Memory Consolidation Processes Research Articles

Impaired Hippocampal Reactivation Preceding Robust Aβ Deposition in a Model of Alzheimer's Disease.

Current therapeutic strategies for Alzheimer's disease (AD) target amyloid-beta (Aβ) fibrils and high molecular weight protofibrils associated with plaques, but other bioactive species may directly contribute to neural systems failure in AD. Employing hippocampal electrophysiological recordings and dynamic calcium imaging across the sleep-wake cycle in young mice expressing human Aβ and Aβ oligomers, we reveal marked impairments of hippocampal function long before amyloid plaques predominate. In slow wave sleep (SWS), Aβ increased the proportion of hypoactive cells and reduced place-cell reactivation. During awake behavior, Aβ impaired theta-gamma phase-amplitude coupling (PAC) and drove excessive synchronization of place cell calcium fluctuations with hippocampal theta. Remarkably, the on-line impairment of hippocampal theta-gamma PAC correlated with the SWS impairment of place-cell reactivation. Together, these results identify toxic effects of Aβ on memory encoding and consolidation processes before robust plaque deposition and support targeting soluble Aβ-related species to treat and prevent AD.

Relationship between sleep disturbance and developmental status in preschool-aged children with developmental disorder

BackgroundSleep has been known to affect childhood development. Sleep disturbance is likely more common in children with developmental delay (DD) than in typical development. There are few studies on the correlation between sleep disturbance and developmental features in children with DD. Therefore, this study aimed to evaluate the associations between the two in children with DD.MethodsA total of 45 children (age range 27.0 ± 11.1) with DD were recruited and evaluated using the Sleep Disturbance Scale for Children (SDSC) and Bayley Scales of Infant and Toddler Development (BSID-III). The outcomes are expressed as means and standard deviations. The correlation between SDSC and BSID-III was assessed using Spearman’s rank correlation test. Multiple regression analysis was performed to investigate the relationship between BSID-III domains and SDSC questionnaire subscales. Statistical significance was set at p < 0.05.ResultsBased on the correlation analysis and subsequent hierarchical regression analysis, cognition and socio-emotional domains of BSID-III were significantly associated with the DOES subscale of the SDSC questionnaire. In addition, the expressive language domain of the BSID-III was found to be associated with the DA subscale of the SDSC questionnaire. It seems that excessive daytime sleepiness might negatively affect emotional and behavioral problems and cognitive function. Also, arousal disorders seem to be related to memory consolidation process, which is thought to affect language expression.ConclusionThis study demonstrated that DA and DOES subscales of the SDSC questionnaire were correlated with developmental aspects in preschool-aged children with DD. Sleep problems in children with DD can negatively affect their development, thereby interfering with the effectiveness of rehabilitation. Identifying and properly managing the modifiable factors of sleep problems is also crucial as a part of comprehensive rehabilitation treatment. Therefore, we should pay more attention to sleep problems, even in preschool-aged children with DD.

Targeted Memory Reactivation during Nonrapid Eye Movement Sleep Enhances Neutral, But Not Negative, Components of Memory.

Emotionally salient components of memory are preferentially remembered at the expense of accompanying neutral information. This emotional memory trade-off is enhanced over time, and possibly sleep, through a process of memory consolidation. Sleep is believed to benefit memory through a process of reactivation during nonrapid eye movement sleep (NREM). Here, targeted memory reactivation (TMR) was used to manipulate the reactivation of negative and neutral memories during NREM sleep. Thirty-one male and female participants encoded composite scenes containing either a negative or neutral object superimposed on an always neutral background. During NREM sleep, sounds associated with the scene object were replayed, and memory for object and background components was tested the following morning. We found that TMR during NREM sleep improved memory for neutral, but not negative scene objects. This effect was associated with sleep spindle activity, with a larger spindle response following TMR cues predicting TMR effectiveness for neutral items only. These findings therefore do not suggest a role of NREM memory reactivation in enhancing the emotional memory trade-off across a 12 h period but do align with growing evidence of spindle-mediated memory reactivation in service of neutral declarative memory.

High frequency oscillations in human memory and cognition: a neurophysiological substrate of engrams?

