The curiosity circuits of our brains.

Every morning, as I am passing through the waking, exercise, and breakfast rituals that finally deliver me to my 'professor is in' office - a converted front bedroom of our house - I marvel at parallel ritualistic behaviors in my two abyssinian 1 year old cats, driven by an almost manic curiosity that impells them to seek new objects, crannies and nooks that hey can explore, occasionally hitting the jackpot of finding a cockroach, or a new object that they can break or brush onto the floor. Curiosity is one of the most important innate drives that they or I posses, and many think it should elevated to join the list of the four F's we teach first year Medical Students (fighting, feeding, fleeing, and fornicating). As Farahbakhsh and Siciliano note in their perspectives article on the work of Ahmadlout et al., "Attraction to the unknown, or curiosity, is a prerequisite for higher-order knowledge. Innate attraction to novelty is thought to be an evolutionary prerequisite for complex learning and guides organisms toward acquisition of adaptive behavioral repertoires."

Ahmadlou et al. have found circuitry in the mouse brain that is necessary for the exploration of new objects and conspecifics. A specific population of genetically identified γ-aminobutyric acid (GABA)—ergic neurons in a brain region called the zona incerta receive excitatory input in the form of novelty and/or arousal information from the prelimbic cortex, and these neurons send inhibitory projections to the periaqueductal gray region. Here is a summary graphic from the perspectives article (click to enlarge):

 

Two promising post-traumatic stress disorder treatments

I want to pass on references to two new approaches to relieving the symptoms of post-traumatic stress disorder (PTSD). Nuwer describes a new study showing that MDMA (known as the party drug Ecstasy, or Molly) can bring relief to PTSD when used in conjunction with talk therapy. Ressler et al. address the problem that human patients cannot be directly re-exposed to trauma-cues of the sort that have been used in animal studies to induce and then disrupt reconsolidation of traumatic memories. They devise a procedure for covertly capturing and attenuating a hippocampu-dependent fear memory in male rats, a procedure that might prove to be useful in human therapy. Here is their abstract:

Reconsolidation may be a viable therapeutic target to inhibit pathological fear memories. In the clinic, incidental or imaginal reminders are used for safe retrieval of traumatic memories of experiences that occurred elsewhere. However, it is unknown whether indirectly retrieved traumatic memories are sensitive to disruption. Here we used a backward (BW) conditioning procedure to indirectly retrieve and manipulate a hippocampus (HPC)-dependent contextual fear engram in male rats. We show that conditioned freezing to a BW conditioned stimulus (CS) is mediated by fear to the conditioning context, activates HPC ensembles that can be covertly captured and chemogenetically activated to drive fear, and is impaired by post-retrieval protein synthesis inhibition. These results reveal that indirectly retrieved contextual fear memories reactivate HPC ensembles and undergo protein synthesis-dependent reconsolidation. Clinical interventions that rely on indirect retrieval of traumatic memories, such as imaginal exposure, may open a window for editing or erasure of neural representations that drive pathological fear.

Gamma-frequency oscillations link different brain regions during learning.

Fernández-Ruiz et al. demonstrate that specific, projected gamma-frequency oscillation patterns dynamically engage functionally related cell assemblies across brain regions in a task-specific manner. I pass along their entire structured abstract:  

INTRODUCTION

Learning induces a dynamic reorganization of brain circuits but the neuronal mechanisms underlying this process are not well understood. Interregional gamma-frequency oscillations (~30 to 150 Hz) have been postulated as a mechanism to precisely coordinate upstream and downstream neuronal ensembles, for example, in the hippocampal system. The lateral (LEC) and medial (MEC) entorhinal cortex receive inputs from two distinct streams of cortical hierarchy (the “what” and the “where” pathways) and convey these neuronal messages to the hippocampus. However, the mechanisms by which such messages are packaged and integrated or segregated by hippocampal circuits had yet to be explored.

