Self‐ and cross‐citations in the Journal of Applied Behavior Analysis and the Journal of the Experimental Analysis of Behavior: 2004‐2018

We examined self‐ and cross‐citations in the Journal of Applied Behavior Analysis (JABA) and the Journal of the Experimental Analysis of Behavior (JEAB) from 2004 through 2018. Mean annual levels of self‐citations for JABA and JEAB were 40.1% and 28.7%, respectively. Overall, 5.1% of JABA citations were JEAB articles, and 2.3% of JEAB citations were JABA articles. Although overall cross‐citation levels were relatively low, 28.7% of the JABA articles reviewed had at least one JEAB citation, and 27.5% of the JEAB articles reviewed had at least one JABA citation. Authors in both journals cited articles addressing the topics of matching and motivating operations. The extent to which the basic and applied sectors of behavior analysis interact depends on how the interaction is measured. Nonetheless, the degree of interaction is growing, which is a good thing for the discipline.     

Beyond inference by eye: Statistical and graphing practices in JEAB, 1992‐2017

Debates about the utility of p values and correct ways to analyze data have inspired new guidelines on statistical inference by the American Psychological Association (APA) and changes in the way results are reported in other scientific journals, but their impact on the Journal of the Experimental Analysis of Behavior (JEAB) has not previously been evaluated. A content analysis of empirical articles published in JEAB between 1992 and 2017 investigated whether statistical and graphing practices changed during that time period. The likelihood that a JEAB article reported a null hypothesis significance test, included a confidence interval, or depicted at least one figure with error bars has increased over time. Features of graphs in JEAB, including the proportion depicting single‐subject data, have not changed systematically during the same period. Statistics and graphing trends in JEAB largely paralleled those in mainstream psychology journals, but there was no evidence that changes to APA style had any direct impact on JEAB. In the future, the onus will continue to be on authors, reviewers and editors to ensure that statistical and graphing practices in JEAB continue to evolve without interfering with characteristics that set the journal apart from other scientific journals.     

A brief nap is beneficial for human route-learning: The role of navigation experience and EEG spectral power

Here, we examined the effect of a daytime nap on changes in virtual maze performance across a single day. Participants either took a short nap or remained awake following training on a virtual maze task. Post-training sleep provided a clear performance benefit at later retest, but only for those participants with prior experience navigating in a three-dimensional (3D) environment. Performance improvements in experienced players were correlated with delta-rich stage 2 sleep. Complementing observations that learning-related brain activity is reiterated during post-navigation NREM sleep in rodents, the present data demonstrate that NREM sleep confers a performance advantage for spatial memory in humans.A growing body of animal and human literature suggests that the consolidation of memories occurs optimally during periods of post-learning sleep. Nonrapid eye movement sleep (NREM), in particular, may be beneficial for the offline consolidation of hippocampus-dependent learning. The neurophysiological basis for this hypothesis is derived largely from electrophysiological studies in rodents, demonstrating that patterns of hippocampal place cell activity first seen during waking exploration are later reexpressed during post-learning sleep (Wilson and McNaughton 1994; Kudrimoti et al. 1999; Nadasdy et al. 1999; Ji and Wilson 2007). Behavioral studies in humans meanwhile demonstrate that NREM sleep is beneficial for declarative memory performance, relative to equivalent periods of wakefulness (Plihal and Born 1997; Tucker et al. 2006). However, the memory tasks typically employed in human research are quite different from those used in rodents, with human studies most often focusing on the memorization of verbal or visual stimuli (Plihal and Born 1997; Schabus et al. 2004; Clemens et al. 2005; Ellenbogen et al. 2006; Tucker et al. 2006; Daurat et al. 2008). Thus far, sleep-dependent memory reactivation has not been established to be directly beneficial for memory performance in an animal model, as the protocols employed in this research typically involve well-learned simple tasks which do not easily lend themselves to measurement of learning across time (Wilson and McNaughton 1994; Kudrimoti et al. 1999). Although the hippocampal memory reactivation described in rodents is a possible explanation for the effect of NREM sleep on human declarative memory, widely divergent methodologies employed across species prohibit confidence in this conclusion.Bridging this conceptual gap, a small handful of studies have begun to explore the relationship between spatial navigation and NREM sleep in humans. Notably, a PET study by Peigneux et al. (2004) demonstrated that learning-related hippocampal activity seen while training on a virtual maze task is again expressed during post-learning human sleep. Furthermore, this hippocampal reactivation strongly predicted overnight improvement on the task (Peigneux et al. 2004). Additional studies have suggested a link between sleep and other types of spatial-related learning, including mental rotation performance (Plihal and Born 1999), the ability to reproduce a complex figure (Clemens et al. 2006; Tucker and Fishbein 2008), performance on a computerized version of Milner''s (1965) “bolt head” maze (Tucker and Fishbein 2008), and memory for the location of verbal information on a screen (Daurat et al. 2008).Yet it remains unclear whether sleep, relative to wakefulness, provides a performance benefit for human route-learning in the context of a realistic spatial environment. Navigation through virtual environments is a strongly hippocampus-dependent task (Peigneux et al. 2004; Astur et al. 2005) and provides an experimental model closely paralleling the spatial exploration tasks employed in the rodent literature. However, the few studies reporting effects of sleep on human navigation performance have been contradictory. Using a navigation task similar to that of Peingeux et al. (2004), Orban et al. (2006) failed to detect any effect of post-learning sleep deprivation on maze performance but did find evidence of altered task-related brain activity, concluding that sleep supports “covert” memory reorganization (Orban et al. 2006). In direct contrast, Ferrara et al. found that spatial memory is improved when a retention interval falls across a night of sleep, relative to when route memory must be retained during daytime wakefulness, or across a night of sleep deprivation (Ferrara et al. 2006, 2008).The present study clarifies these issues by examining the effect of a post-learning nap on complex route-learning in a three-dimensional (3D) virtual environment. When controls are tested at a different time of day than sleep participants, circadian confounds may present a substantial problem. Alternatively, overnight protocols employing sleep-deprived subjects necessarily suffer from confounds related to this sleep deprivation during the retention interval. The use of a daytime nap as a sleep intervention avoids these pitfalls by allowing all subjects to be trained and tested at the same circadian time, and in the absence of sleep deprivation. A series of recent studies confirm that a daytime nap is sufficient to induce performance improvements on declarative and procedural memory tasks, relative to wake subjects (Mednick et al. 2003; Backhaus and Junghanns 2006; Nishida and Walker 2006; Tucker et al. 2006; Lahl et al. 2008; Tucker and Fishbein 2008).Participants (n = 53, 34 female) were trained on a virtual maze-learning task at 12:30 pm. Following training, nap participants lay down for a 1.5-h sleep opportunity. These subjects were allowed to obtain as much NREM sleep as possible but were awoken at the first signs of REM (see Table 

IMPLICATIONS OF BEHAVIORAL PHARMACOLOGY RESEARCH FOR APPLIED BEHAVIOR ANALYSES: JEAB'S SPECIAL ISSUE CELEBRATING THE CONTRIBUTIONS OF JOSEPH V. BRADY (MARCH 1994)

We review four articles from JEAB's March 1994 issue celebrating the contributions of Joseph V. Brady. These articles have implications for studying private events and for studying multiple operants. We suggest that regularly including self-reports about private events in behavioral pharmacological research has resulted in an accumulated knowledge that has facilitated examination of interesting relations among self-reports, environmental factors, and other observable behaviors. Methodological lessons that behavioral pharmacologists have learned regarding the study of multiple operants are also relayed. We provide examples of how these lessons could be useful to applied behavior analysts studying nonpharmacological issues.     