Despite advances in understanding the cellular and molecular processes underlying memory and cognition, and recent successful modulation of cognitive performance in brain disorders, the neurophysiological mechanisms remain underexplored. High frequency oscillations beyond the classic electroencephalogram spectrum have emerged as a potential neural correlate of fundamental cognitive processes. High frequency oscillations are detected in the human mesial temporal lobe and neocortical intracranial recordings spanning gamma/epsilon (60-150 Hz), ripple (80-250 Hz) and higher frequency ranges. Separate from other non-oscillatory activities, these brief electrophysiological oscillations of distinct duration, frequency and amplitude are thought to be generated by coordinated spiking of neuronal ensembles within volumes as small as a single cortical column. Although the exact origins, mechanisms, and physiological roles in health and disease remain elusive, they have been associated with human memory consolidation and cognitive processing. Recent studies suggest their involvement in encoding and recall of episodic memory with a possible role in the formation and reactivation of memory traces. High frequency oscillations are detected during encoding, throughout maintenance, and right before recall of remembered items, meeting a basic definition for an engram activity. The temporal coordination of high frequency oscillations reactivated across cortical and subcortical neural networks is ideally suited for integrating multimodal memory representations, which can be replayed and consolidated during states of wakefulness and sleep. High frequency oscillations have been shown to reflect coordinated bursts of neuronal assembly firing and offer a promising substrate for tracking and modulation of the hypothetical electrophysiological engram.

Role of amygdala astrocytes in different phases of contextual fear memory

Growing evidence indicates a critical role of astrocytes in learning and memory. However, little is known about the role of basolateral amygdala complex (BLA-C) astrocytes in contextual fear conditioning (CFC), a paradigm relevant to understand and generate treatments for fear- and anxiety-related disorders. To get insights on the involvement of BLA-C astrocytes in fear memory, fluorocitrate (FLC), a reversible astroglial metabolic inhibitor, was applied at critical moments of the memory processing in order to target the acquisition, consolidation, retrieval and reconsolidation process of the fear memory. Adult Wistar male rats were bilaterally cannulated in BLA-C. Ten days later they were infused with different doses of FLC (0.5 or 1 nmol/0.5 µl) or saline before or after CFC and before or after retrieval. FLC impaired fear memory expression when administered before and shortly after CFC, but not one hour later. Infusion of FLC prior and after retrieval did not affect the memory. Our findings suggest that BLA-C astrocytes are critically involved in the acquisition/early consolidation of fear memory but not in the retrieval and reconsolidation. Furthermore, the extinction process was presumably not affected (considering that peri-retrieval administration could also affect this process).

TrkB-BDNF Signalling and Arc/Arg3.1 Immediate Early Genes in the Anterior Cingulate Cortex and Hippocampus: Insights into Novel Memory Milestones Through Behavioural Tagging.

In recent years, there has been a surge in interest in investigating the mechanisms underlying memory consolidation. However, our understanding of the behavioural tagging (BT) model and its establishment in diverse brain regions remains limited. This study elucidates the contributions of the anterior cingulate cortex (ACC) and hippocampus in the formation of long-term memory (LTM) employing behaviour tagging as a model for studying the underlying mechanism of LTM formation in rats. Existing knowledge highlights a protein synthesis-dependent phase as imperative for LTM. Brain-derived neurotrophic factor (BDNF) stands as a pivotal plasticity-related protein (PRP) in mediating molecular alterations crucial for long-term synaptic plasticity and memory consolidation. Our study offers evidence suggesting that tropomyosin receptor kinase B (TrkB), the receptor of BDNF, may act as a combined "behavioural tag/PRP". Interfering with the expression of these molecules resulted in impaired LTM after 24h. Furthermore, augmenting BDNF expression led to an elevation in Arc protein levels in both the ACC and hippocampus regions. Introducing novelty around weak inhibitory avoidance (IA) training resulted in heightened step-down latencies and expression of these molecules, respectively. We also demonstrate that the increase in Arc expression relies on BDNF synthesis, which is vital for the memory consolidation process. Additionally, inhibiting BDNF using an anti-BDNF function-blocking antibody impacted Arc expression in both the ACC and hippocampus regions, disrupting the transformations from labile to robust memory. These findings mark the initial identification of a "behavioural tag/PRP" combination and underscore the involvement of the TrkB-BDNF-Arc cascade in the behavioural tagging model of learning and memory.