RATIONALE

Neuronal assemblies firing within gamma time frames in an upstream region can most effectively discharge their downstream partners. This gamma-time-scale organization appears essential for physiological functions because manipulations that impair precision timing of spikes in the hippocampus often affect behavior. However, direct support for distinct gamma-frequency communication in appropriate behavioral situations is missing. To bring physiological operations closer to behavior, we designed “spatial” and “object” learning tasks and examined the selective engagement of gamma-frequency communication between the MEC and LEC inputs and their target neuronal assemblies in the hippocampal dentate gyrus. We combined these correlational observations with optogenetic perturbation of gamma oscillations in LEC and MEC, respectively, to test their roles in pathway-specific neuronal communication and learning.

RESULTS

During spatial learning, fast gamma (100 to 150 Hz) oscillations synchronized MEC and dentate gyrus and entrained predominantly granule cells. During object learning, slow gamma (30 to 50 Hz) oscillations synchronized LEC and dentate gyrus and preferentially recruited mossy cells and CA3 pyramidal neurons, suggesting task-specific routing of MEC and LEC messages in the form of gamma-cycle-spike packets of selected cell types. The low- and high-frequency gamma sub-bands were dominant in the outer and middle third of the dentate molecular layer, respectively, and their amplitude maxima were locked to different phases of theta oscillations.

Gamma frequency optogenenetic perturbation of MEC and LEC led to learning impairments in a spatial and object learning task, respectively. In the same animals, the dentate layer–specific low- and high-frequency gamma sub-bands and spike-gamma LFP coupling were selectively reduced, coupled with deterioration of spatial and object-related firing of dentate neurons.

CONCLUSION

These findings demonstrate that distinct gamma-frequency-specific communication between MEC and LEC and hippocampal cell assemblies are critical for routing task-relevant information, and our selective gamma-band perturbation experiments suggest that they support specific aspects of learning. We hypothesize that sending neuronal messages by segregated gamma-frequency carriers allows a target “reader” area to disambiguate convergent inputs. In general, these results demonstrate that specific projected gamma patterns dynamically engage functionally related cell assemblies across brain regions in a task-specific manner.

False memories can be reversed without damage to true memories.

 Oeberst et al.  demonstrate the effectiveness of source sensitization, which involves alerting participants that their memories could come from external sources, and false memory sensitization, which involves informing individuals that repeatedly being asked to recollect events can produce false memories. The two strategies could be widely implemented in real-world settings and do not require interviewers to know any ground truths.:  

Significance

Human memory is fallible and malleable. In forensic settings in particular, this poses a challenge because people may falsely remember events with legal implications that never actually happened. Despite an urgent need for remedies, however, research on whether and how rich false autobiographical memories can be reversed under realistic conditions (i.e., using reversal strategies that can be applied in real-world settings) is virtually nonexistent. The present study therefore not only replicates and extends previous demonstrations of false memories but, crucially, documents their reversibility after the fact: Employing two ecologically valid strategies, we show that rich but false autobiographical memories can mostly be undone. Importantly, reversal was specific to false memories (i.e., did not occur for true memories).

Abstract

False memories of autobiographical events can create enormous problems in forensic settings (e.g., false accusations). While multiple studies succeeded in inducing false memories in interview settings, we present research trying to reverse this effect (and thereby reduce the potential damage) by means of two ecologically valid strategies. We first successfully implanted false memories for two plausible autobiographical events (suggested by the students’ parents, alongside two true events). Over three repeated interviews, participants developed false memories (measured by state-of-the-art coding) of the suggested events under minimally suggestive conditions (27%) and even more so using massive suggestion (56%). We then used two techniques to reduce false memory endorsement, source sensitization (alerting interviewees to possible external sources of the memories, e.g., family narratives) and false memory sensitization (raising the possibility of false memories being inadvertently created in memory interviews, delivered by a new interviewer). This reversed the false memory build-up over the first three interviews, returning false memory rates in both suggestion conditions to the baseline levels of the first interview (i.e., to ∼15% and ∼25%, respectively). By comparison, true event memories were endorsed at a higher level overall and less affected by either the repeated interviews or the sensitization techniques. In a 1-y follow-up (after the original interviews and debriefing), false memory rates further dropped to 5%, and participants overwhelmingly rejected the false events. One strong practical implication is that false memories can be substantially reduced by easy-to-implement techniques without causing collateral damage to true memories.