Confirmation of linear system theory prediction: Changes in Herrnstein's k as a function of changes in reinforcer magnitude

Eight human subjects pressed a lever on a range of variable-interval schedules for 0.25¢ to 35.0¢ per reinforcement. Herrnstein's hyperbola described seven of the eight subjects' response-rate data well. For all subjects, the y-asymptote of the hyperbola increased with increasing reinforcer magnitude and its reciprocal was a linear function of the reciprocal of reinforcer magnitude. These results confirm predictions made by linear system theory; they contradict formal properties of Herrnstein's account and of six other mathematical accounts of single-alternative responding.     

On the impact of human operant research: Asymmetrical patterns of cross-citation between human and nonhuman research

Reactions to published accounts of research with human subjects, as well as research with nonhuman subjects, were assessed by examining citations in several samples of empirical articles in the Journal of the Experimental Analysis of Behavior. A stable, asymmetrical pattern emerged: Nonhuman research was cited in both human and nonhuman articles, but human research was cited primarily in human articles. Thus, human operant research appears to have had little influence on the nonhuman research which constitutes the bulk of the experimental analysis of behavior. Interpretation of this lack of impact depends on the functions one envisions for human research, several of which are discussed.     

Individual differences in the game motives of Own,Relative, and Joint gain

Two hundred and eighteen undergraduates (94 males and 124 females) made decisions in same-sex dyads across four types of 3-choice decomposed games. An analysis of each subject's choices was performed to see if he or she consistently pursued one of the three motives of Own (Individualism), Relative (Competition) or Joint (Cooperation) gain across all four decomposed games. Sixty-six percent of the subjects manifested such consistency, and sex of subject was unrelated to which goal was pursued. Of the remaining 32%, a sizable subgroup ($\text{1}\text{3}$) was shown to be making its choices in an Altruistic fashion, attempting to maximize the outcomes of the other subject. An analysis of variance of the F scale scores of subjects in these motivational categories yielded an effect (p < .025), with the Competitive group having the highest, and the Altruistic group having the lowest mean authoritarianism score. Correlational analyses indicated negative r's between degree of Competition and F score, positive r's between degree of Altruism and F, but no apparent relation between F and either Individualistic or Joint gain choice.     

Midlife decline in declarative memory consolidation is correlated with a decline in slow wave sleep

Sleep architecture as well as memory function are strongly age dependent. Slow wave sleep (SWS), in particular, decreases dramatically with increasing age, starting already beyond the age of 30. SWS normally predominates during early nocturnal sleep and is implicated in declarative memory consolidation. However, the consequences of changes in sleep across the life span for sleep-associated memory consolidation have not been evaluated so far. Here, we compared declarative memory consolidation (for word-pair associates) during sleep in young and middle-aged healthy humans. The age groups (18–25 vs. 48–55 yr) did not differ with regard to learning performance before retention periods that covered, respectively, the first and second half of nocturnal sleep. However, after early retention sleep, where the younger subjects showed distinctly more SWS than the middle-aged (62.3 ± 3.7 min vs. 18.4 ± 7.2 min, P < 0.001), retrieval of the word pairs in the middle-aged was clearly worse than in the young (P < 0.001). In contrast, declarative memory retention did not differ between groups after late sleep, where retention was generally worse than after early sleep (P = 0.005). Retention of declarative memories was the same in both age groups when sleep periods containing equal amounts of SWS were compared, i.e., across late sleep in the young and across early sleep in the middle-aged. Our results indicate a decline in sleep-associated declarative memory consolidation that develops already during midlife and is associated with a decrease in early nocturnal SWS.     

Critical role of the cholinergic system for object-in-place associative recognition memory

