Iconic memory and visible persistence

There are three senses in which a visual stimulus may be said to persist psychologically for some time after its physical offset. First, neural activity in the visual system evoked by the stimulus may continue after stimulus offset (“neural persistence”). Second, the stimulus may continue to be visible for some time after its offset (“visible persistence”). Finally, information about visual properties of the stimulus may continue to be available to an observer for some time after stimulus offset (“informational persistence”). These three forms of visual persistence are widely assumed to reflect a single underlying process: a decaying visual trace that (1) consists of afteractivity in the visual system, (2) is visible, and (3) is the source of visual information in experiments on decaying visual memory. It is argued here that this assumption is incorrect. Studies of visible persistence are reviewed; seven different techniques that have been used for investigating visible persistence are identified, and it is pointed out that numerous studies using a variety of techniques have demonstrated two fundamental properties of visible persistence: theinverse duration effect (the longer a stimulus lasts, the shorter is its persistence after stimulus offset) and theinverse intensity effect (the more intense the stimulus, the briefer its persistence). Only when stimuli are so intense as to produce afterimages do these two effects fail to occur. Work on neural persistences is briefly reviewed; such persistences exist at the photoreceptor level and at various stages in the visual pathways. It is proposed that visible persistence depends upon both of these types of neural persistence; furthermore, there must be an additional neural locus, since a purely stereoscopic (and hence cortical) form of visible persistence exists. It is argued that informational persistence is defined by the use of the partial report methods introduced by Averbach and Coriell (1961) and Sperling (1960), and the term “iconic memory” is used to describe this form of persistence. Several studies of the effects of stimulus duration and stimulus intensity upon the duration of iconic memory have been carried out. Their results demonstrate that the duration of iconic memory is not inversely related to stimulus duration or stimulus intensity. It follows that informational persistence or iconic memory cannot be identified with visible persistence, since they have fundamentally different properties. One implication of this claim that one cannot investigate iconic memory by tasks that require the subject to make phenomenological judgments about the duration of a visual display. In other words, the so-called “direct methods” for studying iconic memory do not provide information about iconic memory. Another implication is that iconic memory is not intimately tied to processes going on in the visual system (as visible persistence is); provided a stimulus is adequately legible, its physical parameters have little influence upon its iconic memory. The paper concludes by pointing out that there exists an alternative to the usual view of iconic memory as a precategorical sensory buffer. According to this alternative, iconic memory is post-categorical, occurring subsequent to stimulus identification. Here, stimulus identification is considered to be a rapid automatic process which does not require buffer storage, but which provides no information about episodic properties of a visual stimulus. Information about these physical stimulus properties must, in some way, be temporarily attached to a representation of the stimulus in semantic memory; and it is this temporarily attached physical information which constitutes iconic memory.     

The impersistence of false memory persistence

When subjects study lists of thematically related words they sometimes falsely recognise non-presented words related to the theme. The gist extraction account of these findings provided by fuzzy trace theory suggests that false recognition should decline substantially more slowly than true recognition across a delay. In two experiments we demonstrated that corrected recognition of targets and critical lures can decrease by equivalent amounts across a 48-hour delay. However the results for uncorrected recognition were mixed. In Experiment 1 we found evidence that uncorrected recognition of targets declined more rapidly than uncorrected recognition of critical lures. In Experiment 2, we found evidence that uncorrected recognition of targets and critical lures declined at equivalent rates. Results are discussed in terms of their implications for fuzzy trace and source monitoring accounts of false memories.     

Attentional factors in iconic memory and visible persistence

Arrays of 12 fragmentary letters were followed, at various intervals, by one randomly selected complementary letter fragment. On half the trials a partial-report cue (a vertical bar-marker) coincided with the second completion fragment. In Experiment 1 subjects fixated the centre of the to-be-identified letter location, whereas in Experiment 2 subjects fixated the centre of the array. In Experiment 1, the degree of integration and time between successive fragments were inversely related. Integration of fragmentary letters in Experiment 2, however, was uniformly low in the experimental and guessing control conditions. The results were discussed in terms of recent non-traditional accounts of iconic storage that emphasize post-categorical processing.     

Visual persistence and code selection in short-term memory for letters

Four experiments were conducted to examine temporal changes in visual and name codes and the relationship between them. Unlike earlier studies, the design included (a) several levels of visual similarity in addition to the conventional same case and different case conditions and (b) physical- as well as name-match tasks to provide direct evidence about subjects' retention of form information. The main results were as follows: First, the presence of multiple typefonts in the stimulus set does not eliminate convergence between the reaction time functions for the physical- and name-match conditions in a name-match task. Second, inclusion of a physical-match task, requiring subjects to retain form information, does not necessarily eliminate convergence in a primary, name-match task. When the secondary task does reduce convergence, however, the results suggest that it does this through its effect on the name-match function rather than on the physical-match function. Third, apart from difficulties with within-cluster typefont combinations, particularly at long interstimulus intervals, subjects can generally retain and use reliable information about letter form over the ISI range (.5--4.0 sec) used in the experiments. The results were thought to be consistent with the conclusion that convergence results from a combination of (a) a nonoptional decrease in the accessibility of the visual code as a function of increasing ISI and (b) an optional increase in the accessibility of the name code. Under ISI conditions at least, convergence cannot be attributed to either generation of a visual code of the alternative form of the target letter or to the absence of relevant form information.     

