Spatial Memory Research Articles

Sex differences in behavior and glutamic acid decarboxylase in Long Evans rats after prolonged social isolation beginning in adolescence.

Social isolation can have long-term effects on brain development and behavior and increases the risk of developing clinical conditions, including anxiety disorders. One modulator of the stress response is gamma-aminobutyric acid, an inhibitory neurotransmitter synthesized by glutamic acid decarboxylase (GAD). This study examined sex differences in behavior and GAD expression following prolonged social isolation beginning in adolescence in Long Evans rats. Males and females were equally divided into group-housed (GH) and socially isolated conditions on Postnatal Day 28 (n = 8 per group). Beginning 5 weeks later, tests were conducted for anxietylike behaviors (open-field test and elevated plus maze), social interactions (sociability test), and spatial memory (novel object location). Sex differences in behavior were observed, with GH females showing fewer anxietylike behaviors in the open-field test and elevated plus maze and spending more time with objects (sociability task) compared to GH males. Isolation had no effect on males but increased anxiety and reduced neophilic measures in females, removing sex differences. On the sociability task, all groups spent more time with novel rats compared to objects, suggesting social interest was retained after isolation. In the hippocampus, isolation reduced GAD in both sexes, and sex differences were seen (F > M). However, no group differences in behavior were observed in the hippocampal-dependent novel object location task. Our findings suggest that prolonged social isolation beginning in adolescence is anxiogenic for female Long Evans rats. Furthermore, sex and housing impact hippocampal GABA-ergic activity, which may have important implications in the treatment of anxiety disorders. (PsycInfo Database Record (c) 2024 APA, all rights reserved).

Transcriptomic Signature of Spatial Navigation in Brains ofDesert Ants.

Navigation is crucial for central-place foragers to locate food and return to the nest. Cataglyphis ants are renowned for their advanced navigation abilities, relying on landmark cues and path integration. This study aims to uncover the transcriptomic basis of exceptional spatial learning in the central nervous system of Cataglyphis niger. Ants navigated a maze with a food reward, and we examined expression changes linked to correct decisions in subsequent runs. Correct decisions correlated with expression changes in the optic lobes, but not the central brain, showing a downregulation of genes associated with sucrose response and Creb3l1. The latter gene is homologous to Drosophila crebA, which is essential for long-term memory formation. To understand how ants use distance information during path integration, we analyzed expression shifts associated with the last distance traveled. We uncovered a transcriptomic footprint in the central brain, but not in the optic lobes, with genes enriched for energy consumption and neurological functions, including neuronal projection development, synaptic target inhibition, and recognition processes. This suggests that transcriptional activity in the central brain is necessary for estimating distance traveled, which is crucial for path integration. Our study supports the distinct roles of different brain parts for navigation in Cataglyphis ants.

Pre-operative environmental enrichment does not yield a prophylactic effect against traumatic brain injury-induced neurobehavioral deficits

The robustness of environmental enrichment (EE) in ameliorating neurobehavioral and cognitive deficits after experimental traumatic brain injury (TBI) is unequivocal. What is equivocal is whether EE can function as a prophylactic to afford resiliency and neuroprotection against TBI. We hypothesized that pre-operative EE would yield a protective effect against TBI-induced motor, cognitive, and coping deficits, and that further improvements would be conferred when EE is provided before and after TBI. To test the hypotheses, adult male rats received either 4 weeks of EE or standard (STD) housing prior to undergoing a controlled cortical impact of moderate severity (2.8 mm deformation at 4 m/s) or sham injury while under anesthesia. After injury, the rats were randomly assigned to post-operative EE or STD housing. Motor ability, spatial learning, and memory retention were assessed by beam-walk and water maze tests, respectively. Active and passive behavioral coping strategies were evaluated with the shock probe defensive burying (SPDB) test. c-Fos and cortical lesion volume were also quantified. The post-TBI enrichment groups (EE + TBI + EE and STD + TBI + EE) did not differ (p > 0.05) and performed better than the post-TBI STD-housed groups (EE + TBI + STD and STD + TBI + STD) on motor and cognition (p < 0.05). The post-TBI STD groups did not differ, regardless of whether in EE or STD living conditions before injury (p > 0.05). Moreover, both post-TBI enrichment groups performed better in the SPDB test relative to the STD + TBI + STD group (p < 0.05). c-Fos + cells were upregulated in the ipsilateral CA1 in both pre-injury EE groups relative to the pre-injury STD groups (p < 0.05). No statistical differences were observed in cortical lesion volume among the groups. Overall, these data do not support the hypothesis as no neuroprotective effect was observed with 4 weeks of pre-operative EE and no additional benefit was achieved in the TBI group receiving both pre-and-post EE relative to the TBI group receiving only post-EE. However, the data do reinforce the consistency of post-TBI EE in producing robust neurobehavioral benefits, which further supports this paradigm as a relevant preclinical model of neurorehabilitation.