Environmental noise degrades learning and memory

Sobering observations from Zhang et al on our hippocampus-related learning and memory:

Significance

The noise pollution accompanying industrialization is a risk factor to human health. Here, we show in a rodent model that even moderate-level noise at ∼65 dB SPL that has little effect on stress status can substantially impair hippocampus-related learning and memory by altering the plasticity of synaptic transmission. It is possible that because moderately loud noise does not affect peripheral hearing per se, the negative impacts of chronic exposure to such noise are currently not well characterized. Our results indicate the importance of more thoroughly defining these possibly hitherto unappreciated hazards of noise pollution in modern human environments.

Abstract

The neural mechanisms underlying the impacts of noise on nonauditory function, particularly learning and memory, remain largely unknown. Here, we demonstrate that rats exposed postnatally (between postnatal days 9 and 56) to structured noise delivered at a sound pressure level of ∼65 dB displayed significantly degraded hippocampus-related learning and memory abilities. Noise exposure also suppressed the induction of hippocampal long-term potentiation (LTP). In parallel, the total or phosphorylated levels of certain LTP-related key signaling molecules in the synapses of the hippocampus were down-regulated. However, no significant changes in stress-related processes were found for the noise-exposed rats. These results in a rodent model indicate that even moderate-level noise with little effect on stress status can substantially impair hippocampus-related learning and memory by altering the plasticity of synaptic transmission. They support the importance of more thoroughly defining the unappreciated hazards of moderately loud noise in modern human environments.

A review on transcutaneous vagal nerve stimulation.

Colzato and Beste review the literature on cognitive effects of transcutaneous vagus nerve stimulation (tVNS), with a focus on studies on normal subjects suggesting that it might enhance memory and sharpen task relevant representations. I pass on a few clips from their text and also their abstract. Motivated readers can obtain the whole article by emailing me.

The focus of the present review article is not on clinical populations but on healthy humans and how especially auricular tVNS may be a useful neuromodulatory tool in cognitive neuroscience.

Only after commercially available auricular tVNS (NEMOS®) and cervical tVNS (gammaCore®) devices hit the market in the last few years, the idea of using tVNS as a tool for neuromodulation in cognitive neuroscience has been put forward.

Auricular tVNS is applied through a special earplug electrode to the outer ear, sending electrical impulses to the auricular branch of the vagus nerve, also called Alderman's nerve or Arnold's nerve. By doing so, the afferent (i.e., the thick-myelinated Aβ) fibers of Arnold's nerve are excited and the afferent signal propagates from peripheral nerves to nuclei in the brainstem, such as the locus coeruleus (LC) and the NST, and, ultimately, to intracranial subcortical (hippocampus) and cortical structures such as the insula, the prefrontal cortex (PFC) and the motor cortex. To date, auricular tVNS is applied to the left ear because of cardiac safety concerns, even 310 though, recently, these concerns have been challenged.

To date, most tVNS studies use commercially available stimulation devices. Usually, these are equipped with the following fixed parameters: frequency of 25 Hz, 200 μs pulse width, 30s on / 30s off-cycle, and current intensities up to 3 mA. Findings from animal studies, can thus not directly be transferred to study protocols in humans, since stimulation parameters can vary.

The reviewed literature indicates that the modulation of activation in the locus coeruleus and in th hippocampus and related NA release could be regarded as a possible working mechanism for the memory-enhancing effects of tVNS. Second, that increased cortical inhibition in the motor cortex and PFC due to high GABA levels in response to tVNS can facilitate response selection and inhibition processes via sharpening task-relevant representations and inhibiting competing responses.

Here is their abstract:

Brain stimulation approaches are important to gain causal mechanistic insights into the relevance of functional brain regions and/or neurophysiological systems for human cognitive functions. In recent years, transcutaneous vagus nerve stimulation (tVNS) has attracted considerable popularity. It is a noninvasive brain stimulation technique based on the stimulation of the vagus nerve. The stimulation of this nerve activates subcortical nuclei, such as the locus coeruleus and the nucleus of the solitary tract, and from there, the activation propagates to the cortex. Since tVNS is a novel stimulation technique, this literature review outlines a brief historical background of tVNS, before detailing underlying neurophysiological mechanisms of action, stimulation parameters, cognitive effects of tVNS on healthy humans, and, lastly, current challenges and future directions of tVNS research in cognitive functions. Although more research is needed, we conclude that tVNS, by increasing noradrenaline (NA) and gamma-aminobutyric acid (GABA) levels, affects NA and GABA-related cognitive performance. The review provides detailed background information how to use tVNS as a neuromodulatory tool in cognitive neuroscience and outlines important future leads of research on tVNS.