Dopaminergic modulation of the persistence of one-trial hippocampus-dependent memory

The persistence of new memory traces in the hippocampus, encoded following appropriate activation of glutamatergic receptors and the induction of synaptic plasticity, can be influenced by heterosynaptic activation of neuromodulatory brain systems. We therefore investigated the effects of a hippocampus-specific blockade of dopamine D1/D5 receptors on the persistence of spatial memory encoded in one trial using a delayed matching-to-place (DMP) task in a watermaze in which rats learn a new escape location each day. A within-subjects design was used such that both short (20 min) and long (6 h) retention intervals, and both drug (SCH23390, a D1/D5 receptor antagonist) and vehicle (aCSF) infusions were tested on different days in the same animals. Bilateral intrahippocampal infusion of SCH23390 (5 microg in 1 microL per side) prior to trial 1 (encoding) caused a differential impairment as a function of memory delay-with no effect during trial 2 (memory retrieval) after a 20-min interval, but a block of memory at 6 h. Further experiments revealed that infusion of SCH23390 immediately after trial 1 had no effect on retention 6 h later, and the poor memory seen at long retention intervals when the drug was present at encoding was not due to a state-dependent failure of retrieval. These results suggest that activation of D1/D5 receptors during memory encoding is necessary for the formation of a persistent memory trace in the hippocampus. The complementary effects of D1/D5 receptor blockade on the persistence of LTP and the duration of memory are consistent with the idea that changes in synaptic strength underlie memory.     

Participation of hippocampal cholinergic system in memory persistence for inhibitory avoidance in rats

Memory persistence needs a new event of consolidation 12h after the acquisition. We investigated the role of the cholinergic activity on the persistence of memory. For this purpose, we performed the treatments 9 or 12h after acquisition and the memory tested 2 or 7 days after inhibitory avoidance (IA) training. Here we report that activity of medial septum, by transitorily inactivating this structure with lidocaine 12h after IA training, is essential for memory persistence at the 7th day, but not for the formation at the 2nd day. We also report that muscarinic and nicotinic cholinergic receptors of CA1 area are engaged on memory persistence. Since scopolamine (mAChRs antagonist) and mecamylamine (nAChRs blocker) infusions, 12h post-training, demonstrated impairment on long term memory (LTM), persistence on the 7th day but no effect on LTM formation was found on the 2nd day in the IA test. The same effects were found with pirenzepine, an M1 antagonist. No effects on the formation and persistence of memory on the 2nd and 7th days were demonstrated after DHβE infusions (nAChRs subtype antagonist α4β2, α3β2). These findings suggest that mAChR and nAChR at the CA1 area, and also MS activation, are required for the persistence of memory.     

The persistence of memory: Contiguity effects across hundreds of seconds

A contiguity effect-the finding that stimuli that occur close together in time become associated to each other--is observed between words that are separated by several seconds. The traditional account of contiguity effects is that item representations become associated to each other while active in a short-term memory buffer--a limited-capacity store that can hold a small, integral number of items. Participants studied and free recalled 48 lists of words. At the end of the session, participants were given a surprise final free recall test on all of the items from all of the lists. In addition to a standard contiguity effect between items presented at nearby serial positions, we simultaneously observed a contiguity effect between items presented in different lists. This latter contiguity effect extended over several lists, or several hundred seconds, well beyond the range that can be attributed to a buffer holding a small, integral number of items.     

Short-term memory reactivation of a weak CS–US association promotes long-term memory persistence in conditioned odor aversion

In conditioned odor aversion (COA), the association of a tasteless odorized solution (the conditioned stimulus [CS]) with an intraperitoneal injection of LiCl (the unconditioned stimulus [US[), which produces visceral malaise, results in its future avoidance. The strength of this associative memory is mainly dependent on two parameters, that is, the strength of the US and the interstimuli interval (ISI). In rats, COA has been observed only with ISIs of ≤15 min and LiCl (0.15 M) doses of 2.0% of bodyweight, when tested 48 h after acquisition (long-term memory [LTM]). However, we previously reported a robust aversion in rats trained with ISIs up to 60 min when tested 4 h after acquisition (short-term memory [STM]). Since memories get reactivated during retrieval, in the current study we hypothesized that testing for STM would reactivate this COA trace, strengthening its LTM. For this, we compared the LTM of rats trained with long ISIs or low doses of LiCl initially tested for STM with that of rats tested for LTM only. Interestingly, rats conditioned under parameters sufficient to produce STM, but not LTM, showed a reliable LTM when first tested for STM. These observations suggest that under suboptimal training conditions, such as long ISIs or low US intensities, a CS–US association is established but requires reactivation in the short-term in order to persist in the long-term.