The dorsomedial prefrontal cortex prioritizes social learning during rest

Sociality is a defining feature of the human experience: We rely on others to ensure survival and cooperate in complex social networks to thrive. Are there brain mechanisms that help ensure we quickly learn about our social world to optimally navigate it? We tested whether portions of the brain's default network engage "by default" to quickly prioritize social learning during the memory consolidation process. To test this possibility, participants underwent functional MRI (fMRI) while viewing scenes from the documentary film, Samsara. This film shows footage of real people and places from around the world. We normed the footage to select scenes that differed along the dimension of sociality, while matched on valence, arousal, interestingness, and familiarity. During fMRI, participants watched the "social" and "nonsocial" scenes, completed a rest scan, and a surprise recognition memory test. Participants showed superior social (vs. nonsocial) memory performance, and the social memory advantage was associated with neural pattern reinstatement during rest in the dorsomedial prefrontal cortex (DMPFC), a key node of the default network. Moreover, it was during early rest that DMPFC social pattern reinstatement was greatest and predicted subsequent social memory performance most strongly, consistent with the "prioritization" account. Results simultaneously update 1) theories of memory consolidation, which have not addressed how social information may be prioritized in the learning process, and 2) understanding of default network function, which remains to be fully characterized. More broadly, the results underscore the inherent human drive to understand our vastly social world.

Acute pain impairs retention of locomotor learning.

Despite abundant evidence that pain alters movement performance, considerably less is known about the potential effects of pain on motor learning. Some of the brain regions involved in pain processing are also responsible for specific aspects of motor learning, indicating that the two functions have the potential to interact, yet it is unclear if they do. In experiment 1, we compared the acquisition and retention of a novel locomotor pattern in young, healthy individuals randomized to either experience pain via capsaicin and heat applied to the lower leg during learning or no stimulus. On day 1, participants learned a new asymmetric walking pattern using distorted visual feedback, a paradigm known to involve mostly explicit re-aiming processes. Retention was tested 24 h later. Although there were no differences in day 1 acquisition between groups, individuals who experienced pain on day 1 demonstrated reduced retention on day 2. Furthermore, the degree of forgetting between days correlated with pain ratings during learning. In experiment 2, we examined the effects of a heat stimulus alone, which served as a control for (nonpainful) cutaneous stimulation, and found no effects on either acquisition or retention of learning. Thus, pain experienced during explicit, strategic locomotor learning interferes with motor memory consolidation processes and does so most likely through a pain mechanism and not an effect of distraction. These findings have important implications for understanding basic motor learning processes and for clinical rehabilitation, in which painful conditions are often treated through motor learning-based interventions.NEW & NOTEWORTHY Pain is a highly prevalent and burdensome experience that rehabilitation practitioners often treat using motor learning-based interventions. Here, we showed that experimental acute pain, but not a heat stimulus, during locomotor learning impaired 24-h retention of the newly learned walking pattern. The degree of retention loss was related to the perceived pain level during learning. These findings suggest important links between pain and motor learning that have significant implications for clinical rehabilitation.

Sleep Patterns and Associated Insomnia in Junior and Senior Medical Students: A Questionnaire-Based Cross-Sectional Study.

Introduction Appropriate quality and quantity of sleep are critical for good mental health, optimal body functioning, memory consolidation, and other cognitive processes. Objectives To evaluate the sleeping patterns of medical students in Saudi Arabia and their relationships with psychological distress. Methods This was a cross-sectional, self-administered, questionnaire-based study. The study included medical students from a university in Jeddah, Saudi Arabia. The Pittsburgh Sleep Quality Index (PSQI) and the Athens Insomnia Scale (AIS) were used to evaluate the prevalence and burden of inadequate sleep quality and insomnia in the participants. Results The majority of the participants was women (76.6%). Furthermore, most participants (96.2%) were aged between 18 and 24 years old, while 54.4% of the participants were in their senior year. According to the AIS scores (mean: 15.85 ± 4.52), 98.7% of the participants exhibited insomnia symptoms. The PSQI scores (mean: 9.53 ± 5.67) revealed that 70.5% of the participants had poor sleep quality. Students in their fundamental and junior years had significantly higher percentages of insomnia symptoms and poor sleep quality compared with students in their senior years. Conclusion The prevalence of insomnia and poor sleep quality is high among medical students. Therefore, appropriate strategies for early detection and intervention are warranted.