Delayed-and-abbreviated environmental enrichment after traumatic brain injury confers neurobehavioral benefits similar to immediate-and-continuous exposure

Environmental enrichment (EE) consists of increased living space, complex stimuli, and social interaction that collectively confer neurobehavioral benefits in preclinical models of traumatic brain injury (TBI). The typical EE approach entails implementation immediately after surgery and continual exposure, which is not clinically applicable, as TBI patients often only receive rehabilitation after critical care, and then only for a few hours per day. We are focused on developing a clinically relevant model of neurorehabilitation by refining the timing of initiation and duration of EE exposure after TBI. The goal of this experiment is to compare the typical EE approach to paradigms where EE is delayed by 3 or 7 days after TBI and then provided for only 6 h per day, which better mimics the clinic. The hypothesis is that the delayed-and-abbreviated EE paradigms will promote neurobehavioral benefits like the typical approach of immediate-and-continuous exposure. To test the hypothesis, anesthetized adult male rats underwent a controlled cortical impact of moderate severity (2.8 mm deformation at 4 m/s) or sham injury and then were randomly assigned to post-operative EE or standard (STD) housing. Motor ability, spatial learning, and memory retention were assessed. The hypothesis was confirmed as all EE-treated groups performed better than the STD group in all behavioral assessments (p < 0.05) and did not differ from one another (p > 0.05). The ability of EE to provide significant behavioral benefits even when delayed and delivered in moderation affords further support for EE as a preclinical model of neurorehabilitation and offers greater insight into the length of the therapeutic window.

Electroacupuncture inhibits hippocampal oxidative stress and autophagy in sleep-deprived rats through the protein kinase B and mechanistic target of rapamycin signaling pathway.

To investigate the effects of acupuncture on learning and memory impairment, oxidative stress and autophagy induced by sleep depriv ation in rats, and to analyze the related mechanism. Thirty Wistar rats were randomly divided into a normal group, sleep deprivation group and acupuncture group. The rat model of sleep deprivation was established by a modified multiplatform sleep deprivation method. The Baihui (GV20), Shenmen (HT7) and Sanyinjiao (SP6) acupoints of rats were located to give electroacupuncture (density wave, frequency 20 Hz, intensity 1 mA) to maintain the needle feeling, and to keep the needle for 15 min and continuous acupuncture for 7 d. The spatial learning and memory abilities of the rats were detected by the water maze test. The content of malondialdehyde (MDA) and the activities of superoxide dismutase (SOD) and glutathione peroxidase (GPX) in the brain were detected by an assay kit, and the autophagy related proteins light chain 3 alpha (LC3A), light chain 3 beta (LC3B) and Beclin 1 and the activation of the protein kinase B (PKB/AKT) and mechanistic target of rapamycin (mTOR) signaling pathway in the rat's brain were detected by Western blotting. Compared with the normal group, the time spent in the target quadrant (P < 0.05) and the number of times entering the target quadrant (P < 0.05) in the rats of sleep deprivation group were significantly reduced, and the content of MDA was significantly increased (P < 0.01), while the activities of SOD and GPX (P < 0.01) in the brain were significantly decreased, and LC3A Ⅱ/Ⅰ, LC3B Ⅱ/Ⅰ and Beclin 1 increased significantly (P < 0.01), while p-AKT (ser473)/AKT, p-mTOR (ser2448)/mTOR and p-p70s6K (thr389)/p70S6 decreased significantly (P < 0.01). Compared with the sleep deprivation group, the time spent in the target quadrant and the times of entering the target quadrant (P < 0.05) in the rats of acupuncture group after 7 d of treatment were significantly increased, Additionally, the content of MDA was significantly decreased (P < 0.05), while the activities of SOD and GPX (P < 0.05) in the brain were significantly increased. Moreover, the levels of LC3A Ⅱ/Ⅰ, LC3BⅡ/Ⅰ and Beclin 1 decreased significantly (P < 0.05), and that of p-AKT (ser473)/AKT, p-mTOR (ser2448)/mTOR and p-p70s6K (thr389)/p70s6k increased significantly (P < 0.05). Acupuncture can significantly improve the learning and memory damage caused by sleep deprivation and inhibit oxidative stress and autophagy, and its effect is related to the activation of AKT/mTOR signaling.