When we return to the gym...A molecular muscle memory helps retraining of muscles after inactivity.

For me the most deranging part of the current "Stay Home" order that I am obeying during the coronavirus crisis is being unable to do my customary workouts at a gym. It is heartening to see Gretchen Reynolds point to a study that finds that...

...if muscles have been trained in the past, they seem to develop a molecular memory of working out that lingers through a prolonged period of inactivity, and once we start training again, this “muscle memory” can speed the process by which we regain our former muscular strength and size.

Swedish researchers...began by recruiting 19 young men and women who had never played sports or formally exercised at all, so that their muscles were new to formal weight training. They checked these volunteers’ current muscular strength and size, and then had them start training a single leg...one-legged workouts continued for 10 weeks, at which point the researchers re-measured muscles, and then the volunteers stopped their training completely for 20 weeks...After this layoff from working out, they returned to the lab, where the scientists checked the current state of their leg muscles, took muscle biopsies from both legs and had them complete a strenuous leg workout, using both legs this time. Afterward, the researchers biopsied the muscles again. Then they checked the levels of a wide array of gene markers and biochemical signals within the volunteers’ muscle cells that are believed to be related to muscle health and growth.

They found telling differences between the legs that had trained and those that had not, both before and after the lone training session. For one thing, the previously trained leg remained sturdier, having retained about 50 percent of its strength gains during the 20 weeks without exercise.

Taken as a whole..the trained leg’s genetic activity suggests that its muscle cells had become genetically and metabolically more ready to strengthen and grow than the cells in the leg that had not trained before. These findings support the idea that muscle memory can occur at the gene and protein level.

Cannabis increases susceptibility to false memory.

From Kloft et al.:  

Significance

This unique randomized, double-blind, placebo-controlled trial examined the susceptibility to false memories under the influence of cannabis, using a basic (DRM) and two applied (misinformation) paradigms. We used a highly powered experimental design, allowing us to test acute and residual drug effects. To achieve high reproducibility and ecological validity, the misinformation paradigms included an eyewitness and a perpetrator scenario, presented in a virtual-reality environment. We show across different paradigms that cannabis consistently increases susceptibility to false memories. The results have implications for police, legal professionals, and policymakers with regard to the treatment of cannabis-intoxicated witnesses and suspects and the validity of their statements.

Abstract

With the growing global acceptance of cannabis and its widespread use by eyewitnesses and suspects in legal cases, understanding the popular drug’s ramifications for memory is a pressing need. In a double-blind, randomized, placebo-controlled trial, we examined the acute and delayed effects of Δ9-tetrahydrocannabinol (THC) intoxication on susceptibility to false memory in 64 healthy volunteers. Memory was tested immediately (encoding and retrieval under drug influence) and 1 wk later (retrieval sober). We used three different methods (associative word lists and two misinformation tasks using virtual reality). Across all methods, we found evidence for enhanced false-memory effects in intoxicated participants. Specifically, intoxicated participants showed higher false recognition in the associative word-list task both at immediate and delayed test than controls. This yes bias became increasingly strong with decreasing levels of association between studied and test items. In a misinformation task, intoxicated participants were more susceptible to false-memory creation using a virtual-reality eyewitness scenario and virtual-reality perpetrator scenario. False-memory effects were mostly restricted to the acute-intoxication phase. Cannabis seems to increase false-memory proneness, with decreasing strength of association between an event and a test item, as assessed by different false-memory paradigms. Our findings have implications for how and when the police should interview suspects and eyewitnesses.

The role of memory suppression in resilience after trauma.