Object-in-place memory, which relies on the formation of associations between an object and the place in which it was encountered, depends upon a neural circuit comprising the perirhinal (PRH) and medial prefrontal (mPFC) cortices. This study examined the contribution of muscarinic cholinergic neurotransmission within this circuit to such object-in-place associative memory. Intracerebral administration of scopolamine in the PRH or mPFC impaired memory acquisition, but not retrieval and importantly we showed that unilateral blockade of muscarinic receptors simultaneously in both regions in opposite hemispheres, significantly impaired performance. Thus, object-in-place associative memory depends upon cholinergic modulation of neurones within the PRH-PFC circuit.Recognition memory enables individuals to judge whether stimuli have been encountered before. In its most basic form such judgments may be made on the basis of simply whether a stimulus is familiar or novel (familiarity discrimination). However, these judgments may also be made using associations formed between a stimulus and the location or environmental setting in which it was previously encountered. Such object-in-place associative memory in animals is of particular interest as it is acquired rapidly and it requires the integration of object and spatial information and thus has been described as an analog of human episodic memory (Wilson et al. 2008).The perirhinal cortex (PRH) in the medial temporal lobe is a critical neural structure for object recognition and object-in-place associative memory (Bussey et al. 2000; Barker et al. 2007), but unlike object recognition, this memory process is also dependent on the medial prefrontal cortex (mPFC) (Kesner and Ragozzino 2003; Browning et al. 2005; Barker et al. 2007) and crucially it has been shown to depend upon a functional interaction between the PRH and mPFC, with each region making a distinct cognitive contribution to the memory formation (Barker et al. 2007; Barker and Warburton 2008).Having identified two neural regions critical for object-in-place associative memory, we now extend our investigations to explore the underlying cellular mechanisms mediating acquisition or retrieval of this memory process. The present study focused on the neurotransmitter acetylcholine as cholinergic innervation of the PRH is crucial for familiarity discrimination (Tang et al. 1997; Easton and Gaffan 2001; Warburton et al. 2003; Abe et al. 2004; Winters and Bussey 2005). In contrast, the role of muscarinic receptor neurotransmission in the PRH or mPFC in object-in-place associative memory is unknown. Further, while it might appear that object recognition memory and object-in-place memory are likely to share common neural substrates, recent data from our laboratory suggest that this may not be the case (Griffiths et al. 2008).To explore the importance of muscarinic cholinergic neurotransmission within the PRH-mPFC circuit for object-in-place memory, rats were implanted with bilateral cannulae aimed at the PRH or mPFC or both regions to allow direct intracerebral administration of scopolamine during distinct stages of an object-in-place task. Memory performance was tested following either a short (5 min) or long (1 h) retention delay. All animal procedures were performed in accordance with the United Kingdom Animals Scientific Procedures Act (1986) and associated guidelines. Details of the surgery, infusion procedures, behavioral testing, and histology have been published previously (Barker and Warburton 2008). Briefly, male DA rats (230–250 g, Bantin and Kingman, UK) housed under a 12-h/12-h light/dark cycle (light phase 18:00–6:00 h), were anesthetized with isoflurane (induction 4%, maintenance 2%–3%) and surgically implanted with bilateral cannulae aimed at either the PRH or mPFC or both regions. After a two-week recovery period all rats were handled, habituated, and then tested in the object-in-place memory task.Sample phase: Each rat was placed in a black open-topped wooden arena (50 × 90 × 100 cm) containing four different objects (A, B, C, D) constructed from “Duplo” (Lego UK Ltd.). The walls of the arena were surrounded with a black cloth to a height of 1.5 m, and the floor covered with sawdust. The objects were placed 15 cm from the walls (see Fig. 1A) and each rat was allowed to explore the objects for 5 min, after which it was removed for the delay (5 min or 1 h). Exploratory behavior was defined as the animal directing its nose toward the object at a distance of <2 cm. Any other behavior, such as looking around while sitting on or resting against the object, was not recorded. Subjects that failed to complete a minimum of 15-s exploration in the sample phase or 10 s of exploration in the test phase were excluded from the analysis.Open in a separate windowFigure 1.Diagrammatic representations of the individual infusion sites in each animal. (A) Bilateral medial prefrontal (mPFC) group. (B) Bilateral perirhinal (PRH) group. (C) The mPFC infusion sites of the PRH+mPFC group. (D) The PRH infusion sites of the PRH+mPFC group. All of the infusion sites were within the PRH or mPFC.Test phase: Two of the objects, e.g., B and D, exchanged positions and the subjects were replaced in the arena for 3 min. The time spent exploring the two objects that had changed position was compared to the time spent exploring the two objects that had remained in the same position. If object-in-place memory is intact, subjects spend more time exploring the “moved” objects, compared to the “unmoved” objects. Scopolamine hydrobromide (Sigma-Aldrich) dissolved in sterile 0.9% saline solution was administered at a dose of 10 μg/μL per hemisphere (Schroeder and Packard 2002; Warburton et al. 2003; Winters et al. 2006); control infusions consisted of saline. The infusions were given either 15 min before the sample phase or 15 min before the test phase. At the end of the experiment, each rat was anesthetized and perfused transcardially. Coronal brain sections (40 μm) were stained with cresyl-violet to verify the cannulae locations. All the rats in the PRH group had the tip of the bilateral cannulae in the PRH and all the rats in the mPFC group had tips in the ventral portion of the prelimbic or dorsal portion of the infralimbic region of the prefrontal cortex (Fig. 1B). From unpublished observations, using Indian ink and radiolabeled scopolamine, the region infused is estimated to be 1–1.5 mm³, and largely confined to perirhinal cortex or the prelimbic/infralimbic regions of the prefrontal cortex. This spread is consistent with previously quoted results in other brain regions (Martin 1991; Izquierdo et al. 2000; Attwell et al. 2001). Figure 2, A and B show the performance of the rats receiving bilateral infusions of scopolamine or vehicle into either the PRH (n = 12) or mPFC (n = 12) 15 min prior to the sample phase. After a minimum of 48 h, vehicle or scopolamine was infused in a cross-over design and the animal retested using different objects. A three-way ANOVA (drug × region × delay) showed that scopolamine infusion into either region significantly impaired the acquisition of object-in-place memory (main effect of drug F _(1,35) = 63.87, P < 0.001). The magnitude of the deficit was similar irrespective of the region into which scopolamine was infused (region F _(1,35) < 1.0) or the delay employed (delay F _(1,35) < 1.0). Further analyses to examine whether individual groups discriminated between the objects, using a within subjects t-test (two-tailed), confirmed that vehicle-treated animals in the PRH and mPFC groups showed a significant preference for the moved objects over the objects that had remained in the same position, irrespective of the retention delay (PRH 5 min t ₍₉₎ = 2.96, P < 0.02; 1 h t ₍₁₀₎ = 5.71, P < 0.001: mPFC 5 min t ₍₅₎ = 5.47, P < 0.005; 1 h t ₍₁₁₎ = 9.89, P < 0.001), while scopolamine infusion into the PRH or mPFC significantly disrupted the animal''s ability to discriminate (PRH 5min t ₍₉₎ = 0.13, P = 0.9; 1 h t ₍₁₀₎ = 0.92, P = 0.38: mPFC 5 min t ₍₅₎ = 0.051, P = 0.961; 1 h t ₍₁₁₎ = 0.68, P = 0.51). Scopolamine was without effect on the total amount of exploration completed in the sample or test phases (all Fs < 1.0).Open in a separate windowFigure 2.Discrimination between the objects was calculated using a discrimination ratio, which takes into account individual differences in the total amount of exploration. The discrimination ratio is calculated as follows: the difference in time spent by each animal exploring objects that changed position compared to the objects that remained in the same position divided by the total time spent exploring all objects. (A) Infusion of scopolamine (Scop) into the perirhinal cortex (PRH) significantly impaired performance in the object-in-place task following a 5 min and a 1 h delay. (B) Infusion of scopolamine (Scop) into the medial prefrontal cortex (mPFC) significantly impaired performance in the object-in-place task following a 5 min and a 1 h delay. Illustrated for each group is the mean (+ SEM) discrimination ratio. * P < 0.05; ** P < 0.01; and *** P < 0.001 difference between groups.It could be argued that the impairment produced by intracortical infusions of scopolamine following a short delay, reflects an effect on retrieval as well as acquisition. Therefore, we examined the effect of pretest administration of scopolamine (infusion 15 min before the start of the test phase) in the mPFC or PRH following a 1 h delay. No significant impairments were