The dynamic and malleable nature of memories is a well-studied phenomenon. Traditionally, for memory formation to occur, a set of processes collectively known as consolidation are thought to be needed in order to stabilize memories, making them susceptible to modification during this period (Dudai et al. 2015). More recently a slightly distinct theory, known as memory integration, was proposed according to which memories are rapidly formed during learning without the need for consolidation, but any relevant information around the event can be integrated modifying them (Gisquet-Verrier and Riccio 2019). Common to both theories though, is that memories alternate between an inactive and an active state and modifications can mostly occur during the active state, which lasts for some time after learning, or during its reactivation due to retrieval (Lee et al. 2017; Albo and Gräff 2018; Gisquet-Verrier and Riccio 2019). Thus, memory malleability is explained either because consolidation can be altered or because additional information can be integrated with the initial memory (Bailey et al. 1996; Dudai 2004; Wixted 2004; Alberini et al. 2006; Lee et al. 2008, 2017; McGaugh and Roozendaal 2009; Roesler and Schröder 2011; Dudai et al. 2015; Nader 2015; Crossley et al. 2019; Gisquet-Verrier and Riccio 2019).In conditioned odor aversion (COA), an odorized tasteless solution (conditioned stimulus, CS) whose ingestion is followed by gastrointestinal malaise (unconditioned stimulus, US) is rejected in future encounters (conditioned response, CR). In most COA studies, a robust aversion has been observed only when the interstimulus interval (ISI) is ∼5 min, and no significant aversion can be seen when the ISI is >15 min (Hankins et al. 1973; Palmerino et al. 1980; Ferry et al. 1995, 1996; Ferry and di Scala 1997; Ferry et al. 2006; Chapuis et al. 2007). This observation has been attributed to a short-lasting memory of the odor that becomes unavailable for its association with the US after ISI >15 min. However, in all these instances the CR was measured 48 h after conditioning (LTM test), leaving up the possibility that CS–US association was formed but somehow did not last till the long-term. In keeping with this possibility, we previously reported a significant aversion during a test performed 4 h after conditioning (i.e., STM test) in rats trained with ISIs up to 60 min, three times longer than previously described (Tovar-Díaz et al. 2011). The LTM, however, was not tested so no further insight was provided regarding its persistence due to STM reactivation.Thus, in the current paper we hypothesized that a STM test would reactivate the initial memory, allowing it to further consolidate/integrate the information and to persist in the LTM. To test this possibility, we trained independent groups of rats with reduced US intensities or prolonged ISIs in a standard two-bottle choice COA paradigm and tested them twice at 4 and 48 h after conditioning. Our findings suggest that COA takes place under milder US and longer ISIs than previously thought and reactivating this memory during the STM test promotes its persistence in the LTM test.     