Early excitatory-inhibitory cortical modifications following skill learning are associated with motor memory consolidation and plasticity overnight

Consolidation of motor memories is vital to offline enhancement of new motor skills and involves short and longer-term offline processes following learning. While emerging evidence link glutamate and GABA dynamics in the primary motor cortex (M1) to online motor skill practice, its relationship with offline consolidation processes in humans is unclear. Using two-day repeated measures of behavioral and multimodal neuroimaging data before and following motor sequence learning, we show that short-term glutamatergic and GABAergic responses in M1 within minutes after learning were associated with longer-term learning-induced functional, structural, and behavioral modifications overnight. Furthermore, Glutamatergic and GABAergic modifications were differentially associated with different facets of motor memory consolidation. Our results point to unique and distinct roles of Glutamate and GABA in motor memory consolidation processes in the human brain across timescales and mechanistic levels, tying short-term changes on the neurochemical level to overnight changes in macroscale structure, function, and behavior.

Temporal cluster-based organization of sleep spindles underlies motor memory consolidation.

Sleep benefits motor memory consolidation, which is mediated by sleep spindle activity and associated memory reactivations during non-rapid eye movement (NREM) sleep. However, the particular role of NREM2 and NREM3 sleep spindles and the mechanisms triggering this memory consolidation process remain unclear. Here, simultaneous electroencephalographic and functional magnetic resonance imaging (EEG-fMRI) recordings were collected during night-time sleep following the learning of a motor sequence task. Adopting a time-based clustering approach, we provide evidence that spindles iteratively occur within clustered and temporally organized patterns during both NREM2 and NREM3 sleep. However, the clustering of spindles in trains is related to motor memory consolidation during NREM2 sleep only. Altogether, our findings suggest that spindles' clustering and rhythmic occurrence during NREM2 sleep may serve as an intrinsic rhythmic sleep mechanism for the timed reactivation and subsequent consolidation of motor memories, through synchronized oscillatory activity within a subcortical-cortical network involved during learning.

Neurotrophin-3 into the insular cortex strengthens conditioned taste aversion memory

Memory consolidation is an essential process of long-term memory formation. Neurotrophins have been suggested as key regulators of activity dependent changes in the synaptic efficacy and morphology, which are considered the downstream mechanisms of memory consolidation. The neurotrophin 3 (NT-3), a member of the neurotrophin family, and its high affinity receptor TrkC, are widely expressed in the insular cortex (IC), a region with a critical role in the consolidation of the conditioned taste aversion (CTA) paradigm, in which an animal associates a novel taste with nausea. Nevertheless, the role of this neurotrophin in the cognitive processes that the IC mediates remains unexamined. To answer whether NT-3 is involved in memory consolidation at the IC, adult male Wistar rats were administered with NT-3 or NT-3 in combination with the Trk receptors inhibitor K252a into the IC, immediately after CTA acquisition under two different conditions: a strong-CTA (0.2 M lithium chloride i.p.) or a weak-CTA (0.1 M lithium chloride i.p.). Our results show that NT-3 strengthens the memory trace of CTA, transforming a weak conditioning into a strong one, in a Trk-dependent manner. The present evidence suggests that NT-3 has a key role in the consolidation process of an aversive memory in a neocortical region.

Research on the relationship between episodic memory and sleep in human

This paper reviews and analyzes the important "memory" aspect of brain science, mainly through reading and summarizing the existing literature to explain the relationship between episodic memory and sleep. A large amount of literature on Google scholar shows that sleep plays an important role in consolidating episodic memories, and gives experiments and evidence to support this idea. The study found that slow-wave sleep is an important period for memory consolidation, and that different stages of sleep also play a part in the memory consolidation process. Various experiments have demonstrated the important link between sleep and episodic memory storage, which means that memory quality is closely related to sleep. This paper also contains two hypotheses for the process of memory Consolidation: the "Active System Consolidation Hypothesis" and the "Synaptic Homeostasis Hypothesis". In the course of research, we haven't seen much literature supporting the existence of episodic memory in animals, but they do have memories that look a lot like episodic memory, which most scientists call "episodic-like memory."