Behavioral effects of two cannabidiol and cannabigerol-rich formulas on mice

Cannabis sativa L. produces more than 100 specific bioactive compounds, known as cannabinoids. The major non-psychotropic Cannabis constituent is cannabidiol (CBD), which displays beneficial properties in a variety of medical conditions. However, the potential therapeutic role of other minor phytocannabinoids, such as cannabigerol (CBG), and their use in combination with CBD, has remained largely unexplored. In this study, we wanted to assess the in vivo effects of two novel non-psychotropic cannabinoid formulas, both containing relatively high percentages of CBD but differing mainly for CBG content, hereafter called CBG+ and CBG- formulas. We employed different behavioral tests to evaluate the effects of these formulas at three different dosages on mice locomotor activity, anxiety-related behaviors, short-term memory and sociability. We found that these two formulas display unique behavioral profiles: CBG+ formula produced an increase in mice locomotor activity and displayed anxiolytic properties, whereas both formulas improved spatial short-term memory and social interactions. The results obtained suggest that different combinations of phytocannabinoids are able to determine different behavioral effects and highlight the importance of studying the effects of less known phytocannabinoids (like CBG), which used in combination with other phytocannabinoids can change the profile of action of other active compounds (such as CBD).

Intranasal administration of dextran-pramlintide polyelectrolyte complex-coated nanoemulsions improves cognitive impairments in a mouse model of Alzheimer's disease

Nasal delivery has emerged as a non-invasive route to administer drugs for brain delivery. In particular, polyelectrolyte complexes-based nanocarriers have been demonstrated to be advantageous for nasal delivery of peptide drugs and vaccines. Pramlintide (Pram) is a peptide that emerges as a novel neuroprotective strategy to modify the pathogenesis of Alzheimer's disease (AD). In this study, we examined the effects of the intranasal administration of dextran-pramlintide polyelectrolyte complex-coated nanoemulsions (PEC-NEDexS/Pram) in an experimental model of AD induced by intracerebroventricular (i.c.v.) infusion of amyloid-beta (Aβ1–42) peptide in mice. PEC-NEDexS/Pram displayed droplet size lower than 200 nm and a negatively charged surface. The locomotor activity of the animals was not affected by the i.c.v. Aβ1–42 injection or Pram treatment. On the other hand, the intranasal administration of PEC-NEDexS/Pram at a dose of 100 μg/day for 14 consecutive days restored the impairment induced by Aβ1–42 injection in the discriminative learning and the short-term spatial reference memory of mice. However, Pram treatment did not alter the Aβ1–42-induced anhedonic behavior, oxidative stress parameters, or the pre-synaptic SNAP-25 and post-synaptic PSD-95 levels in the hippocampus and prefrontal cortex. These findings indicate cognitive-enhancing properties of intranasal Pram administration in an animal model of AD.