A brief retraining regulates the persistence and lability of a long-term memory

An experience extending the persistence of a memory after training Aplysia californica with inedible food also allows a consolidated memory to become sensitive to consolidation blockers. Long-term (24 h) memory is initiated by 5 min of training and is dependent on protein synthesis during the first few hours after training. By contrast, a more persistent (48 h) memory is dependent on a longer training session and on a later round of protein synthesis. When presented 24 h after training, a 3-min training that produces no memory alone can cause a memory that would have persisted for only 24 h to persist for 48 h. After a 48 h memory has been consolidated, 3 min of training also makes the memory sensitive to a protein-synthesis inhibitor. These findings suggest that a function of allowing a consolidated memory to become sensitive to blockers of protein synthesis may be to allow the memory to become more persistent.Long-term memory of an experience is dependent on a consolidation process that follows the experience. Before the memory is consolidated it is labile and can be disrupted (Lechner et al. 1999; Dudai 2004; Alberini and Taubenfeld 2008), particularly by blocking mRNA and protein synthesis (Alberini and Taubenfeld 2008; Klann and Sweatt 2008), which are needed to produce the changes in synaptic structure and function that underlie long-term memory (Sigurdsson et al. 2007; Bailey and Kandel 2008; De Roo et al. 2008). After long-term memory is established by the initial stages of consolidation, later rounds of consolidation may be needed to extend the persistence of the memory (Wittenberg and Tsien 2002; Bekinschtein et al. 2007). Consolidated memories may also be modified when they are retrieved (Dudai 2006; Alberini and Taubenfeld 2008). Retrieving a memory by exposure to the conditioned stimulus, or by re-experiencing aspects of the original training, can destabilize it and initiate an additional protein-synthesis-dependent process of memory stabilization (Nader 2003; Dudai 2006; Alberini and Taubenfeld 2008). The aim of this communication is to explore whether an experience that alone does not cause long-term memory can make a memory more persistent and can also destabilize a consolidated memory and makes it labile.Training Aplysia californica with inedible food until they stop responding to the food initiates long-term memory that can be measured as a reduction in the time to stop responding. Long-term memory is present 1, 2, and 7 d after a single training session (Schwarz et al. 1991). We examined some of the parameters of training that lead to persistence of memory by determining whether shorter training sessions also produce a persistent long-term memory.As in previous studies (Schwarz et al. 1991; Botzer et al. 1998; Lyons et al. 2005), Aplysia californica were trained with inedible food, the seaweed Ulva wrapped in plastic net. This food induced biting, leading to food entering the mouth. Animals then attempted to swallow the food. The netted food cannot be swallowed and it became lodged in the buccal cavity, producing repetitive failed swallowing responses. Food eventually left the buccal cavity. The experimenter continued to hold the food against the lips, inducing further biting responses, entries into the mouth, and failed swallows. As training proceeded many bites failed to cause entry of food into the mouth. When food did enter the mouth it stayed within for progressively shorter periods, eliciting fewer attempted swallows. In all animals, food was in the mouth eliciting failed attempts to swallow for at least 100 sec of the initial training, since previous experience showed that such animals almost always show long-term memory. Animals in which food was not in the mouth for 100 sec during training were discarded. A full training session until animals stop responding to food requires 10–25 min of training (Fig. 1). Such a training session caused long-term memory measured after 24 h or after 48 h (Fig. 1A). Memory was measured by comparing the time to stop responding to inedible food during training to the time to stop responding when animals were tested 24 or 48 h later, in a procedure identical to that during training. All tests of memory were performed using a blind procedure in which the experimenter was unaware of the previous training procedure.Open in a separate windowFigure 1.Memory 24 and 48 h after different training procedures. The figure shows the time to stop responding in a group of naïve animals trained with a full training session (training continued until animals stop responding to food), as well as the time to stop responding on memory trials 24 and 48 h later (N = 38 naïve animals [naïve animals were run as controls for the various other groups and data from the naïve animals were then combined. There was no significant difference between the various groups of naïve animals: P = 0.405, F_(5,32) = 1.053]); (A) N = 13 animals tested 24 h after a full training; N = 6 animals tested 48 h after a full training; (B) N = 9 animals tested 24 h after a 5-min training; N = 17 animals tested 48 h after a 5-min training; (C) N = 14 animals tested 24 h after a 3-min training; (D) N = 7 animals tested 48 h after a 5-min training, plus an additional 3-min training 24 h later. A one-way analysis of variance showed significant differences between the seven groups shown (P < 0.001, F_(6,97) = 11.95). A post-hoc test (Student-Newman-Keuls, α = 0.05) showed that there were no significant differences between the time to stop in naïve animals and in animals tested 48 h after a 5-min training, or in animals tested 24 h after a 3-min training, indicating that these treatments did not cause memory. By contrast, the times to stop in these three groups were significantly different from that in the other four groups, which were not significantly different from one another. These findings indicate significant memory 24 or 48 h after a full training, as well as 24 h after 5 min of training, and 48 h after 5 min of training with 3 min of reminder training, with no differences in memory after these 4 treatments. Standard errors are shown.We examined whether abbreviated training also caused long-term memory. First, we examined long-term memory when training is stopped after 5 min. During the first 5 min of a full training session, food is in the mouth, and animals are attempting to swallow for a mean of 70% of the time in the mouth during a full training session. Attempts to swallow are an integral part of the training (Katzoff et al. 2006). We confirmed an earlier finding (Botzer et al. 1998) that a 5-min training produced long-term memory measured 24 h after the training (Fig. 1B). However, we have now found that training animals for only 5 min did not cause long-term memory measured 48 h after training (Fig. 1B). A training session that was stopped after 3 min did not give rise to long-term memory measured at 24 h (Fig. 1C), indicating that the last 2 min of a 5-min training are necessary for the production of 24 h memory. These findings allowed us to examine the possible effects of an experience which itself does not cause memory, 3 min of training on memory persistence and memory lability.A 5-min training session gives rise to memory after 24 h, but not after 48 h, whereas additional training gives rise to 48 h memory. Must the additional training take the form of continuing to train animals during the initial training session, or can an additional 3 min