Mary et al. report the neural differences that control the retrieval of traumatic memories in 102 individuals who were affected by the Paris terror attacks but who dealt with these memories in different ways: 55 developed posttraumatic stress disorder (PTSD), and 47 did not. The used functional magnetic resonance imaging to measure how the dorsolateral prefrontal cortex (DLPFC), a core hub of the brain control system, regulated and suppressed memory activity during the reexperiencing of these intrusive memories. Their abstract:

In the aftermath of trauma, little is known about why the unwanted and unbidden recollection of traumatic memories persists in some individuals but not others. We implemented neutral and inoffensive intrusive memories in the laboratory in a group of 102 individuals exposed to the 2015 Paris terrorist attacks and 73 nonexposed individuals, who were not in Paris during the attacks. While reexperiencing these intrusive memories, nonexposed individuals and exposed individuals without posttraumatic stress disorder (PTSD) could adaptively suppress memory activity, but exposed individuals with PTSD could not. These findings suggest that the capacity to suppress memory is central to positive posttraumatic adaptation. A generalized disruption of the memory control system could explain the maladaptive and unsuccessful suppression attempts often seen in PTSD, and this disruption should be targeted by specific treatments.

Skill development - the intelligence vs. practice debate reframed

Vaci et al. note that what is often overlooked in the nature vs. nurture debate is the fact that both factors interact with each other:

The relative importance of different factors in the development of human skills has been extensively discussed. Research on expertise indicates that focused practice may be the sole determinant of skill, while intelligence researchers underline the relative importance of abilities at even the highest level of skill. There is indeed a large body of research that acknowledges the role of both factors in skill development and retention. It is, however, unknown how intelligence and practice come together to enable the acquisition and retention of complex skills across the life span. Instead of focusing on the 2 factors, intelligence and practice, in isolation, here we look at their interplay throughout development. In a longitudinal study that tracked chess players throughout their careers, we show that both intelligence and practice positively affect the acquisition and retention of chess skill. Importantly, the nonlinear interaction between the 2 factors revealed that more intelligent individuals benefited more from practice. With the same amount of practice, they acquired chess skill more quickly than less intelligent players, reached a higher peak performance, and arrested decline in older age. Our research demonstrates the futility of scrutinizing the relative importance of highly intertwined factors in human development.

Twitter is making us dumber.

Stanley-Becker points to some research providing hardly surprising evidence that communicating about complex issues using 280 character chunks of text dumbs down the understanding of twitter users. Using Twitter to teach literature has an overall negative effect on students’ average achievement, with the effect being strongest on students who usually perform better. Numerous schools have started to utilize twitter discussion among students assuming that this would enhance intellectual attainment, but in fact it undermines it.

Re-skilling the brain.

For the first time, Oby et al (open source, nice graphics) observe the new neural activity patterns that cause a new learned behavior.

Significance

Consider a skill you would like to learn, like playing the piano. How do you progress from “Chopsticks” to Chopin? As you learn to do something new with your hands, does the brain also do something new? We found that monkeys learned new skilled behavior by generating new neural activity patterns. We used a brain–computer interface (BCI), which directly links neural activity to movement of a computer cursor, to encourage animals to generate new neural activity patterns. Over several days, the animals began to exhibit new patterns of neural activity that enabled them to control the BCI cursor. This suggests that learning to play the piano and other skills might also involve the generation of new neural activity patterns.

Abstract

Learning has been associated with changes in the brain at every level of organization. However, it remains difficult to establish a causal link between specific changes in the brain and new behavioral abilities. We establish that new neural activity patterns emerge with learning. We demonstrate that these new neural activity patterns cause the new behavior. Thus, the formation of new patterns of neural population activity can underlie the learning of new skills.

Mechanism of exercise and antioxidant stimulation of memory and new nerve cell growth

On reading this article by Yook et al. I promptly ordered a bottle of 10 mg astaxanthin capsules to add to my normal array of supplements (and exercise).

Significance

Leptin (LEP, a small protein hormone), produced and acting in the hippocampus, mediates enhancement by mild exercise (ME) of hippocampus-related memory and neurogenesis, which are further increased by an antioxidant carotenoid, astaxanthin (AX). Both are facilitated by the administration of ME or AX alone. The up-regulation of the LEP gene and LEP protein expression in the hippocampus by ME is further elevated when combined with AX. Consistently, the combined interventions increased hippocampal LEP protein. In LEP-deficient ob/ob mice, LEP replacement in the brain restored the ability of ME+AX to enhance hippocampal function. Thus, a combined lifestyle intervention based on ME, including yoga and tai chi, and specific dietary supplements that include antioxidants may together improve cognition and possibly retard cognitive decline in humans.