Particulate matter induced cognitive impairments via endoplasmic reticulum stress-mediated damage to mitochondria-associated endoplasmic reticulum membranes in immature rats

Particulate matter (PM) exposure has been increasingly recognized as detrimental to cognitive function and is associated with neurodevelopmental disorders. Mitochondria-associated endoplasmic reticulum membranes (MAMs) form an integrated interface between mitochondria and the endoplasmic reticulum (ER), facilitating crucial cellular functions. Prolonged ER stress (ERS) is implicated in various pathological states in the nervous system. MAMs and ERS may play vital roles in adverse effects of early-life PM exposure on cognitive abilities. This study investigated whether ERS plays a role in PM-induced MAMs dysfunction, leading to neuronal damage and cognitive impairments in early postnatal rats. Using a rat model with PM exposure concentrations of 2 and 10 mg/kg from postnatal Day 3 (PND3) to PND28, we observed that PM exposure resulted in anxiety-like behavior and impaired spatial working memory. The protein levels of ERS markers, including GRP78 and CHOP, were significantly increased in response to PM exposure. Western blot, transmission electron microscopy (TEM), and immunofluorescence analyses revealed decreased MAMs-related proteins and disrupted MAM structure and function caused by PM exposure. Administration of the ERS inhibitor 4-phenylbutyric acid (4-PBA) ameliorated these effects, restoring MAMs integrity and improving cognitive deficits. These findings highlighted the key role of ERS-MAMs dysfunction in PM-induced neurotoxicity and cognitive impairments, providing a new perspective and strategy for the prevention of cognitive deficits in early age with PM exposure.

Ameliorative effects of Akkermansia muciniphila on anxiety-like behavior and cognitive deficits in a rat model of Alzheimer’s disease

Alzheimer’s Disease (AD) is the primary neurodegenerative disorder in the elderly, lacking a definitive treatment. The gut microbiota influences the gut-brain axis by aiding in hypothalamic–pituitary–adrenal (HPA) axis development and neuromodulator production. Research links AD and gut microbiota, suggesting gut microbiota regulation could be a therapeutic approach for AD. This study explores Akkermansia muciniphila’s impact on preventing AD. This research investigates the effect of A. muciniphila consumption (1 × 109 CFU) on tau protein-induced AD rats compared to a control group. Rats were divided into four groups: sham, sham + Akk, AD (tau-induced rats), and AD + Akk (tau-induced rats treated with A. muciniphila). A. muciniphila gavage lasted five weeks. Rats underwent qRT-PCR analysis to assess mRNA expression of pro-inflammatory factors (TNF-α, IL-6, IL-1β, IFN-γ) in the hippocampus. Behavioral tests included Morris Water Maze (MWM), Passive Avoidance Memory Test (Shuttle box), Elevated Plus Maze (EPM), and marble burying. After five weeks of A. muciniphila treatment, anxiety-like behavior significantly decreased. The AD group receiving A. muciniphila showed improved spatial and recognition memory compared to the AD group. Pro-inflammatory cytokine levels (TNF-α, IL-1β, IL-6, IFN-γ) decreased. A. muciniphila effectively reduces cognitive impairments and anxiety-related behavior, showing promise as an AD therapeutic by influencing the gut-brain axis.

Fasudil attenuates lipopolysaccharide-induced cognitive impairment in C57BL/6 mice through anti-oxidative and anti-inflammatory effects: Possible role of aquaporin-4

IntroductionProcesses that generate systemic inflammation are strongly associated with neurodegenerative diseases. This study aimed to explore the potential anti-oxidative and anti-inflammatory effects of fasudil and its role in modulating aquaporin-4 (AQP-4) to improve cognitive impairment in a systemic inflammation model induced by lipopolysaccharide (LPS). Methodfourty C57BL/6 mice were assigned to four groups, including sham, LPS, sham+fasudil, and LPS+fasudil). Intraperitoneal LPS was given (500μg/kg/day) at hours 0, 24, 48, and 72, and fasudil (30mg/kg) administered intraperitoneal injections 2hours after LPS injection. The open field, Y-maze, and Novel object tasks was used to assess learning and memory. The levels of malondialdehyde (MDA), superoxide dismutase (SOD), interleukin-10 (IL-10), and tumor necrosis factor-α (TNF-α) in the hippocampus also measured as markers of oxidative stress and inflammation. Furthermore, the expression of AQP-4 measured in the intact and experimental groups. ResultsThe results showed that Fasudil significantly improved memory and anxiety behavior induced by LPS in the open field maze, spatial recognition memory in the Y-maze, and performance in the novel object recognition task. It also mitigates hippocampal MDA and SOD levels. Additionally, fasudil ameliorated LPS-induced hippocampal levels of TNFα and IL-10 and increased hippocampal levels of AQP-4 expression in mice. ConclusionOur results suggest that fasudil in the LPS model of systemic inflammation could improve cognition by suppressing oxidative stress and inflammation and increasing AQP-4 protein expression. These findings highlighted the potential of fasudil as a neuroprotective agent. However, further research is required to fully understand its neuroprotective properties in the treatment of neurodegenerative disorders.

