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Luminescent rare-earth-based nanoparticles have been increasingly used in nanomedicine due to their excellent physicochemical properties, such as biomedical imaging agents, drug carriers, and biomarkers. However, biological safety of the rare-earth-based nanomedicine is of great significance for future development in practical applications. In particular, biological effects of rare-earth nanoparticles on human's central nervous system are still unclear. This study aimed to investigate the potential toxicity of rare-earth nanoparticles in nervous system function in the case of continuous exposure. Adult ICR mice were randomly divided into seven groups, including control group (receiving 0.9% normal saline) and six experimental groups (10 mice in each group). Luminescent rare-earth-based nanoparticles were synthesized by a reported co-precipitation method. Two different sizes of the nanoparticles were obtained, and then exposed to ICR mice through caudal vein injection at 0.5, 1.0, and 1.5 mg/kg body weight in each day for 7 days. Next, a Morris water maze test was employed to evaluate impaired behaviors of their spatial recognition memory. Finally, histopathological examination was implemented to study how the nanoparticles can affect the brain tissue of the ICR mice. Two different sizes of rare-earth nanoparticles have been successfully obtained, and their physical properties including luminescence spectra and nanoparticle sizes have been characterized. In these experiments, the rare-earth nanoparticles were taken up in the mouse liver using the magnetic resonance imaging characterization. Most importantly, the experimental results of the Morris water maze tests and histopathological analysis clearly showed that rare-earth nanoparticles could induce toxicity on mouse brain and impair the behaviors of spatial recognition memory. Finally, the mechanism of adenosine triphosphate quenching by the rare-earth nanoparticles was provided to illustrate the toxicity on the mouse brain. This study suggested that long-term exposure of high-dose bare rare-earth nanoparticles caused an obvious damage on the spatial recognition memory in the mice.

IntroductionFalse contextual fear memory has been attributed to a time-dependent loss of precision in contextual memory representations. In this study, we investigated the role of protein kinase M zeta (PKMζ), a key molecule in the maintenance of hippocampus-dependent long-term memory, in false contextual fear memory within the dorsal (dHPC) and ventral hippocampus (vHPC).MethodsTwo weeks prior to behavioral testing, male C57BL/6J mice (7–10 weeks old) received bilateral injections of adeno-associated virus (AAV PHP.eB) into the dHPC or vHPC to induce PKMζ knockdown (PKMζ KD), overexpression of wild-type PKMζ (PKMζ WT), or kinase-inactive PKMζ (PKMζ K281R). False contextual fear memory was assessed by measuring freezing behavior in Context B at 3 and 24 h following exposure to Context A with or without unconditioned stimulus presentation [US(+) and US(−), respectively]. Spatial recognition memory was evaluated using the two-trial novel arm recognition test in the Y-maze.ResultsAs shown in our previous work, mice exhibited freezing in Context B after receiving a US in Context A, whereas mice that did not receive such a stimulus showed minimal freezing. These data confirmed that freezing in Context B reflects false contextual fear memory. False fear responses were evident at 3 h and were further increased at 24 h. Freezing at 24 h was markedly enhanced in dHPC PKMζ knockdown mice compared with that in AAV control-injected mice. PKMζ WT overexpression prevented the increase in freezing at 24 h, whereas PKMζ K281R overexpression mimicked the effects of PKMζ KD. Furthermore, PKMζ knockdown in the dHPC impaired spatial recognition memory, indicating that hippocampus-dependent spatial processing was disrupted. In contrast, PKMζ manipulation in the vHPC did not affect false contextual fear memory but did impair spatial recognition memory.DiscussionThese findings are consistent with the possibility that functional loss of PKMζ in the dHPC affects contextual memory processes in a manner that may contribute to the time-dependent increase in false contextual fear and impaired spatial recognition memory.

In the present study we investigated the efficacy of the differential outcomes procedure (DOP) to improve visuospatial working memory in patients with Alzheimer's disease and mild cognitive impairment (MCI). The DOP associates correct responses to the to-be-remember stimulus with unique outcomes. Eleven patients diagnosed with Alzheimer's disease, 11 participants with MCI, and 17 healthy matched controls performed a spatial delayed memory task under the DOP and a control condition (non-differential outcomes -NOP-). We found that performance (terminal accuracy) was significantly better in the DOP condition relative to the NOP condition in all three groups of participants. AD patients performed worse, and took longer to benefit from the DOP. In line with previous animal and human research, we propose that the DOP activates brain structures and cognitive mechanisms that are less affected by healthy and pathological aging, optimizing in this way the function of the cognitive system.

Background: Scientific interest has grown in naturally derived compounds capable of supporting or enhancing cognitive performance. Tanacetum vulgare L. is an abundant source of secondary metabolites and has been associated with a broad range of biological activities; however, its potential influence on cognitive function remains largely unexplored. Methods: The present study explored the effects of T. vulgare essential oil (EO) on cognitive performance, hippocampal brain-derived neurotrophic factor (BDNF) expression, and histomorphological alterations in a rat model. Animals were administered T. vulgare EO at doses of 0.5 and 1.5 mL/kg for 28 days and were subjected to a series of behavioral tests after one week of pretreatment. Results: Both doses of EO facilitated the formation of short- and long-term memory traces in the inhibitory avoidance tasks, with a more pronounced effect observed at the lower dose, whereas improvement in passive learning was evident only at the higher dose. Spatial and recognition memory were enhanced at both doses. EO treatment significantly increased hippocampal BDNF expression without inducing pathological alterations. Conclusions: These findings suggest that T. vulgare EO may improve specific hippocampal-dependent cognitive functions, with upregulation of hippocampal BDNF representing a potential underlying mechanism.