Neuroplasicity and the developmental dyslexia intervention

A growing body of literature suggests that timing plays a critical role in neuroplasticity processes and the molecular mechanisms necessary for learning and memory [1, 2]. Of particular significance to remedial education is identifying the time parameters for primary stimulation that are necessary and sufficient, the time frame relevant for transitioning to long-term memory, and the appropriate periods for restimulation. The translation of short-term stimulation into long-term memory is regulated by diverse processes that are mechanistically distinct and activated by synaptic activity [1], while also relying on protein and glycoprotein synthesis [3] and myelination processes. The current research explores the potential benefits of incorporating neuroscience research on the timing of neuroplasticity mechanisms in designing intervention programs for individuals with developmental dyslexia, specifically focusing on enhancing cognitive functions and skills crucial for reading. Based on available evidence, we have determined optimal training and break time periods for a 10-year-old child with developmental dyslexia resulting from multiple deficits. During the 21-day intervention program, 12 training sessions were conducted each day, commencing at 8 or 9 am and held hourly thereafter. Each session comprised a brief, targeted training exercise ranging from 3 to 7 minutes, depending on the child’s aptitude, followed by a playing session or computer game lasting up to 15 minutes. A 40-minute break followed each session. Brief training sessions were required due to the swift exhaustion of the subject child. The sessions were selected based on the evidence that brief stimulation can still result in a high level of CERB phosphorylation, even if it lasts only a few minutes [4]. Playing sessions were necessary for supporting the child’s motivation throughout the lengthy and intensive intervention program, and the activities performed during these sessions were pertinent to developing specific skills. The duration of the breaks was determined by evidence indicating the time required for primary memory consolidation processes and protein synthesis necessary for long-lasting synaptic plasticity. We have made an effort to eliminate any potential sources of emotional engagement or significant new information during breaks, allowing the initial stage of memory consolidation to occur without any unnecessary disruption. During the training sessions, various tasks were used to target specific types of processing such as phonological, visual, speech, and multimodal processing (e.g., visual-motor, audio-visual, or reading). Each session exclusively focused on one type of exercise. In our prior study [5], we discussed the linguistic aspects of the program and the exercises employed. Significant progress was achieved as a result of the 21-day intervention, surpassing the progress achieved in three years of schooling and during traditional remediation programs with speech therapists that lasted 1–3 sessions per week for 40–120 minutes. Following the intensive intervention, supportive training was continued for one year while considering the crucial timing for neuroplasticity. Afterward, the child reached a normative level of reading, and the effect was maintained throughout their entire period of school education. Based on the timing of neuroplasticity processes, this is the first intensive intervention program experience for dyslexia that we are aware of. Intensive remediation programs, based on relevant findings regarding the mechanisms of memory consolidation, may enhance neural memory trace reinforcement. However, further research is necessary to optimize the timing and length of sessions and identify the most effective combination of linguistic and neurophysiological aspects for intervention.

The role and mechanisms of sleep on memory consolidation

In addition to its physiological functions, sleep also has a consolidating effect on memory, and current research has found sleep could promote the consolidation of declarative, procedural, and emotional memory. Possible mechanisms of sleep-enhanced memory include the the systemic consolidation theory, dual-process theory, the synaptic homeostasis theory, and the sequence hypothesis. In the future, more research need to examine the neural mechanisms of sleep-enhanced memory consolidation, and the use of simultaneous EEG-MRI will be a meaningful attempt to help us better understand the specific neural processes of sleep-enhanced memory consolidation.

The neural circuits and molecular mechanisms underlying fear dysregulation in posttraumatic stress disorder.

Post-traumatic stress disorder (PTSD) is a stress-associated complex and debilitating psychiatric disorder due to an imbalance of neurotransmitters in response to traumatic events or fear. PTSD is characterized by re-experiencing, avoidance behavior, hyperarousal, negative emotions, insomnia, personality changes, and memory problems following exposure to severe trauma. However, the biological mechanisms and symptomatology underlying this disorder are still largely unknown or poorly understood. Considerable evidence shows that PTSD results from a dysfunction in highly conserved brain systems involved in regulating stress, anxiety, fear, and reward circuitry. This review provides a contemporary update about PTSD, including new data from the clinical and preclinical literature on stress, PTSD, and fear memory consolidation and extinction processes. First, we present an overview of well-established laboratory models of PTSD and discuss their clinical translational value for finding various treatments for PTSD. We then highlight the research progress on the neural circuits of fear and extinction-related behavior, including the prefrontal cortex, hippocampus, and amygdala. We further describe different molecular mechanisms, including GABAergic, glutamatergic, cholinergic, and neurotropic signaling, responsible for the structural and functional changes during fear acquisition and fear extinction processes in PTSD.