Abstract

Regular exercise and dietary supplements with antioxidants each have the potential to improve cognitive function and attenuate cognitive decline, and, in some cases, they enhance each other. Our current results reveal that low-intensity exercise (mild exercise, ME) and the natural antioxidant carotenoid astaxanthin (AX) each have equivalent beneficial effects on hippocampal neurogenesis and memory function. We found that the enhancement by ME combined with AX in potentiating hippocampus-based plasticity and cognition is mediated by leptin (LEP) made and acting in the hippocampus. In assessing the combined effects upon wild-type (WT) mice undergoing ME with or without an AX diet for four weeks, we found that, when administrated alone, ME and AX separately enhanced neurogenesis and spatial memory, and when combined they were at least additive in their effects. DNA microarray and bioinformatics analyses revealed not only the up-regulation of an antioxidant gene, ABHD3, but also that the up-regulation of LEP gene expression in the hippocampus of WT mice with ME alone is further enhanced by AX. Together, they also increased hippocampal LEP (h-LEP) protein levels and enhanced spatial memory mediated through AKT/STAT3 signaling. AX treatment also has direct action on human neuroblastoma cell lines to increase cell viability associated with increased LEP expression. In LEP-deficient mice (ob/ob), chronic infusion of LEP into the lateral ventricles restored the synergy. Collectively, our findings suggest that not only h-LEP but also exogenous LEP mediates effects of ME on neural functions underlying memory, which is further enhanced by the antioxidant AX.

Synchronizing rhythmic brain circuits improves working memory in older adults.

Our short term memory depends on theta rhythms (~6-10 Hz) and gamma rhythms (~25-100 Hz) in different parts of our brain being coupled and in synchrony with each other. They become increasingly uncoordinated as we age, resulting in observable cognitive decline by the time we reach 60 or 70 years of age. Reinhart and Nguyen compare the working memory of subjects in their 20s with 60-70 year olds, and find that 25 min of noninvasive stimulation, frequency-tuned to individual brain network dynamics, dramatically improves the working memory of the older group, making it similar to the younger group.

Understanding normal brain aging and developing methods to maintain or improve cognition in older adults are major goals of fundamental and translational neuroscience. Here we show a core feature of cognitive decline—working-memory deficits—emerges from disconnected local and long-range circuits instantiated by theta–gamma phase–amplitude coupling in temporal cortex and theta phase synchronization across frontotemporal cortex. We developed a noninvasive stimulation procedure for modulating long-range theta interactions in adults aged 60–76 years. After 25 min of stimulation, frequency-tuned to individual brain network dynamics, we observed a preferential increase in neural synchronization patterns and the return of sender–receiver relationships of information flow within and between frontotemporal regions. The end result was rapid improvement in working-memory performance that outlasted a 50 min post-stimulation period. The results provide insight into the physiological foundations of age-related cognitive impairment and contribute to groundwork for future non-pharmacological interventions targeting aspects of cognitive decline.

The Neuroscience of ‘Rock-a-Bye Baby’

I've always wondered why I sleep like a baby when on a boat being slowly rocked by waves, so was intrigued by Friedman's recent piece pointing to work by Perrault et al. showing that a slow rocking motion not only improves sleep but also can help people consolidate memories overnight. This is because continuous rocking stimulation strengthens deep sleep via the neural entrainment of intrinsic sleep oscillations. The Perrault et al. summary:

Highlights

•Rocking boosts deep sleep, sleep maintenance, and memory in healthy sleepers

•Fast spindles increase during rocking and synchronize with the slow oscillation up-state

• Rocking-induced overnight memory improvement relates to increased sigma activity

