirchhoff et al, 2000; Preston et al, 2010) and animal studies (Zola-Morgan and Squire, 1986; Beason-Held et al, 1999; for review see: Eichenbaum, 2000; Squire et al, 2004) have implicated the hippocampus (HC), parahippocampal cortex (PHC), entorhinal cortex (EC), and perirhinal cortex (PrC) as critical for Hippocampal subfields, MTL, and ongoing encoding long-term episodic encoding. Within the hippocampal memory system, recent work has shown that subsets of neurons in the EC, PrC, and hippocampal subfields CA1 and CA3 are known to possess these characteristics (Klink and Alonso, 1997; Young et al, 1997; Tahvildari et al, 2007; Yoshida et al, 2008; Navaroli et al, 2012; Jochems and Yoshida, 2013; Knauer et al, 2013) These data have led to the idea persistent spiking may act as an episodic memory buffer, supporting long-term encoding of information past the duration of a sensory event, and suggest a neural mechanism sufficient for short-term maintenance of novel stimuli (Lisman and Idiart, 1995; Jensen and Lisman, 1996; Fransén et al, 2002; Koene et al, 2003; McGaughy et al, 2005). In support of this hypothesis, electrophysiological recordings in awake, behaving monkeys and rats have shown persistent, stimulus selective activity in EC neurons during the delay period of delayed (non-) match to sample tasks (Suzuki et al, 1997; Young et al, 1997)
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