found (mean discrimination ratio ± SEM: PRH vehicle 0.38 ± 0.07, scopolamine 0.46 ± 0.11; mPFC vehicle 0.37 ± 0.08, scopolamine 0.44 ± 0.05), confirmed by a nonsignificant drug effect (F _(1,14) < 1.0, P > 0.1) and nonsignificant drug × area interaction (F _(1,14) = <  1.0, P > 0.1). In addition all groups significantly discriminated between the moved objects compared to objects in the same location (PRH vehicle t ₍₇₎ = 4.95, P < 0.01; PRH scopolamine t ₍₇₎ = 3.45, P < 0.05; mPFC vehicle t ₍₇₎ = 4.26, P < 0.01; mPFC scopolamine t ₍₇₎ = 8.37, P < 0.01). Scopolamine was without effect on the total amount of exploration completed in the test phase (drug × region F _(1,14) < 1.0, P > 0.05).To evaluate the importance of intrahemispheric interactions between these cortical regions and the cholinergic system, a third group of animals had cannulae implanted into both the PRH and mPFC (n = 12). In this experiment the behavioral effects of unilateral scopolamine infusions into the PRH and mPFC in the same hemisphere (Scop Ipsi) were compared with the effects of unilateral scopolamine infusions into opposite hemispheres (Scop Contra). The animals assigned to the Scop Ipsi group on day one, received infusions into opposite hemispheres (Scop Contra) on day two (minimum of 48 h later). Likewise, the animals in the Scop Contra group on day one, received ipsilateral infusions on day two. Figure 3 shows discrimination performance following a 5 min or 1 h delay. A two-way within-subject ANOVA revealed that the Scop Contra group was significantly impaired (infusion F _(1,20) = 44.35, P < 0.001) irrespective of the delay (infusion × delay F _(1,20) < 1.0, P < 0.05). Further analysis confirmed that the Scop Contra group failed to discriminate between the moved and unmoved objects (5 min t ₍₁₀₎ = 0.70, P > 0.1; 1 h t ₍₁₀₎ = 1.03, P > 0.1), while the Scop Ipsi group preferentially explored the moved objects (5 min t ₍₁₀₎ = 9.99, P < 0.0001; 1 h t ₍₁₀₎ = 4.34, P = 0.001).Open in a separate windowFigure 3.Unilateral scopolamine infusions into the PRH and mPFC in opposite hemispheres (Scop Contra) impaired object-in-place performance following both a 5 min and a 1 h delay. Scopolamine infusions into both the PRH and mPFC in the same hemisphere (Scop Ipsi) had no effect on performance following either delay. ** P < 0.01 and *** P < 0.001 difference between groups.Scopolamine was without effect on overall exploration levels during the sample (infusion × delay F _(1,20) < 1.0, P > 0.05; infusion F _(1,20) < 1.0, P > 0.05; delay F _(1,20) < 1.0, P > 0.05) or test phases (infusion × delay F _(1,20) < 1.0, P  >  0.05; infusion F _(1,20)  <  1.0, P > 0.05). There was a significant main effect of delay (F _(1,20) = 10.67, P < 0.01), as the Scop Ipsi and Scop Contra groups completed a greater amount of exploration in the test phase following a 1 h delay compared to a 5 min delay.These results demonstrate that acquisition, but not retrieval of object-in-place memory, is dependent upon muscarinic cholinergic neurotransmission in both the mPFC and PRH. Thus, acute bilateral administration of scopolamine directly into the mPFC or PRH before the sample phase impaired both short- and long-term memory performances. In contrast administration of scopolamine into either the mPFC or PRH prior to the test phase had no effect. Significantly, co-administration of scopolamine into the PRH and mPFC in opposite hemispheres produced a significant impairment in both short-term and long-term object-in-place memory compared to performance following co-administration of scopolamine into the PRH and mPFC in the same hemisphere. Thus, concomitant activation of cholinergic muscarinic receptors is necessary in both regions for the formation of object-in-place associative recognition memory.Our previous studies investigating the role of the mPFC and PRH in object-in-place associative memory suggest that these regions make different cognitive contributions to this mnemonic process. Thus, the PRH appears to be primarily involved in the acquisition of “object” information, while we have hypothesized that the role of the mPFC is to integrate object and place information (Barker et al. 2007). As administration of scopolamine into either region disrupted performance following a long- or short-retention delay, the present data suggest that the neural mechanisms underlying both these different cognitive processes must be dependent upon cholinergic neurotransmission.The results demonstrate that muscarinic receptor neurotransmission is clearly critical for acquisition of the object-in-place task as no impairment was produced when scopolamine was administered only prior to the test phase. While the current study is the first to investigate the importance of cholinergic neurotransmission in object-in-place associative memory, a number of previous studies have shown that intra-PRH infusions of scopolamine block discrimination of novel and familiar objects when administered prior to the sample phase, but not when administered immediately after the sample phase or prior to the test phase (Aigner and Mishkin 1986; Aigner et al. 1991; Warburton et al. 2003; Winters et al. 2006). Thus, together these results support the hypothesis that muscarinic cholinergic neurotransmission within the PRH is necessary for encoding representations of new visual stimuli for subsequent recognition (Turchi et al. 2005), but not for the retrieval of such information. The present results also show for the first time that muscarinic receptor neurotransmission within the mPFC is crucial for the encoding, but not the retrieval of object-in-place memory.It may be argued that the disruptions in performance following administration of scopolamine reflect disruptions in attentional processing. Indeed muscarinic cholinergic neurotransmission in the prefrontal cortex has been implicated in both mnemonic and attentional processes (Voytko et al. 1994; Everitt and Robbins 1997; Chudasama et al. 2004; Dalley et al. 2004). However, deficits in attentional processing are typically observed when the attentional demands of the tasks are high, for example, when very short (millisecond) stimulus exposure times are used (Chudasama et al. 2004; Dalley et al. 2004). In the present study, the exposure time to the stimuli is relatively long (minutes); further there was no evidence of a drug-associated change in explorative behavior following either an infusion into the mPFC or PRH or simultaneously into both regions. Thus, it seems unlikely that the impairments in memory observed can be attributed purely to an attentional deficit, although it is possible that during the encoding of the object-in-place task attentional processes are also recruited involving the cholinergic afferents to the mPFC or PRH.The results showing that simultaneous muscarinic cholinergic blockade in the PRH and mPFC produces a significant impairment in performance support our previous findings of a neural system for object-in-place memory and extend these findings to show that cholinergic neurotransmission is a key component within the system. Our results also support those studies in primates demonstrating a circuit involving the basal forebrain, frontal cortex, and inferior temporal cortex is necessary for object memory encoding (Easton et al. 2002; Easton and Parker 2003).Results from our laboratory have shown that the maintenance of long-term, but not short-term, object-in-place memory is critically dependent upon concurrent NMDA receptor activation in the PRH and mPFC (Barker and Warburton 2008), while short-term object-in-place performance is dependent upon kainate receptor activation in the PRH. Hence, we have argued that there may be multiple cellular mechanisms underlying encoding of information for the short or long term. The present study contrasts with these findings as it demonstrates the necessity for muscarinic receptor activation for both short- and long-term object-in-place memory. Primate studies have indicated that a synergistic interaction between the cholinergic and glutamatergic systems plays an important role in the regulation of visual recognition memory (Matsuoka and Aigner 1996). Hence, further investigations are warranted to explore such interactions in the rat; for example, an interaction between NMDA and muscarinic receptor neurotransmission may mediate long-term recognition memory, while a kainate–muscarinic receptor interaction may mediate short-term recognition memory. Further, the extent to which the contribution of the cholinergic system to encoding of object-in-place memory within the PRH-mPFC system is the same for both short- or long-term memory is unknown.Our results have demonstrated that when a subject is required to use information concerning an association between an object and a place to produce a behavioral response, muscarinic cholinergic receptors in the mPFC are involved. Further, the object-in-place task requires the subject to acquire and remember the topographical relationship between the objects, a process that is known to depend upon the parietal cortex (Goodrich-Hunsaker et al. 2005). The precise contribution of object and spatial information processing in the parietal cortex to the operation of the PRH-mPFC circuit has yet to be determined.In conclusion, the cholinergic projections to the PRH and mPFC originating in the basal forebrain (Wenk et al. 1980) are an important component of the neural mechanisms underlying short- and long-term object-in-place associative memory.     