of training that itself does not cause 24 h memory enhance the effect of a 5 min of training? To test the ability of a 3-min training to enhance memory, animals were trained with either a full training session, or with a training session that was abbreviated after 5 min. One group of animals trained for 5 min received an additional 3-min training 24 h after the initial training, whereas another group did not. Memory was tested 24 h later, 48 h after the initial training. Animals receiving a full training, and animals receiving a 5-min training plus a reminder consisting of a 3-min additional training, displayed 48 h memory (Fig. 1D; for a fuller presentation of this experiment, see Supplemental material), whereas animals receiving only a 5-min training, with no additional training, showed no 48 h memory. These data show that a 3-min training, which is itself ineffective in producing memory 24 h later, can lead to significant memory when it follows a 5-min training, which itself would not produce 48 h memory.In other learning tasks it has been shown that long-term memory is not a unitary process. An earlier round of protein synthesis is necessary for 24 h memory, but a more persistent memory (>24 h), and the synaptic plasticity underlying it, are dependent on later rounds of protein synthesis (Giustetto et al. 2003; Bekinschtein et al. 2007; Miniaci et al. 2008). We therefore examined whether 24 and 48 h memory differ in their dependence on protein synthesis adjacent to training, or on protein synthesis 6 h after training. The protein-synthesis inhibitor anisomycin was injected into the hemolymph either 10 min before training or 6 h after training. Animals were injected with a 1 cc solution of anisomycin at a concentration that caused a 10 µM concentration within the animals. This concentration blocks protein synthesis in ganglia (Schwartz et al. 1971). Controls were injected with 1 cc of artificial seawater (ASW–NaCl 460 mM, KCl 10 mM, CaCl₂ 11 mM, MgCl₂ 55 mM, and NaHCO₃ 5 mM). Treatment with anisomycin just before training blocked 24 h memory, but anisomycin treatment 6 h after training did not prevent the appearance of 24 h memory, indicating that 24 h memory is consolidated within the first 6 h after training (note that Fig. 2A shows the percent change in time to stop responding during the test of memory, with respect to the time to stop during training). By contrast, 48 h memory was blocked by anisomycin treatment 6 h after training (Fig. 2B), whereas treatment with ASW did not block 48 h memory.Open in a separate windowFigure 2.Protein synthesis dependence of 24 and 48 h memory. Data shows the memory test 24 or 48 h after training as a percent change [−([train-test]/train) × 100] from the initial training session. All tests of memory were after a full training session until animals stopped responding to the food. Memory was tested via two-tailed paired t-tests, in which the time to stop responding in a given animal during the initial training was compared with the time to stop responding 24 or 48 h later, when animals were tested. A significant decrease in the time to stop responding was used as an indicator of memory. Treatments showing such a decrease are marked (*). Standard errors are shown. (A) Anisomycin treatment blocks 24 h memory when applied just before training, but not when applied 6 h after training. Control animals (N = 8) not treated with anisomycin displayed significant 24 h memory (P < 0.001, t₍₇₎ = 10.15). Anisomycin applied 10 min before the training (N = 9) blocked memory, as shown by a lack of significant decrease in the time to stop between the initial training and the test after 24 h (P = 0.96, t₍₈₎ = 0.05). By contrast, application of anisomycin 6 h after the initial training (N = 7) did not block memory measured 24 h after training, as shown by significant savings after 24 h (P = 0.05, t₍₆₎ = 2.45). (B) Forty-eight hour memory is dependent on a later stage of protein synthesis. Anisomycin (N = 26), but not ASW (N = 5) applied 6 h after training blocks 48 h memory, as shown by significant memory after treatment with ASW (P = 0.007, t₍₄₎ = 5.08) but not with anisomycin (P = 0.49, t₍₂₅₎ = 0.69). However, a 3-min reminder training 24 h after the training (N = 12) rescues 48 h memory after it was blocked by anisomycin treatment 6 h after training (P = 0.01, t₍₁₁₎ = 2.93).Memory 48 h after training is dependent on protein synthesis 6 h after training. As shown above, 3 min of training can establish 48 h memory after a 5-min training that alone is too brief to establish 48 h memory. Can 3 min of training also establish 48 h memory after it has been blocked by inhibiting protein synthesis at 6 h? To test this possibility, animals were trained with inedible food until they stopped responding, and were then treated with either ASW or anisomycin 6 h later. One group of animals also received 3 min of training with inedible food 24 h after the initial training. When tested 48 h after training, memory was present in animals treated with ASW and in animals that had received the additional 3-min training, but not in animals receiving only the anisomycin treatment (Fig. 2B). This finding indicates that a 3-min training that is effective in causing 48 h memory after 5 min of training can also rescue 48 h memory after it has been blocked by anisomycin.If 3 min of training saves a blocked 48 h memory, it could also amplify an already-formed 48 h memory. We tested the effect on 48 h memory of a 3-min training 24 h after a full training session, which alone produces 48 h memory. There was no significant difference in memory between animals tested 24 h after training, and animals receiving a 3-min retraining, and then tested 48 h after training, indicating that the 3-min training did not affect the already consolidated 48 h memory (Fig. 3, cf. column 1 and column 3).Open in a separate windowFigure 3.Brief training makes memory labile. Twenty-four hours after training with inedible food, animals were treated with anisomycin, or with ASW. The animals treated with ASW (N = 9), as well as one of the two groups treated with anisomycin (N = 9), were also given a 3-min training session 10 min later. Memory was then tested again 24 h later, 48 h after the training, by comparing the time to stop measured 48 h after training with the time to stop measured during the original training session, using a two-tailed paired t-test. A significant decrease in the time to stop responding was used as an indicator of memory. Data are also shown for 24 h memory after a full training session, to allow a test of whether a 3-min retraining at 24 h improves memory tested at 48 h. Treatment with anisomycin alone (N = 8) did not block 48 h memory (P = 0.002, t₍₇₎ = 4.66). The 3-min reminder training plus treatment with ASW also did not block 48 h memory (P = 0.001, t₍₈₎ = 5.02). By contrast, when the 3-min reminder training was preceded by anisomycin treatment, there was no significant difference between training and the 48 h test (P = 0.27, t₍₈₎ = 1.18), indicating that the 3-min reminder allowed the anisomycin to block 48 h memory. Note that there is also no significant difference in savings after the 3-min training following ASW treatment and 24 h memory following training (P = 0.13, t₍₁₀₎ = 1.63), indicating that the 3-min training on day 2 alone did not affect memory.The 3-min training does not affect an already-formed 48 h memory, but does cause effects 24 h later if the memory is not fully consolidated. Formation of a long-term memory requires protein