• Continuous rocking stimulation actively entrains intrinsic sleep oscillations

Summary

Sensory processing continues during sleep and can influence brain oscillations. We previously showed that a gentle rocking stimulation (0.25 Hz), during an afternoon nap, facilitates wake-sleep transition and boosts endogenous brain oscillations (i.e., EEG spindles and slow oscillations [SOs]). Here, we tested the hypothesis that the rhythmic rocking stimulation synchronizes sleep oscillations, a neurophysiological mechanism referred to as “neural entrainment.” We analyzed EEG brain responses related to the stimulation recorded from 18 participants while they had a full night of sleep on a rocking bed. Moreover, because sleep oscillations are considered of critical relevance for memory processes, we also investigated whether rocking influences overnight declarative memory consolidation. We first show that, compared to a stationary night, continuous rocking shortened the latency to non-REM (NREM) sleep and strengthened sleep maintenance, as indexed by increased NREM stage 3 (N3) duration and fewer arousals. These beneficial effects were paralleled by an increase in SOs and in slow and fast spindles during N3, without affecting the physiological SO-spindle phase coupling. We then confirm that, during the rocking night, overnight memory consolidation was enhanced and also correlated with the increase in fast spindles, whose co-occurrence with the SO up-state is considered to foster cortical synaptic plasticity. Finally, supporting the hypothesis that a rhythmic stimulation entrains sleep oscillations, we report a temporal clustering of spindles and SOs relative to the rocking cycle. Altogether, these findings demonstrate that a continuous rocking stimulation strengthens deep sleep via the neural entrainment of intrinsic sleep oscillations.

Social networks explain academic success and failure.

Interesting work from Stadtfeld et al.:

Significance

Understanding the factors that explain academic failure and success of university students is a core interest of educational researchers, teachers, and managers. We demonstrate how the dynamic social networks that informally evolve between students can affect their academic performance. We closely followed the emergence of multiple social networks within a cohort of 226 undergraduate university students. They were strangers to each other on their first day at university, but developed densely knit social networks through time. We show that functional studying relationships tended to evolve from informal friendship relations. In a critical examination period after one year, these networks proved to be crucial: Socially isolated students had significantly lower examination grades and were more likely to drop out of university.

Abstract

Academic success of students has been explained with a variety of individual and socioeconomic factors. Social networks that informally emerge within student communities can have an additional effect on their achievement. However, this effect of social ties is difficult to measure and quantify, because social networks are multidimensional and dynamically evolving within the educational context. We repeatedly surveyed a cohort of 226 engineering undergraduates between their first day at university and a crucial examination at the end of the academic year. We investigate how social networks emerge between previously unacquainted students and how integration in these networks explains academic success. Our study measures multiple important dimensions of social ties between students: their positive interactions, friendships, and studying relations. By using statistical models for dynamic network data, we are able to investigate the processes of social network formation in the cohort. We find that friendship ties informally evolve into studying relationships over the academic year. This process is crucial, as studying together with others, in turn, has a strong impact on students’ success at the examination. The results are robust to individual differences in socioeconomic background factors and to various indirect measures of cognitive abilities, such as prior academic achievement and being perceived as smart by other students. The findings underline the importance of understanding social network dynamics in educational settings. They call for the creation of university environments promoting the development of positive relationships in pursuit of academic success.

How exercise protects memory.

Gretchen Reynolds points to an interesting study on a mouse model for Alzheimer's disease by Lourenco et al. showing that exercise causes an increase in the level of a small protein,irisin, that boosts synaptic plasticity and memory. Here is the technical abstract:

Defective brain hormonal signaling has been associated with Alzheimer’s disease (AD), a disorder characterized by synapse and memory failure. Irisin is an exercise-induced myokine released on cleavage of the membrane-bound precursor protein fibronectin type III domain-containing protein 5 (FNDC5), also expressed in the hippocampus. Here we show that FNDC5/irisin levels are reduced in AD hippocampi and cerebrospinal fluid, and in experimental AD models. Knockdown of brain FNDC5/irisin impairs long-term potentiation and novel object recognition memory in mice. Conversely, boosting brain levels of FNDC5/irisin rescues synaptic plasticity and memory in AD mouse models. Peripheral overexpression of FNDC5/irisin rescues memory impairment, whereas blockade of either peripheral or brain FNDC5/irisin attenuates the neuroprotective actions of physical exercise on synaptic plasticity and memory in AD mice. By showing that FNDC5/irisin is an important mediator of the beneficial effects of exercise in AD models, our findings place FNDC5/irisin as a novel agent capable of opposing synapse failure and memory impairment in AD.