RISKY CHOICE IN PIGEONS AND HUMANS: A CROSS‐SPECIES COMPARISON

Pigeon and human subjects were given repeated choices between variable and adjusting delays to token reinforcement that titrated in relation to a subject's recent choice patterns. Indifference curves were generated under two different procedures: immediate exchange, in which a token earned during each trial was exchanged immediately for access to the terminal reinforcer (food for pigeons, video clips for humans), and delayed exchange, in which tokens accumulated and were exchanged after 11 trials. The former was designed as an analogue of procedures typically used with nonhuman subjects, the latter as an analogue to procedures typically used with human participants. Under both procedure types, different variable‐delay schedules were manipulated systematically across conditions in ways that altered the reinforcer immediacy of the risky option. Under immediate‐exchange conditions, both humans and pigeons consistently preferred the variable delay, and indifference points were generally ordered in relation to relative reinforcer immediacies. Such risk sensitivity was greatly reduced under delayed‐exchange conditions. Choice and trial‐initiation response latencies varied directly with indifference points, suggesting that local analyses may provide useful ancillary measures of reinforcer value. On the whole, the results indicate that modifying procedural features brings choices of pigeons and humans into better accord, and that human—nonhuman differences on risky choice procedures reported in the literature may be at least partly a product of procedural differences.     

Lemurs and macaques show similar numerical sensitivity

We investigated the precision of the approximate number system (ANS) in three lemur species (Lemur catta, Eulemur mongoz, and Eulemur macaco flavifrons), one Old World monkey species (Macaca mulatta) and humans (Homo sapiens). In Experiment 1, four individuals of each nonhuman primate species were trained to select the numerically larger of two visual arrays on a touchscreen. We estimated numerical acuity by modeling Weber fractions (w) and found quantitatively equivalent performance among all four nonhuman primate species. In Experiment 2, we tested adult humans in a similar procedure, and they outperformed the four nonhuman species but showed qualitatively similar performance. These results indicate that the ANS is conserved over the primate order.     

JEAB And JABA On The World Wide Web: A Report To Readers (Editorial)

The Journal of the Experimental Analysis of Behavior (JEAB) and the Journal of Applied Behavior Analysis (JABA) have both established home pages on the World Wide Web. Their addresses are:

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Information Processing and Decision-Making in Pathological Worriers and their Potential Role in Mechanisms of Generalized Anxiety Disorder

Systematic information processing and decision-making under uncertainty are key constructs of new conceptions explaining the severity of pathological worry. The current study attempted to analyze their usefulness in subclinical and clinical groups. In the first phase of the study (N = 251) participants were examined with the Penn State Worry Questionnaire (PSWQ), a GP consultationrelated survey, and a screening survey for generalized anxiety disorder (GAD). In the second phase (N = 220), the State-Trait Anxiety Inventory, the PSWQ, and tasks measuring systematic information processing (SIP) versus heuristic reasoning (HR) were applied. In the third phase (N = 60), GAD (n = 30) and healthy control (n = 30) groups were examined with the above methods and the Iowa Gambling Task (IGT). In the low risk group, a relationship between mood and the representativeness heuristic (ρ = 0.50), as well as anchoring and adjustment heuristic (anxiety-related stimuli) was found (ρ = −0.53). In the GAD group, significant correlations between the PSWQ score, the IGT loss avoidance score (ρ = 0.40), and total IGT score (ρ = 0.48) were found. The results did not confirm a particular usefulness of the systematic/heuristic information processing construct in subclinical and clinical groups. Theory-consistent results were rather found in the nonclinical groups. Nevertheless, the data revealed some interesting findings supporting potential explanatory power of some theoretical models.     

Development of a structured psychiatric interview for children: Agreement between child and parent on individual symptoms

To test the reliability of children's reporting as compared with that of their mothers, a highly structured psychiatric diagnostic interview was used with 307 subjects, ages 6 through 16. Another interviewer gave each mother a similar interview about the child. Responses of each mother-child pair to 168 questions were compared using the kappa statistic. Highest agreement was found on questions concerning symptoms that are concrete, observable, severe, and unambiguous. Mothers tended to report significantly more behavioral symptoms, and children more subjective symptoms. Reasons for low kappas and asymmetrical reporting of symptoms are discussed.     

The WIG (weighted individual and group) shrinkage estimator

Regularization, or shrinkage estimation, refers to a class of statistical methods that constrain the variability of parameter estimates when fitting models to data. These constraints move parameters toward a group mean or toward a fixed point (e.g., 0). Regularization has gained popularity across many fields for its ability to increase predictive power over classical techniques. However, articles published in JEAB and other behavioral journals have yet to adopt these methods. This paper reviews some common regularization schemes and speculates as to why articles published in JEAB do not use them. In response, we propose our own shrinkage estimator that avoids some of the possible objections associated with the reviewed regularization methods. Our estimator works by mixing weighted individual and group (WIG) data rather than by constraining parameters. We test this method on a problem of model selection. Specifically, we conduct a simulation study on the selection of matching‐law‐based punishment models, comparing WIG with ordinary least squares (OLS) regression, and find that, on average, WIG outperforms OLS in this context.     

Selective enhancement of fear learning and resistance to extinction in a mouse model of acute early life trauma

Early life stress (ELS) experiences can cause changes in cognitive and affective functioning. This study examined the persistent effects of a single traumatic event in infancy on several adult behavioral outcomes in male and female C57BL/6J mice. Mice received 15 footshocks in infancy and were tested for stress-enhanced fear learning, extinction learning, discrimination and reversal learning, and novel object recognition. Infant trauma potentiated fear learning in adulthood and produced resistance to extinction but did not influence other behaviors, suggesting restricted effects of infant trauma on behaviors reliant on cortico-amygdala circuitry.