Category boundaries modulate memory in a place-cell-like manner

Concepts describe how instances of the same kind are related, enabling the categorization and interpretation of new information.1,2 How concepts are represented is a longstanding question. Category boundaries have been considered defining features of concept representations, which can guide categorical inference,3 with fMRI evidence showing category-boundary signals in the hippocampus.4,5 The underlying neural mechanism remains unclear. The hippocampal-entorhinal system, known for its spatially tuned neurons that form cognitive maps of space,6,7 may support conceptual knowledge formation, with place cells encoding locations in conceptual space.4,8,9,10,11 Physical boundaries anchor spatial representations and boundary shifts affect place and grid fields,12,13,14,15,16 as well as human spatial memory,17,18,19 along manipulated dimensions. These place cell responses are likely driven by boundary vector cells, which respond to boundaries at specific allocentric distances and directions,20,21,22,23 the neural correlates of which have been identified in the subiculum and entorhinal cortex20,24,25. We hypothesize similar patterns of memory adaptations in response to shifting category boundaries. Our findings show that after category boundary shifts, participants' memory for category exemplars distorts along the changed dimension, mirroring place field deformations. We demonstrate that the boundary vector cell model of place cell firing best accounts for these distortions compared with alternative geometric explanations. Our study highlights a role of category boundaries in human cognition and establishes a new complementary link between hippocampal coding properties with respect to boundaries and human concept representation, bridging spatial and conceptual domains.

Trimethylamine N-Oxide Aggravates Neuro-Inflammation via lncRNA Fendrr/miR-145-5p/PXN Axis in Vascular Dementia Rats.

Vascular dementia (VaD) is the second most common dementia in the world. An increasing number of studies have demonstrated the important role of long non-coding RNAs (lncRNAs) in VaD. Our previous investigation demonstrated that Trimethylamine-N-oxide (TMAO) exacerbates cognitive impairment and neuropathological alterations in VaD rats. Thus, we hypothesized that TMAO could play an injury role in VaD by regulating lncRNAs. The rats using the bilateral common carotid artery (2VO) model were administered TMAO (120 mg/kg) for 8 consecutive weeks, 4weeks preoperatively and 4weeks postoperatively. High-throughput sequencing was conducted to investigate the effects of TMAO treatment on lncRNA expression in rat hippocampus and bioinformatics analysis was performed to identify potential downstream targets. Reverse transcription-quantitative polymerase chain reaction (RT-qPCR) was used to detect the levels of lncRNA fetal-lethal noncoding developmental regulatory RNA (Fendrr), miR-145-5p, and paxillin (PXN). Learning and spatial memory capacities were measured, as well as inflammatory factors. Nissl staining was used to observe neuronal injury in the CA1 area of the hippocampus. Furthermore, we used the Fendrr loss-of-function assay, miR-145-5p gain-of-function assays and PXN loss-of-function assay to explore the mechanisms by which TMAO acts on VaD. TMAO administration upregulated lncRNA Fendrr expression in the rat hippocampus, while the damaging effects of TMAO were counteracted after knockdown of Fendrr. Fendrr exhibits highly expressed in 2VO rats and sponged miR-145-5p, which targets PXN. Silencing of Fendrr or PXN, or promotion of miR-145-5p improved neurological function injury, reduced neuronal damage, as well as repressed inflammation response. Inhibition of miR-145-5p abrogated up Fendrr knockdown mediated influence on 2VO rats. The results of this study indicated that TMAO inhibits the miR-145-5p/PXN axis by increasing the Fendrr expression, thus exacerbating the development of VaD.