Watching memories change the brain - a challenge to the traditional view

I pass on both the Science Magazine summary of Brodt et al., as well as the summary graphic in a review of their article by Assaf, and finally the Brodt et al. abstract:

How fast do learning-induced anatomical changes occur in the brain? The traditional view postulates that neocortical memory representations reflect reinstatement processes initiated by the hippocampus and that a genuine physical trace develops only through reactivation over extended periods. Brodt et al. combined functional magnetic resonance imaging (MRI) with diffusion-weighted MRI during an associative declarative learning task to examine experience-dependent structural brain plasticity in human subjects (see the Perspective by Assaf). This plasticity was rapidly induced after learning, persisted for more than 12 hours, drove behavior, and was localized in areas displaying memory-related functional brain activity. These plastic changes in the posterior parietal cortex, and their fast temporal dynamics, challenge traditional views of systems memory consolidation.

Models of systems memory consolidation postulate a fast-learning hippocampal store and a slowly developing, stable neocortical store. Accordingly, early neocortical contributions to memory are deemed to reflect a hippocampus-driven online reinstatement of encoding activity. In contrast, we found that learning rapidly engenders an enduring memory engram in the human posterior parietal cortex. We assessed microstructural plasticity via diffusion-weighted magnetic resonance imaging as well as functional brain activity in an object–location learning task. We detected neocortical plasticity as early as 1 hour after learning and found that it was learning specific, enabled correct recall, and overlapped with memory-related functional activity. These microstructural changes persisted over 12 hours. Our results suggest that new traces can be rapidly encoded into the parietal cortex, challenging views of a slow-learning neocortex.

Social learning circuits in the brain.

Allsop et al. at MIT, observe brain circuits that let an animal learn from the experience of others: 


Highlights

•Neurons in cortex and amygdala respond to cues that predict shock to another mouse 

•Cortex → amygdala neurons preferentially represent socially derived information 

•Cortical input to amygdala instructs encoding of observationally learned cues 

•Corticoamygdala inhibition impairs observational learning and social interaction 

Summary

Observational learning is a powerful survival tool allowing individuals to learn about threat-predictive stimuli without directly experiencing the pairing of the predictive cue and punishment. This ability has been linked to the anterior cingulate cortex (ACC) and the basolateral amygdala (BLA). To investigate how information is encoded and transmitted through this circuit, we performed electrophysiological recordings in mice observing a demonstrator mouse undergo associative fear conditioning and found that BLA-projecting ACC (ACC→BLA) neurons preferentially encode socially derived aversive cue information. Inhibition of ACC→BLA alters real-time amygdala representation of the aversive cue during observational conditioning. Selective inhibition of the ACC→BLA projection impaired acquisition, but not expression, of observational fear conditioning. We show that information derived from observation about the aversive value of the cue is transmitted from the ACC to the BLA and that this routing of information is critically instructive for observational fear conditioning.

REM sleep in naps and memory consolidation in typical and Down syndrome children.

From Spano et al.:

Sleep is recognized as a physiological state associated with learning, with studies showing that knowledge acquisition improves with naps. Little work has examined sleep-dependent learning in people with developmental disorders, for whom sleep quality is often impaired. We examined the effect of natural, in-home naps on word learning in typical young children and children with Down syndrome (DS). Despite similar immediate memory retention, naps benefitted memory performance in typical children but hindered performance in children with DS, who retained less when tested after a nap, but were more accurate after a wake interval. These effects of napping persisted 24 h later in both groups, even after an intervening overnight period of sleep. During naps in typical children, memory retention for object-label associations correlated positively with percent of time in rapid eye movement (REM) sleep. However, in children with DS, a population with reduced REM, learning was impaired, but only after the nap. This finding shows that a nap can increase memory loss in a subpopulation, highlighting that naps are not universally beneficial. Further, in healthy preschooler’s naps, processes in REM sleep may benefit learning.