33 Associations Between Long-Term Forgetting and Slow Wave Activity in Autosomal-Dominant Alzheimer’s Disease: Findings from the Colombia-Boston (COLBOS) Biomarker Study

Objective:Sleep contributes to memory retention and recall. Alzheimer’s disease (AD) patients experience decreased slow wave activity (SWA) during sleep. This decrease in SWA is associated with impaired memory consolidation (Lee et al., 2020). Long-term forgetting (LTF) over days or weeks has been linked to memory consolidation deficits and has been suggested as an early marker of AD that could be useful for identifying at-risk individuals for preclinical AD trials (Weston et al., 2018). Here, we examined associations between LTF and SWA in a sample of Presenilin-1 (PSEN1) E280A mutation carriers with autosomal dominant Alzheimer’s disease and non-carrier family members. Carriers of this mutation usually develop dementia in their forties (Fuller et al., 2019).Participants and Methods:Fourteen cognitively unimpaired PSEN1-E280A mutation carriers and sixteen age-matched non-carriers (mean age: 34.2 years) from the Colombia-Boston (COLBOS) biomarker study were included. Participants completed an overnight polysomnogram (PSG) and memory testing (NEUROPSI Word List) at 3-time points: 1) the night before PSG: immediate recall (Day1-ImmRecall) and a 20-minute delayed recall (Day1-DelayedRecall), 2) recall the following day (Day2-recall), and 3) recall one week later (Day7-recall). SWA was measured as the ratio 0. 6-1Hz/0.6-4Hz in frontopolar and frontotemporal regions and was calculated for sleep stages N2+N3 (slow wave sleep) based on an automated staging algorithm. Each participant’s LTF was calculated as the percent retention between Day 1 immediate recall and Day 7 recall (Butler, 2009). Mann-Whitney U tests were used to compare differences in recall, SWA, and LTF between groups. Spearman’s correlation was used to examine the associations between memory recall at different time points and SWA, as well as between LTF and SWA.Results:On Day 1, carriers had lower performance in immediate recall (p=0.02), compared to non-carriers, but there were no group differences in the 20-minute delayed recall. Carriers also recalled fewer words on Day 2 (p=0.03) and Day 7 (p=0.009) and had greater LTF (p=0.03). There were no group differences in SWA. In our overall sample, worse performance on word list delayed recall on Day 1, Day 2, and Day 7 was associated with less SWA across both frontotemporal (Day1: p=0.04, Day2: p=0.02, Day7: p=0.02) and frontopolar (all Ps&lt;0.01) regions. In carriers, only worse performance on Day 1 delayed recall was associated with lower SWA in the frontopolar region (r= 0.535; p=0.049). Memory recall on other days was not associated with SWA in any brain regions. Additionally, greater LTF was associated with less SWA across both frontopolar (r= 0.507; p=0.005) and frontotemporal regions (r= 0.463 p= 0.01).Conclusions:Preliminary findings suggest that long-term forgetting is associated with less slow- wave activity in preclinical autosomal dominant Alzheimer’s disease. These results also suggest that SWA may be related to pre-sleep learning and subsequent overnight memory consolidation processes. LTF testing may be useful in selecting individuals for preclinical AD trials. Future research on the impact of slow wave activity on LTF may be useful in identifying ways to enhance short- and long-term memory consolidation in individuals at greater risk for dementia.

The modulation of emotional memory consolidation by dream affect

IntroductionResearch in the field of cognitive neuroscience has focused on the role of sleep in various neurocognitive processes such as memory consolidation. However, an area that has not been adequately researched is the role of dreaming in this memory process. This study aimed to determine the relationship between affect experienced in dreams and emotional memory consolidation. Considering that REM dreams are laden with emotion and that emotion enhances memory, one possibility is that dream affect could also play a role in emotional memory consolidation. We hypothesised that greater dream-related affect would be associated with greater memory retention of emotional but not neutral information.Methods126 healthy participants, aged 18–35, were recruited for the online study, of which 103 participants had valid data (female: n =73). On the night of the study, participants viewed a series of pictures from the South African Affective Picture System (SA-APS) in an online session. Afterwards, they verbally recalled as many pictures as possible. The following morning, they were asked to recall any dreams and rate the emotional intensity of their dreams. Participants then again verbally recalled all the pictures that they could remember from the previous night.ResultsContrary to the prediction, dream-related affect, regardless of valence, did not predict memory consolidation of positive or negative information. Instead, increases in dream-related affect, and especially anxiety were predictive of better memory retention of all information. The findings also showed that an increase in negative affect in dreams predicted better memory retention of negative information.DiscussionOur results suggest that dream affect is an important modulator of memory consolidation processes occurring during sleep. Furthermore, increased negative affect may indicate which experiences are salient and require consolidation to form long-lasting memories that can guide future behaviour.ConclusionThese findings have implications for psychiatric disorders, such as major depression, which is characterised by negative affect and increased memory sensitivity to negative stimuli.