YTHDF1 gene inhibits epilepsy progression by epigenetic activation of PTEN gene

Epilepsy is a common chronic neurological disorder with high prevalence that profoundly affects millions of people worldwide. Inflammatory dysregulation affects central nervous system disorders including epilepsy, and YTHDF1, the most common "reader" of m6A and m6A-binding protein, can attenuate the inflammatory response and activate PTEN, and here we aimed to investigate its effect on epilepsy through epigenetics. All mice were injected intraperitoneally with 12 mg/kg of sea manic acid to establish an epilepsy model, and the epileptic behaviors of the mice were classified into 6 grades; epileptic behaviors of grade 3 or above were defined as seizures, and consecutive epileptic seizures of more than 30 min were considered as successful modeling. Mouse behavior was examined using the Morris Water Maze tracking assay; inflammatory factors IL-6, TNF-α, and IL-1β were detected by qPCR/WB/ELISA; cell activity was analyzed by CCK-8; apoptotic markers were identified by immunofluorescence assay and Western blot analysis. YTHDF1 knockout mice have poor spatial memory capacity and sensitivity to external stimuli. Under the influence of YTHDF1, the neuroinflammation and nseuron death decreased. YTHDF1 works by repressing the production of pro-inflammatory cytokines and the activation of astrocytes. It was found that YTHDF1 epigenetically activates PTEN through m6A modification, activates glial cells and represses pro-inflammatory cytokines production and inhibits the development of epilepsy.

Microglial priming by IFN-γ involves STAT1-mediated activation of the NLRP3 inflammasome.

Inflammatory and immune responses in the brain that contribute to various neuropsychiatric disorders may begin as microglial "priming". Interferon (IFN)-γ is known to cause microglial priming, but the mechanism is unclear. We examined the effects of IFN-γ on gene expression, microglial activation, inflammatory and immune responses and activity of the NLRP3 inflammasome in primary microglia and in the brains of mice. Our results showed that treating microglial cultures with IFN-γ induced a hedgehog-like morphology and upregulated markers of microglial activation (CD86, CD11b) and pro-inflammatory molecules (IL-1β, IL-6, TNF-α, iNOS), while downregulating markers of microglial homeostasis (CX3CR1, CD200R1), anti-inflammatory molecules (MCR1, Arg-1) and neurotrophic factors (IGF-1, BDNF). IFN-γ also upregulated markers of NLRP3 inflammasome activation (NLRP3, caspase-1, gasdermin D, IL-18). This particular transcriptional profiling makes IFN-γ-primed microglia with exaggerated responses upon lipopolysaccharide (LPS) stimulation. The level of NLRP3, caspase-1, gasdermin D, IL-1β, IL-18, TNF-α and iNOS in microglia cultures treated with both IFN-γ and LPS were highest than with either one alone. Injecting IFN-γ into the lateral ventricle of mice induced similar morphological and functional changes in hippocampal microglia as in primary microglial cultures. The effects of IFN-γ on NLRP3 inflammasome and microglia from cultures or hippocampus were abolished when STAT1 was inhibited using fludarabin. Injecting mice with IFN-γ alone or together with LPS induced anxiety- and depression-like behaviors and impaired hippocampus-dependent spatial memory; these effects were mitigated by fludarabin. IFN-γ primes microglia by activating STAT1, which upregulates genes that activate the NLRP3 inflammasome. Inhibiting the IFN-γ/STAT1 axis may be a way to treat neurodegenerative diseases and psychiatric disorders that involve microglial priming.

A Computer Vision System for an Automated Scoring of a Hand-drawn Geometric Figure