synthesis, and recalling a consolidated memory can make a memory sensitive to inhibitors of protein synthesis (Nader et al. 2000). Does a 3-min training 24 h after an initial full training initiate a renewed dependence of 48 h memory on protein synthesis? Animals were trained to criterion and then subjected to either anisomycin, or ASW, 24 h later. Both groups then received a 3-min reminder training 10 min later. Memory was then assessed 24 h later (48 h after initial training). There was significant memory 48 h after the training after treatment with ASW, but not after treatment with anisomycin, indicating that the 3-min reminder training restored the ability of anisomycin to block memory (Fig. 3).Our data have shown that 3 min of training with inedible food alone does not produce long-term memory (Fig. 1), and does not amplify an already established 48 h memory (Fig. 3). Nonetheless, 3 min of training induces a protein-synthesis-dependent state in which memory can be modified (Figs. 2, ​,3).3). After a previous training leading to only 24 h memory (Fig. 1), or after a treatment blocking 48 h memory, the 3-min training makes the memory more persistent (Fig. 2). In addition, after a 48 h memory has already been consolidated, 3 min of training makes the memory labile, so that it can be blocked by inhibitors of protein synthesis (Fig. 3).Reconsolidation is a process by which a consolidated memory returns to a protein-synthesis-dependent labile state by retrieving the memory (e.g., Nader et al. 2000; Sangha et al. 2003; Kemenes et al. 2006). In learning that food is inedible 3 min of training makes the memory labile. There has been much speculation on the possible function of memory reconsolidation. It has been suggested that the destabilization of memory by retrieval could function as a means to update and modify the magnitude and the persistence of the original memory trace (Dudai 2002, 2006). There is good evidence that reconsolidation can update (Rodriguez-Ortiz et al. 2005; Morris et al. 2006), strengthen (Frenkel et al. 2005; Tronson et al. 2006; Lee 2008), or modify (Rossato et al. 2006) memories, as well as block them (Nader et al. 2000), but the possible role of reconsolidation in regulating memory persistence has not been examined. Indeed, many of the previous studies on reconsolidation used a conditioned stimulus (CS) alone as a reminder, and thereby caused extinction along with reconsolidation (Eisenberg et al. 2003; Pedreira and Maldonado 2003), rather than causing a strengthening of memory. Previous studies have indicated that after memory is initially consolidated, its persistence is dependent on successive waves of protein synthesis (Giustetto et al. 2003; Bekinschtein et al. 2007; Miniaci et al. 2008) and that reactivation of a memory improves its persistence (Spear 1973). Later waves of protein synthesis affecting persistent memories could be modulated or modified by retrieving a memory.We have taken advantage of a memory task affecting Aplysia feeding to examine the possibility that memory retrieval via a brief additional training affects later waves of protein synthesis, and thereby affects the persistence of a memory. We found that pairing a brief additional training with block of protein synthesis blocks memory (Fig. 3). We also found that a more persistent memory measured at 48 h is dependent on a longer training session (Fig. 1), and a later wave of protein synthesis (Fig. 2) than is 24 h memory. Retrieval of memory by a 3-min retraining can establish 48 h memory even when the latter portion of training is absent (Fig. 1), or when the later wave of protein synthesis is blocked (Fig. 2). This finding suggests that the initial experience required to establish 48 h memory, as well as the wave of protein synthesis elicited by this experience, can be deferred. A later experience, and a later wave of protein synthesis, can substitute for the absence of experience in the initial training, or for the blocked wave of protein synthesis. In addition to creating a more persistent memory, a 3-min retraining also makes a consolidated memory sensitive to blocking by inhibitors of protein synthesis (Fig. 3). Thus, a function of experiences that permit reconsolidation may also be to extend the persistence of a memory.In our study we cannot exclude the possibility that the 3-min retraining does more than just retrieve memory, and thereby make it labile. The increased persistence of memory could be caused by processes initiated by the 3-min training, such as increased consolidation, that are not related to the ability of the added training to make the memory labile. Indeed, previous studies have suggested that memory consolidation and reconsolidation may utilize different molecular mechanisms (Taubenfeld et al. 2001; Lee et al. 2004; Alberini 2005). The different molecular mechanisms activated by consolidation or reconsolidation have been used to classify the process by which retrieval affects memory, although use of the molecular markers to classify a behavioral process is controversial (Nader et al. 2005). Such studies have shown that changing a memory when it is retrieved sometimes utilizes a molecular mechanism for consolidation (Tronel et al. 2005), and sometimes for reconsolidation (Lee 2008). In the learning task utilized we have not examined separate molecular markers for consolidation and reconsolidation, raising the possibility that a 3-min retraining affects persistence by activating molecular mechanisms that are specifically associated with a separate round of consolidation, rather than activating reconsolidation.Memory reconsolidation also affects a number of other molluscan learning paradigms (Sekiguchi et al. 1997; Sangha et al. 2003; Gainutdinova et al. 2005; Kemenes et al. 2006). In some, the memory becomes labile when animals are exposed to a CS alone, which does not itself create memory, whereas in others the memory becomes labile only when the CS is paired with an unconditioned stimulus (US), as in the original training (see Eisenhardt and Stollhoff 2008). In our experiments, memory was made labile by a second training session, which was shorter than that needed to itself create memory. It will be of interest to determine whether components of the experience alone in which animals learn that food is inedible do not give rise to memory, such as lip stimulation alone (Schwarz et al. 1988), can also give rise to reconsolidation, although they would not cause a more persistent memory.Where in the Aplysia nervous system are molecular changes related to reconsolidation and the persistence of memory localized? The earliest molecular changes leading to long-term memory that a food is inedible (e.g., increased expression of C/EBP and sensorin), are localized to the buccal ganglia, specifically to a population of mechanoafferents (Levitan et al. 2008a,b). It is possible that the later molecular changes leading to a persistent memory are also localized to these neurons, similar to the localization to the same sensory neurons of earlier and later molecular events leading to long-term facilitation underlying sensitization in Aplysia (Miniaci et al. 2008). However, it is also possible that the later phases of consolidation, and reconsolidation, may arise by molecular changes localized to other sites with the Aplysia nervous system, similar to the movement of earlier and later phases on long-term declarative memories from the hippocampus to the neocortex (Squire and Kandel 1999). Future studies will need to examine these points.     