Exposure to traumatic events early in childhood is associated with the development of psychiatric disorders (Copeland et al. 2018) and deficits in cognitive and affective functioning (Pechtel and Pizzagalli 2011) in adulthood. In humans, early life stress (ELS) is defined as experiencing traumatic events in childhood (Pechtel and Pizzagalli 2011). Rodent models of ELS suggest that acute versus chronic stress may differentially alter systems that regulate the stress response, producing different behavioral outcomes in adulthood (Pryce et al. 2002; Musazzi et al. 2017).Stress-enhanced fear learning (SEFL), a powerful preclinical model of PTSD- and addiction-like behaviors, captures the enduring, maladaptive effects of a single traumatic event on behavior (Rau et al. 2009; Meyer et al. 2013; Radke et al. 2019). In these studies, exposure to 15 footshocks enhances contextual fear conditioning later in life. For infant SEFL, enhanced contextual fear conditioning occurs months after the initial stressful experience and in the absence of memory for the context in which ELS was experienced (Poulos et al. 2014; Quinn et al. 2014). SEFL protocols have been used to model adult or infant trauma in rats (e.g., Rau et al. 2009; Poulos et al. 2014; Quinn et al. 2014) and have been extended to adult mice (Sillivan et al. 2017; Hassien et al. 2020; Pennington et al. 2020). However, to our knowledge, no studies have established the use of acute, infant footshock as a model of ELS in mice.We sought to characterize the effects of acute, infant trauma exposure across several types of learning in adult mice. We tested mice exposed to 15 footshocks on postnatal day (PND) 17 for contextual fear learning, extinction of fear, discrimination and reversal learning, and novel object recognition. Our results suggest that exposure to acute infant trauma enhances fear learning and resistance to extinction in adulthood, but does not alter other types of learning.Male and female C57BL/6J mice were generated from breeding pairs from The Jackson Laboratory. Mice were group-housed (two to four mice/cage) post-weaning and were provided food and water ad libitum, unless otherwise specified. Mice were on a 12:12 light/ dark cycle. Other than trauma exposure, all behavioral tests were conducted during adulthood (PND 60+). Animals were cared for in accordance with the guidelines set by the National Institutes of Health and all procedures were approved by the Institutional Animal Care and Use Committee at Miami University.We first established that exposure to infant footshock produces enhanced contextual fear conditioning in adulthood. Mice were placed in a MED-Associates conditioning chamber (context A) on PND 17 (Fig. 1A; after Quinn et al. 2014). Context A was brightly lit, contained a uniform grid floor, was scented with vanilla (50%), and was cleaned with odorless 5% sodium hydroxide. Mice received either 0 or 15 footshocks (1 mA, 1 sec) during a 60-min session beginning 180 sec following placement in the chamber. Progressive scan video cameras containing visible light filters monitored mice throughout the session. Video Freeze software (Med Associates, Inc.) analyzed the video and data were expressed as percent of time spent freezing during the session. Fear conditioning experiments were powered to detect sex differences with an n of eight per sex. Because differences were not observed when sex was included as a factor in analyses, all reported results represent data from both sexes. Due to computer malfunction, fear conditioning sessions from 14 mice were hand scored according to standard time-sampling procedures (Chowdhury et al. 2005) and data from three mice had to be excluded on extinction session 2.Open in a separate windowFigure 1.Acute infant trauma produces stress-enhanced fear learning in adulthood. (A) Experimental timeline and visual representation of context A and context B. Infant trauma consisted of 15 footshocks or no footshocks on PND 17 in context A. Adult fear conditioning consisted of one footshock (black bars) or no footshock (blue bars) on PND 60 in context B. Extinction was assessed in context B. Memory of the infant trauma was assessed in context A. Stress enhanced fear learning (SEFL) was observed in mice who were exposed to early life stress (15 shocks) and fear conditioning (one shock) for extinction test 1 (B) and extinction test 2 (C). (*) P < 0.05, (**) P < 0.01 versus no/one shock group (Holm–Sidak test). (D) Mice showed little freezing, indicating an absence of fear memory for the infant trauma in context A. Data are means ± SEM.Contextual fear conditioning occurred on PND 60 in a novel context (context B). Context B was dark with a staggered grid floor and cleaned and scented with acetic acid (5%). Baseline freezing during the first 180 sec in this novel context was assessed and used to measure generalization between the stress exposure context (context A) and the novel fear conditioning context (context B). Mice received either 0 or 1 footshocks (1 mA, 1 sec) 180 sec into a 3.5-min session. Thus, there were four groups (infant trauma/adult fear conditioning): no/no shock, n = 14; 15/no shock, n = 15; no/one shock, n = 15; and 15/one shock, n = 18. To test extinction of fear memory, mice were reintroduced to context B for two 8-min sessions, separated by 24 h. Finally, mice were reintroduced to context A for an 8-min retention test of the original context.Mice exposed to 15 footshocks in infancy and conditioned with one footshock as adults exhibited robust SEFL. There were no differences in baseline freezing during the adult fear conditioning session (infant trauma: F_(1,47) = 2.67, P = 0.109, no/no shocks = 0.26 ± 0.15; no/one shock = 2.17 ± 0.64; 15/no shocks = 2.14 ± 0.76; 15/one shock = 7.17 ± 3.25; all data mean ± SEM). For extinction sessions (Fig. 1B,C), a mixed-effects analysis identified main effects of trauma (F_(1,58) = 5.68, P = 0.020), fear conditioning (F_(1,58) = 12.40, P < 0.001), and session (F_(1,55) = 5.25, P = 0.026). There was a significant interaction between fear conditioning and session (F_(1,55) = 7.10, P = 0.010). Two-way ANOVA was next used to examine each test session. For session 1 (Fig. 1B), there were main effects of trauma (F_(1,58) = 5.72, P = 0.020) and fear conditioning (F_(1,58) = 21.10, P < 0.001). The interaction of trauma and fear conditioning did not reach the threshold for significance (F_(1,58) = 2.87, P = 0.096). Follow-up Holm Sidak''s tests revealed that adult fear conditioning produced greater freezing in mice exposed to infant footshock vs. trauma-naïve mice (P = 0.008). For the second extinction test (Fig. 1C), the main effects of trauma (F_(1,55) = 3.72, P = 0.059) and fear conditioning (F_(1,55) = 3.92, P = 0.053) approached the threshold for significance. Follow-up Holm Sidak''s tests revealed that trauma-exposed mice froze more than trauma-naïve mice following adult fear conditioning only (P = 0.042). When tested for memory of the context used for trauma-exposure on PND 17 (context A), mice demonstrated minimal freezing and two-way ANOVA found no significant main effects or interactions (Fs < 1.39) (Fig. 1D). Percent freezing in infancy and in extinction test 1 in adulthood were correlated (r = −0.481, P = 0.043) for the 15/one group alone. Activity bursts in infancy did not correlate with freezing behavior in adulthood. These results indicate that mice exposed to infant trauma who experienced fear conditioning in adulthood exhibited SEFL on the first and second extinction sessions but the memory of the trauma experience was not retained into adulthood.Since PTSD is associated with deficits in fear extinction (Zuj et al. 2016), we next examined extinction learning using 30-min sessions (Fig. 2A). Mice were exposed to acute infant trauma (0 or 15 footshocks) on PND 17. On PND 60, mice were reintroduced to context A for an 8-min test of memory for the original ELS context prior to fear conditioning (no/one shock = 2.41 ± 0.58; 15/one shock = 3.50 ± 0.42; no/three shocks = 1.86 ± 0.43). On PND 61 fear conditioning occurred in context B. Since we observed that trauma-naïve mice displayed very little fear conditioning following one footshock (Fig. 1B,C), mice in this experiment received either one or three footshocks during adult fear conditioning. There were three groups (infant trauma/adult fear conditioning): no/one shock, n = 17; 15/one shock, n = 17; no/three shocks, n = 18. Retention of fear memory was tested for five subsequent days (PND 62–66) in context B during 30-min sessions.Open in a separate windowFigure 2.Extinction of fear learning is impaired following acute infant trauma. (A) Experimental timeline. Infant trauma consisted of 15 footshocks or no footshocks on PND 17 in context A. Adult fear conditioning consisted of one (yellow symbols) or three (blue symbols) footshocks in trauma-naïve mice and one footshock (black symbols) in trauma-exposed mice in context B. Memory of the infant trauma was assessed in context A. Mice received five extinction sessions in context B. (B) On extinction day 1, trauma-exposed mice initially froze at the same level as trauma-naïve mice conditioned with three footshocks but fear persisted longer, demonstrating within-session resistance to extinction. (*) P < 0.05, (**) P < 0.01 15/one shock group versus no/one shock group; (^#) P < 0.05 15/one shock group versus no/three shocks group; (^†) P < 0.05, (^‡) P < 0.01 no/one shock group versus no/three shock group (Holm–Sidak test). (C) Freezing was averaged across the first 8 min of each extinction session. Trauma-exposed mice demonstrated resistance to extinction across sessions. On session 1, both trauma-exposed (15/one shock group) and mice conditioned with three footshocks (no/three shock group) had elevated freezing compared to mice conditioned with one footshock. On session 2, freezing in trauma-exposed mice