Visual Reproduction is a condition to measure Visual Spatial Memory as one of the cognitive domains commonly used to measure visuo-spatial memory. Geometric figures serve as stimulus material, and probands have to reproduce the figures from memory through a hand drawing. The scoring of the drawing has subjective elements. This study aims to evaluate the scoring criteria for the Figural Reproduction Test (FRT), part of the Indonesian Neuropsychological Test Battery, and to develop and evaluate an automated scoring system based on computer vision technology (FRT-CVAS). Scoring evaluation conducted by Cohen Kappa analysis, accuracy, sensitivity, and specificity. The analyzes of the three criteria of the manual confirmed a subjective element in the scoring of the shape of triangles by a moderate (0.74) inter-rater agreement; this agreement could be improved to 0.84 by a slight modification of its criteria. FRT-CVAS, based on computer vision’s identification of the different elements of the hand drawing, was developed and trained using 290 drawings. The system was additionally tested by comparing its scoring with the scoring of two independent raters on 120 drawings from a second data set. FRT-CVAS recognized all elements, and its comparison between human raters showed a high accuracy and sensitivity (minimally 0.91), while the specificity was 0.80 for one of the three criteria. FRT-CVAS offers a highly standardized, consistent, precise, and objective output from the first card in the FRT. This approach is advantageous to data-hungry alternatives such as deep learning when applied to the automated scoring of hand drawings with relatively little data available for training.

Differences in memory performance: The effects of sex and reproductive experience on object recognition memory in high- and low-yawning Sprague‒Dawley rats

The novel object recognition (NOR) test is an efficient way to measure nonspatial memory in rodents. The NOR performance of female and male rats is sexually dimorphic because memory performance is better in the former than in the latter. In females, maternal experience enhances spatial memory. We used the NOR test to evaluate short- and long-term recognition memory in both sexes in the high- and low-yawning sublines of rats (HY and LY, respectively), which were generated via a strict inbreeding process from the Sprague‒Dawley (SD) strain for more than ninety generations. Additionally, we evaluated the effect of maternal experience using nulliparous, primiparous, biparous, and multiparous HY, LY and SD dams. Our results revealed that LY rats presented less thigmotaxis, with lower central square crosses and more vertical exploration in the open-field arena, suggesting that they experienced anxiety. Additionally, LY males performed significantly better than LY females in short- and long-term NOR memory, and LY males performed significantly better than SD rats did. Among females, two maternal experiences negatively affected short-term memory in the LY and HY sublines with respect to primiparous dams, and HY dams had better memory performance in the NOR test than did SD dams. Our findings suggest that the yawning sublines are suitable for studying the neurobiological basis of different memory processes under different endocrine conditions in highly inbred groups of rats.

The Impact of Science, Environment, Technology, and Society (SETS) Learning Model Integrated with Google Earth on Spatial Thinking Ability in Senior High School

Developing spatial thinking skills in students often poses a challenge for Geography teachers in Indonesia. The concept of spatial relationships in geography places spatial thinking as a distinct aspect of intelligence, enabling individuals to identify patterns and trends in spatial change. Therefore, appropriate models and strategies are needed to develop spatial thinking skills. This study aims to determine the effect of the Science, Environment, Technology and Society (SETS) learning model integrated with Google Earth on students' spatial thinking ability. This research is a quasi-experiment with posttest-only design nonequivalent groups that uses a quantitative approach with the inferential statistical method using the Independent sample t-test parametric test. The subjects of this study were randomly selected XI grade students from SMAN 10 Malang including, XI-C class as the experimental class and XI-D as the control class. The research instruments used are seven essay questions on spatial thinking ability. The data obtained will be analyzed using parametric statistics Independent sample t-test and obtained sig value. (2-tailed) 0.041. The mean value of the experimental class is greater (80.14) than the mean value of the control class (72.08). It can be concluded that the Science, Environment, Technology, and Society (SETS) model integrated with Google Earth affects students' spatial thinking ability on the material of Disaster and Environment class XI SMAN 10 Malang City. Another finding of this study is that three syntaxes are dominant in bringing up and developing students' spatial thinking ability, namely initiation, concept development formation, and concept application.