Multiple processes in prospective memory retrieval: factors determining monitoring versus spontaneous retrieval

Theoretically, prospective memory retrieval can be accomplished either by controlled monitoring of the environment for a target event or by a more reflexive process that spontaneously responds to the presence of a target event. These views were evaluated in Experiments 1-4 by examining whether performing a prospective memory task produced costs on the speed of performing the ongoing task. In Experiment 5, the authors directly tested for the existence of spontaneous retrieval. The results supported the multiprocess theory (M. A. McDaniel & G. O. Einstein, 2000) predictions that (a) spontaneous retrieval can occur and can support good prospective memory and (b) depending on task demands and individual differences, people rely to different degrees on monitoring versus spontaneous retrieval for prospective remembering.     

On the persistence of very early memory traces in psychoanalysis, myth, and religion

It is tentatively proposed that fragments of certain early perceptual experiences of the parental objects such as the sight of the face and the breast of the mother, the smiling or angry expression of the face, the pleasing or disagreeable character of the voice, the soft touch or rough handling, the sight of the hands may occasionally be recoverable in the course of analysis. Some mythological figures and religious symbols may also hark back to similar motifs. The relation of this material to early modes of perception and the beginnings of object relations is examined. The data are correlated with the findings of child observation and of modern experimental psychology.     

Late expression of brain-derived neurotrophic factor in the amygdala is required for persistence of fear memory

In many instances, increase in neuronal activity can induce biphasic secretion of a modulator. The initial release of the modulator triggers the induction of synaptic plasticity, whereas the second-phase release reinforces the efficacy of synaptic transmission and growth of dendrites and axons. In this study, we showed that fear conditioning not only induced the first but also a second peak of brain-derived neurotrophic factor (BDNF) expression. Fluorescent immunohistostaining confirmed that BDNF expression increased at 1 and 12 h after conditioning and returned to baseline at 30 h after conditioning. Mature BDNF expression increased in a similar manner. TrkB-IgG or K252a infusion before training impaired fear memory on days 1 and 7 after training. In contrast, TrkB-IgG or K252a infusion 9 h after fear conditioning did not affect memory retention on day 1 after training but impaired fear memory on day 7 after training. Fear conditioning significantly enhanced Zif268 expression in the amygdala at 12 h after training; this enhanced expression was completely inhibited by TrkB-IgG infusion 9 h after training. The level of growth-associated protein 43 (GAP-43), a marker of newly formed synapses, in the amygdala increased 7 days after fear conditioning. Moreover, conditioned rats had higher AMPA/NMDA ratio than unpaired rats. These results suggest that consolidated memory could be continuously modulated by previous molecular changes produced during memory acquisition.     

The persistence of content-specific memory operations: Priming effects following a 24-h delay

The duration of long-term semantic priming is typically described in minutes. Woltz and Was (2007) found that priming effects following processing in working memory were relatively long-lasting, reporting there was no decrease in priming effects following 32 intervening Stroop-like trials. These findings were interpreted as an increased availability of long-term memory elements, in part due to memory for prior operations, and as not being solely explicable by spreading-of-activation accounts of priming. The present study was designed to test the persistence of these effects following a 24-h delay. In the present study, priming effects were found to be present following a minimum of a 24-h delay between processing of information in working memory and measures of increased availability of long-term memory elements. The results are discussed, in the context of long-term semantic priming, as being the result of persistent memory for prior cognitive operations.     

The persistence of inferences in memory for younger and older adults: Remembering facts and believing inferences

Research shows that younger adults have difficulty forgetting inferences that they make after reading a passage, even if the information that the inferences are based on is later shown to be untrue. The present study examined the effects of these inferences on memory in the lab and tested whether older adults, like younger adults, are influenced by the lingering effects of false inferences. In addition, this study examined the nature of these inferences, by examining younger and older adults’ subjective experiences and confidence associated with factual recall and incorrect inference recall. The results showed that younger and older adults were equally susceptible to the continued influence of inferences. Both younger and older adults tended to remember facts from the stories but to believe their inferences, although confidence judgments did not differ for facts and inferences.     

The roles of working memory and intervening task difficulty in determining the benefits of repetition

Memory is better when learning events are spaced, as compared with massed (i.e., the spacing effect). Recent theories posit that retrieval of an item’s earlier presentation contributes to the spacing effect, which suggests that individual differences in the ability to retrieve an earlier event may influence the benefit of spaced repetition. The present study examined (1) the difficulty of task demands between repetitions, which should modulate the ability to retrieve the earlier information, and (2) individual differences in working memory in a spaced repetition paradigm. Across two experiments, participants studied a word set twice, each separated by an interval where duration was held constant, and the difficulty of the intervening task was manipulated. After a short retention interval following the second presentation, participants recalled the word set. Those who scored high on working memory measures benefited more from repeated study than did those who scored lower on working memory measures, regardless of task difficulty. Critically, a crossover interaction was observed between working memory and intervening task difficulty: Individuals with low working memory scores benefited more when task difficulty was easy than when it was difficult, but individuals with high working memory scores produced the opposite effect. These results suggest that individual differences in working memory should be considered in optimizing the benefits of repetition learning.     