remained elevated and was greater than in the other two groups. (**) P < 0.01 15/one shock group versus no/one shock group. (^##) P < 0.01 15/one shock group versus no/three shocks group. (^†) P < 0.05 no/one shock group versus no/three shocks group (Holm–Sidak test). Data are means ± SEM.On the first extinction session, there were significant main effects of time (F_(29,1421) = 2.23, P < 0.001) and group (F_(2,49) = 3.54, P = 0.037) and a significant interaction (F_(58,1421) = 1.93, P < 0.001). Holm–Sidak follow-up comparisons revealed that trauma-exposed mice (15/one shock) and mice conditioned with three footshocks during adulthood (no/three shocks) froze more than the no/one shock group during the first 3 min (P < 0.05 for minute 1 and P < 0.01 for minutes 2 and 3) of the first extinction session (Fig. 2B). Trauma-exposed mice continued to freeze more than the no/one shock group during minutes 4–7 (P < 0.01) and minute 11 (P < 0.05). Freezing in the no/3 shocks group was similar to trauma-exposed mice for the first 4 min but diminished sooner, evidenced by a significant difference between these groups during minutes 5, 6, and 9 (P < 0.05). These results suggest that conditioning with three footshocks produces similar levels of fear in trauma-naïve mice as conditioning with one footshock in trauma-exposed mice, but that within-session extinction is delayed in the trauma-exposed group.To examine extinction across the five sessions, we averaged freezing during the first 8 min of each session. We found significant main effects of session (F_(4,196) = 22.92, P < 0.001) and group (F_(2,49) = 6.38, P = 0.003) and a significant interaction (F_(8,196) = 2.75, P = 0.007). Holm–Sidak follow-up comparisons revealed that mice exposed to infant trauma (15/one shock) and mice in the no/three shock group froze more than those in the no/one shock group on extinction session 1 (P < 0.01 and P < 0.05, respectively) (Fig. 2C). On session 2, freezing was greater in trauma-exposed mice versus both other groups (P < 0.01). Percent freezing in infancy did not correlate with freezing behavior in adulthood. Activity bursts in infancy correlated with freezing behavior in adulthood on extinction test 1 (r = −0.558, P = 0.020). These results further suggest that infant trauma produces resistance to extinction.To determine whether the behavioral alterations observed in mice exposed to infant trauma extend to other types of learning, we tested the effects of infant footshock on operant discrimination and reversal learning for food reward and novel object recognition. For discrimination and reversal learning, we used a subset of mice from the first experiment (no shock = 20, 15 shocks = 17) restricted to 85% of free-feeding weight. Mice underwent one habituation day with ten 14-mg grain pellets (Bio Serv) in their home cages. The following day, mice began 15-min training sessions in a standard mouse operant chamber (Med Associates). There were two nose-poke holes and a reward receptacle on one wall of the chamber and a house light and speaker on the opposite wall. The chamber was housed in a sound and light-attenuating box and connected to a computer for data collection (Med-PC V software suite). For all sessions, the house light was off and lights in the nose-poke holes were on. Following a correct response, a 2-sec, 65-dB tone sounded and there was a timeout period of 20 sec following reward delivery during which the lights above the nose-poke holes were off and no rewards could be earned.During the first session, 30 pellets were automatically delivered into the reward receptacle. Next, mice were trained to respond for the food reward on a fixed ratio 1 (FR1) schedule by responding at either nose-poke hole until meeting criterion of 30 responses in 15-min. For discrimination, mice were trained to respond at the active nose-poke hole (100% probability of reward), which was randomly assigned to the left or right side. The contingencies of the active and inactive nose-pokes holes were reversed once criterion was met (≥30 rewards with 85% reinforced responses over two consecutive sessions).Neither sex nor adult fear conditioning affected any measure of discrimination and reversal learning, so all results are reported collapsed across these two factors. Two trauma-exposed females did not acquire the discrimination in 25 sessions and were not advanced to reversal. Data were analyzed using mixed-effects analyses with phase (i.e., acquisition and reversal) as the within-subjects factor. There were no differences between groups in the total number of sessions required to complete discrimination (no shock = 5.70 ± 0.69; 15 shock = 6.82 ± 1.50) or reversal (no shock = 9.40 ± 0.98; 15 shock = 7.73 ± 1.21). Mice made more total reinforced (main effect of phase: F_(1,33) = 11.62, P = 0.002) and total nonreinforced (main effect of phase: F_(1,33) = 42.54, P < 0.001) responses during reversal but there were no effects of infant trauma on behavior (Fig. 3A,B). These results indicate that acute infant trauma does not influence acquisition of operant discrimination learning or behavioral flexibility in adulthood.Open in a separate windowFigure 3.Acute infant trauma does not affect discrimination and reversal learning or novel object recognition. (A,B) Following infant trauma on PND 17 (no footshock, blue, or 15 footshocks, black), adult mice were trained to respond for a food pellet in an operant, spatial discrimination and reversal learning task. Following acquisition of the discrimination (left or right nose-poke hole reinforced 100% of the time) the contingencies of the responses were reversed. Mice made more total reinforced (A) and unreinforced (B) responses during reversal versus acquisition across sessions ([**] P < 0.01, main effect of training phase) but there were no effects of infant trauma exposure. (C) A separate cohort of mice exposed to infant trauma (no or 15 footshocks on PND 17) was tested for novel object recognition by assessing exploration of a novel object 1 and 24 h after exposure to the familiar object. Mice explored the novel object more ([**] P < 0.01, main effect of object, main effect of testing session, and interaction of object × testing session) but there were no effects of infant trauma exposure. Data are means ± SEM.In a new cohort of mice (no shock = 16, 15 shocks = 16), novel object recognition following infant footshock was tested. In adulthood, mice were handled for 1–3 min for two consecutive days. The following day, mice were placed in 20 × 18 × 25-cm apparatus with white floors and patterned walls (Panlab) for a 10-min habituation session to the chamber. Twenty-four hours later, mice were returned to the apparatus now containing two sample objects for 10-min initial exposure to the objects (two identical small plastic caps, 0.8 cm tall with a 2.1-cm diameter) placed in the back right and left corners of the apparatus. One hour later, mice were returned to the apparatus for a 3-min session (1-h test) where one of the sample objects was replaced with a novel object (a 2.5 × 1.2 × 1.5-cm Lego tower). The object replaced was alternated for each mouse. Mice were returned to the same box 24 h later for another 3-min session (24-h test) with the opposite cap replaced with a second novel object (a 3 × 1.5-cm black binder clip). ANY-maze software recorded each session. Time spent interacting with each object was measured by two independent raters and averaged (after Bevins and Besheer 2006).A three-way ANOVA revealed a significant main effect of object (familiar vs. novel; F_(1,60) = 59.84, P < 0.001). There was also a main effect of testing session (1-h vs. 24-h test; F_(1,60) = 7.89, P = 0.007) and an interaction of object × testing session (F_(1,60) = 11.48, P = 0.001) (Fig. 3C,D). Interrater reliability was confirmed using Pearson''s correlation (r = 0.942). These results indicate that acute infant trauma does not influence hippocampal-dependent object recognition memory.Our results demonstrate that an acute traumatic experience during infancy affects some learned behaviors during adulthood. As previously reported in rats (Quinn et al. 2014; Poulos et al. 2014), 15 footshocks on PND 17 increased adult contextual fear conditioning in mice. We also demonstrated for the first time that the infant SEFL protocol produces resistance to extinction (within-session and between-session) and that behavior in a discrimination and reversal learning task and a novel object recognition task are unaffected. These findings establish the use of infant footshock to study SEFL in mice and further support the use of this paradigm as a model of PTSD-like behavior.The effects observed here differ from those commonly observed following chronic ELS manipulations such as limited nesting and bedding (Ivy et al. 2008; Molet et al. 2016) or maternal separation (Nishi et al. 2014). Chronic ELS impairs acquisition of fear conditioning in adult rodents (Kosten et al. 2006; Stevenson et al. 2009; Lesuis et al. 2019) and performance on hippocampal-dependent memory tasks (Rice et al. 2008; Naninck et al. 2015), for example. These behavioral differences suggest that acute and chronic infant stressors alter neural circuits in unique ways that are worthy of further study.Since the tasks used here rely on distinct neural circuits, the current results provide novel insight into how acute infant trauma impacts brain function. The effects of acute ELS were restricted to fear acquisition and extinction, suggesting alterations in cortico-amygdala circuits (Tovote et al. 2015). However, preservation of novel object recognition as well as discrimination and reversal learning suggest that hippocampal and striatal circuits likely remain intact (Cohen and Stackman 2015; Izquierdo et al. 2017). These findings can guide future studies concerning the neural mechanisms of acute ELS effects on behavior.     