Extract of Angelica keiskei Leaves Attenuates Spatial Memory Impairment on the D-galactose Model of Brain Aging in Mice

Aging is a complex and inexorable phenomenon, entailing several physiological changes. Impaired memory skills are associated with cell death in the hippocampus as a result of the age-related buildup of free radicals. D-galactose can artificially accelerate brain aging, causing memory impairment in mice due to neuroinflammation and oxidative stress. Numerous phytoconstituents found in Angelica keiskei possess anti-oxidant, anti-inflammatory, and memory-enhancing properties. In this study, we sought to determine the effects of an ethanol extract from the leaves of A. keiskei (EELAK) on spatial memory in mice with impaired memory functions due to D-gal. Here, we showed that administering 300 mg/kg BW/day of D-gal orally for a duration of 28 days significantly decreased spatial memory as quantified by the Morris Water Maze, and this was linked to a marked increase in hippocampal acetylcholinesterase (AChE), inflammation, and oxidative stress. The spatial memory of D-gal-induced mice was markedly enhanced by 20 mg/kg BW/day of EELAK, demonstrating its potent memory-boosting properties. The mice treated with EELAK also showed a notable decrease in hippocampal neuroinflammation (p65 NF-kB, NO, and TNF-α protein) and an increase in antioxidant activity (elevated SOD activity and reduced MDA levels), suggesting its potent neuroprotective activity. In conclusion, our results establish for the first time that by reducing oxidative stress and neuroinflammation, EELAK enhances spatial memory. Hence, for the prevention and treatment of age-related neurodegenerative illnesses like Alzheimer's disease, EELAK may be a useful therapeutic approach.

Measures of spatial memory, peripheral inflammation and negative emotional state predict social-cognitive skills in healthy aging cats

Aging is a complex, multidimensional process. Normative aging is typically accompanied by declines in several cognitive domains, including memory and social cognition. As aging progresses, the often-overlooked early manifestations of cognitive decline can advance, leading to an inability to adapt to new situations and environments. Potential mechanisms influencing cognitive decline remain elusive, but, among other mechanisms, inflammaging, an age-related increase in the chronic production of pro-inflammatory mediators, and emotional stress are implicated. Cognitive function in cats is under-researched, with no studies on the link between potential risk factors and cognitive signs in aging subjects. Understanding this link is essential as it may facilitate the early identification of cognitive decline and encourage preventative, individualized interventions. We carried out a citizen science study to investigate, for the first time, the relationship between cognitive functions, stress, and the inflammatory markers interleukin (IL)-1β and IL-10 in 44 healthy, privately owned pet cats (7–14 years of age), who underwent standardized testing in their home environment. A task was employed to test spatial memory, requiring the cat to recall the location of a food-baited container. An unsolvable task was used to assess cats' social cognition and cognitive flexibility by measuring how they used referential communication (i.e., gaze alternation between the apparatus and the caregivers) compared to their persistence in trying to obtain food which was out of reach. Generalized linear regression analysis, conducted while adjusting for demographic factors and stress behaviors, revealed: 1) a predictive positive relationship connecting spatial memory and the use of social referencing with the caregiver (more gaze alternation) in the unsolvable task, highlighting the importance of the interplay between cognitive domains in sustaining complex behaviors, and 2) a reduced engagement in social referencing toward caregivers (less gaze alternation) in the presence of higher serum levels of IL-1β in the unsolvable task, especially as cats get older. A cat’s social cognitive performance was also negatively predicted by stress-related behaviors, which is not surprising given that cats are sentient creatures whose everyday behavior is also influenced by emotional states. These findings provide new insights into the crosstalk between different cognitive domains during aging and the potential contributions of emotions and inflammation to cognitive changes in healthy aging cats. Further research using this multidimensional approach will help explore these mechanisms of cognitive aging and potential markers for early detection of cognitive changes in older cats, which is critical for timely interventions.

In vivo neuroprotective effect of Guaiacum officinale leaf extracts in scopolamine-induced cognitive impairment model

ABSTRACT The phytochemical composition and neuroprotective potential of the ethanolic extract of Guaiacum officinale leaves against scopolamine-induced amnesia were investigated. Spatial memory was evaluated through the Morris water maze, while the entire brain was assessed for acetylcholinesterase (AchE), malondialdehyde (MDA), and superoxide dismutase (SOD) levels. The presence of glycosides, alkaloids, steroids, terpenoids, flavonoids, and saponins was detected in the ethanolic extract through phycological analysis. The findings suggested that the ethanolic extract alleviated scopolamine-induced spatial memory impairments caused by scopolamine and decreased the AchE activity. The study also detailed MDA, SOD, transfer latency periods, and acetylcholine esterase levels in both normal and extract-treated groups.