The persistence of thought: evidence for a role of working memory in the maintenance of task-unrelated thinking

Tasks that tax working memory (WM) have consistently been found to decrease mind wandering. These findings may indicate that maintenance of mind wandering requires WM resources, such that mind wandering cannot persist when WM resources are being consumed by a task. An alternative explanation for these findings, however, is that mind wandering persists without the support of WM but is nonetheless decreased during any demanding task because good task performance requires that attention be restricted from task-unrelated thought (TUT). The present study tested these two competing theories by investigating whether individuals with greater WM resources mind-wander more during an undemanding task, as would be predicted only by the theory that WM supports TUT. We found that individuals with higher WM capacity reported more TUT in undemanding tasks, which suggests that WM enables the maintenance of mind wandering.     

Loss and persistence of implicit memory for sound: Evidence from auditory stream segregation context effects

An important question is the extent to which declines in memory over time are due to passive loss or active interference from other stimuli. The purpose of the present study was to determine the extent to which implicit memory effects in the perceptual organization of sound sequences are subject to loss and interference. Toward this aim, we took advantage of two recently discovered context effects in the perceptual judgments of sound patterns, one that depends on stimulus features of previous sounds and one that depends on the previous perceptual organization of these sounds. The experiments measured how listeners’ perceptual organization of a tone sequence (test) was influenced by the frequency separation, or the perceptual organization, of the two preceding sequences (context1 and context2). The results demonstrated clear evidence for loss of context effects over time but little evidence for interference. However, they also revealed that context effects can be surprisingly persistent. The robust effects of loss, followed by persistence, were similar for the two types of context effects. We discuss whether the same auditory memories might contain information about basic stimulus features of sounds (i.e., frequency separation), as well as the perceptual organization of these sounds.     

Eye movements as a gatekeeper for memorization: evidence for the persistence of attentional sets in visual memory search

Attention is known to serve multiple goals, including the selection of information for further perceptual analysis (selection for perception) and for goal-directed behavior (selection for action). Here, we study the role of overt attention (i.e., eye movements) as a gatekeeper for memorization processes (selection for memorization). Subjects memorized complex multidimensional stimulus displays and subsequently indicated whether a specific (probe) item was present. In Experiment 1 we utilized an incidental learning setting where in the beginning only a subset of display stimuli was relevant, whereas in a transfer block all stimuli were possible probe items. In Experiment 2, we used an explicit learning setting within a between-group design. Response times and gaze patterns indicated that subjects learned to ignore irrelevant stimuli while forming memory representations. The findings suggest that complex feature binding processes in peripheral vision may serve to guide overt selective attention, which eventually contributes to filtering out irrelevant information even in highly complex environments. Gaze patterns suggested that attentional control settings persisted even when they were no longer required.     

Structure-from-motion: dissociating perception, neural persistence, and sensory memory of illusory depth and illusory rotation

In the structure-from-motion paradigm, physical motion on a screen produces the vivid illusion of an object rotating in depth. Here, we show how to dissociate illusory depth and illusory rotation in a structure-from-motion stimulus using a rotationally asymmetric shape and reversals of physical motion. Reversals of physical motion create a conflict between the original illusory states and the new physical motion: Either illusory depth remains constant and illusory rotation reverses, or illusory rotation stays the same and illusory depth reverses. When physical motion reverses after the interruption in presentation, we find that illusory rotation tends to remain constant for long blank durations (T _blank ≥ 0.5 s), but illusory depth is stabilized if interruptions are short (T _blank ≤ 0.1 s). The stability of illusory depth over brief interruptions is consistent with the effect of neural persistence. When this is curtailed using a mask, stability of ambiguous vision (for either illusory depth or illusory rotation) is disrupted. We also examined the selectivity of the neural persistence of illusory depth. We found that it relies on a static representation of an interpolated illusory object, since changes to low-level display properties had little detrimental effect. We discuss our findings with respect to other types of history dependence in multistable displays (sensory stabilization memory, neural fatigue, etc.). Our results suggest that when brief interruptions are used during the presentation of multistable displays, switches in perception are likely to rely on the same neural mechanisms as spontaneous switches, rather than switches due to the initial percept choice at the stimulus onset.     

Adaptive memory: determining the proximate mechanisms responsible for the memorial advantages of survival processing

J. S. Nairne, S. R. Thompson, and J. N. S. Pandeirada (2007) suggested that our memory systems may have evolved to help us remember fitness-relevant information and showed that retention of words rated for their relevance to survival is superior to that of words encoded under other deep processing conditions. The authors present 4 experiments that uncover the proximate mechanisms likely responsible. The authors obtained a recall advantage for survival processing compared with conditions that promoted only item-specific processing or only relational processing. This effect was eliminated when control conditions encouraged both item-specific and relational processing. Data from separate measures of item-specific and relational processing generally were consistent with the view that the memorial advantage for survival processing results from the encoding of both types of processing. Although the present study suggests the proximate mechanisms for the effect, the authors argue that survival processing may be fundamentally different from other memory phenomena for which item-specific and relational processing differences have been implicated. (PsycINFO Database Record (c) 2010 APA, all rights reserved).