Irrational choice behavior in human and nonhuman primates

Choice behavior in humans has motivated a large body of research with a focus on whether decisions can be considered to be rational. In general, humans prefer having choice, as do a number of other species that have been tested, even though having increased choice does not necessarily yield a positive outcome. Humans have been found to choose an option more often only because the opportunity to select it was diminishing, an example of a deviation from economic rationality. Here we extend this paradigm to nonhuman primates in an effort to understand the mechanisms underlying this finding. In this study, we presented two groups of laboratory monkeys, capuchins (Cebus apella) and rhesus macaques (Macaca mulatta), as well as human subjects, with a computerized task in which subjects were presented with two differently colored icons. When the subject selected an icon, differing numbers of food pellets were dispensed (or points were assigned), making each icon correspond to a certain level of risk (one icon yielded 1 or 4 pellets/points and the other yielded 2 or 3). Initially, both options remained constantly available and we established choice preference scores for each subject. Then, we assessed preference patterns once the options were not continuously available. Specifically, choosing one icon would cause the other to shrink in size on the screen and eventually disappear if never selected. Selecting it would restore it to its full size. As predicted, humans shifted their risk preferences in the diminishing options phase, choosing to click on both icons more equally in order to keep both options available. At the group level, capuchin monkeys showed this pattern as well, but there was a great deal of individual variability in both capuchins and macaques. The present work suggests that there is some degree of continuity between human and nonhuman primates in the desire to have choice simply for the sake of having choice.     

Sex as Reported in a Recent Sample of Psychological Research

This study is a follow up on the study done by Sara Schwabacher (1972). All the articles in this study were taken from the Journal of Personality and Social Psychology 1974, volume 30, and were reviewed for sex of subjects, type of conclusions drawn, and whether sex was mentioned in the abstract, introduction, or methods section. These results were compared to the Schwabacher study in order to discover if the conditions noted in her study continue to prevail, or whether there has been a change in scientific sampling and reporting procedures.
Contrary to the previous study, the percentage of all male studies show a sharp drop of 15% while all female studies rose 22%. When comparing the amount of single sex studies overgeneralized, all-male studies remained proportionately the same, whereas overgeneralized all-female studies showed an increase of 35.5%. In addition more both-sex articles checked for sex differences than previously reported. The authors discuss the results in relation to the women's movement and scientific decision making. Three suggestions for scientific reporting and procedures are made.