N-Formyl-Methionyl-Leucyl-Phenylalanine Plays a Neuroprotective and Anticonvulsant Role in Status Epilepticus Model.

Status epilepticus (SE) is described as continuous and self-sustaining seizures, which triggers hippocampal neurodegeneration, inflammation, and gliosis. N-formyl peptide receptor (FPR) has been associated with inflammatory process. N-formyl-methionyl-leucyl-phenylalanine (fMLP) peptide plays an anti-inflammatory role, mediated by the activation of G-protein-coupled FPR. Here, we evaluated the influence of fMLP peptides on the behavior of limbic seizures, memory consolidation, and hippocampal neurodegeneration process. Male Wistar rats (Rattus norvegicus) received microinjections of pilocarpine in hippocampus (H-PILO, 1.2mg/μL, 1μL) followed by fMLP (1mg/mL, 1μL) or vehicle (VEH, saline 0.9%, 1μL). During the 90min of SE, epileptic seizures were analyzed according to the Racine's Scale. After 24h of SE, memory impairment was assessed by the inhibitory avoidance test and the neurodegeneration process was evaluated in hippocampal areas. There was no change in latency and number of wet dog shake (WDS) after administration of fMLP. However, our results showed that the intrahippocampal infusion of fMLP reduced the severity of seizures, as well as the number of limbic seizures. In addition, fMLP infusion protected memory dysfunction followed by SE. Finally, the intrahippocampal administration of fMLP attenuated the process of neurodegeneration in both hippocampi. Taken together, our data suggest a new insight into the functional role of fMLP peptides, with important implications for their potential use as a therapeutic agent for the treatment of brain disorders, such as epilepsy. Schematic drawing on the neuroprotective and anticonvulsant role of fMLP during status epilepticus. Initially, a cannula was implanted in hippocampus and pilocarpine/saline was administered into the hippocampus followed by fMLP/saline (A-C). fMLP reduced seizure severity and neuronal death in the hippocampus, as well as protecting against memory deficit (D).

Effect of reindeer pituitary peptide extract on cognitive functions in rats with changes light regime

BACKGROUND: Disruption of circadian rhythms can cause significant damage to sensory processing, learning, and memory. At the same time, the structure of the endogenous biological clock contributes to the adaptation of the organism to changes in the conditions for the existence of a biosystem in the external environment. The possibility of synchronization of the endogenous rhythms of the organism with disturbed light periodicity is an urgent problem of modern society, where different rhythms of labor, motor, cognitive activity are used.&#x0D; AIM: To study the effect of peptides from the pituitary gland of the Reindeer on the parameters of cognitive functions in rats with a long-term change in the light regime on models with altered cellular oscillation due to oxidative stress caused by poisoning of animals with sodium thiopental in a half-lethal dose.&#x0D; MATERIALS AND METHODS: The study was conducted on 56 white Wistar male rats after acute poisoning with sodium thiopental at a dose of 85 mg/kg under conditions of light desynchronosis. In the passive avoidance conditioned reflex test, the cognitive functions of animals were assessed after a two-week pharmacological correction with a cellular extract of the pituitary gland of the Reindeer at a dose of 100 mg/kg.&#x0D; RESULTS: The peptide extract of the pituitary gland of the Reindeer contributes to the change in the higher integrative functions of the central nervous system in case of disturbed periodicity of the light signal. The results obtained indicate the chronobiotic activity of the peptide extract of the pituitary gland of the Reindeer at a dose of 100 g/kg when administered intranasally.&#x0D; CONCLUSIONS: The light regime change for 1 month under conditions of altered cellular oscillation led to impaired of the higher integrative functions of the central nervous system in rats, which was accompanied by an increase in the rate of reflex extinction and a disturbance of the processes of memory consolidation; under conditions of constant light, these disorders are more pronounced. The result of the pharmacological correction of these changes with the reindeer pituitary peptide extract was an improvement in the processes of memory consolidation and information reproduction (an increase in the number of trained animals with a change in the light regime).