Lithium is a drug used for the treatment of bipolar disorder. It has several mechanisms of action, and recently it is shown that lithium can antagonize the 5-HT1B/1D serotonin receptors. Sumatriptan is a 5-HT1B/1D receptor agonist used for the treatment of cluster headaches and migraine which might cause memory impairment as a potential side effect. In this study, effects of lithium on sumatriptan-induced memory impairment have been determined in a two-trial recognition Y-maze and passive avoidance tests. Male mice weighing 25-30 g were divided into several groups randomly. In Y-maze test, effects of lithium (1,5,10,20,40,80 mg/kg) and sumatriptan (1,5,10 mg/kg) were assessed on memory acquisition, then lithium (0.1,1,10 mg/kg) and sumatriptan (1,10 mg/kg) were studied in passive avoidance test. Effects of lithium (1mg/kg) on sumatriptan (10 mg/kg)-induced memory impairment were studied in both of tests. The present study demonstrated that sumatriptan impaired memory in Y-maze and passive avoidance tests (P<0.05, P<0.01, respectively). Lithium did not show any significant effect on memory function compared to saline-treated control group in both tests (P>0.05), but significantly reversed sumatriptan-induced memory impairment in Y-maze and passive avoidance tests (P<0.001, P<0.05, respectively). It is concluded that lithium reverses the sumatriptan-induced memory impairment probably through 5-HT1B/1D receptors antagonism.

A previous study in the rat has shown that systemic injection of two CCK-B agonists, BC264 and BC197, induced opposing effects on the retrieval phase of a spatial recognition memory task. The present study was designed to investigate the mechanisms underlying these effects at the level of the dopaminergic system. Rats were injected IPly with BC264 (0.3 microg/kg) or BC197 (30 microg/kg) and with D1 or D2 agonists and antagonists. The cognitive performances of rat were analysed on the retrieval phase of a spatial recognition memory task. The extracellular levels of dopamine were quantified in the anterior nucleus accumbens after injection of BC197 (3, 30 and 300 microg/kg IP), using the microdialysis technique on freely moving rats. Local injection of the D2 antagonist, sulpiride (2.5 ng/microl) was performed in the anterior nucleus accumbens and the cognitive performances analysed following systemic injection of BC264 (0.3 microg/kg). The improvement and the impairment of performance induced respectively by BC264 and BC197 were suppressed by peripheral administration of sulpiride, showing that these opposing effects were both mediated by the stimulation of D2-like receptors. However, different dopaminergic pathways seem to be involved in the effects of the two CCK-B agonists. Indeed, systemic administration of BC197 did not induce the increase of extracellular dopamine levels observed with BC264. Furthermore, local injection of sulpiride, in the anterior nucleus accumbens, completely suppressed the cognitive enhancing effect of BC264. These findings suggest that the D2-mediated deficit in the performance induced by BC197 involves brain structures other than the anterior nucleus accumbens. They also demonstrate a critical role of dopaminergic transmission within the anterior nucleus accumbens in the improving effect induced by BC264 in a spatial memory task.

Limited longitudinal research examining developmental changes in visuospatial working memory (WM) among children and adolescents with autism spectrum disorder (ASD) has prompted our investigation. We assessed 123 autistic children and adolescents and 145 typically developing controls (TDC) using the Cambridge Neuropsychological Test Automated Battery at baseline (Time 1 [mean age ± SD]: ASD: 13.04 ± 2.86; TDC: 11.53 ± 2.81) and 2-9 years later (Time 2: ASD: 18.08 ± 3.17; TDC: 16.41 ± 3.09) to measure changes of visuospatial (working) memory over time. The linear mixed model was used to compare the differences between ASD and TDC and estimate the effect of changes over time, age, ASD diagnosis, and interactions of Time×Age×ASD. The overall Age×ASD effect was calculated in the spline regression. Autistic children and adolescents exhibited significantly poorer performance on all spatial tasks and some visual tasks than their TDC counterparts at Time 1 and Time 2, after adjusting for sex, age, attention deficit/hyperactivity disorder (ADHD), and full-scale intelligence quotient. There was an overall improvement from Time 1 to Time 2 across all tasks with significant Age×Time interactions. Significant Age×ASD interactions were observed in the delayed matching to sample, pattern recognition memory (PRM), spatial span (SSP), and spatial working memory (SWM) tasks with no significant Time×ASD interactions. In the quadratic nonlinear model, Age×ASD interactions were significant in PRM and SSP. Despite significant improvements during the follow-up period, autistic children and adolescents continue to experience persistent deficits in SWM, with a weaker age-related improvement in visuospatial WM than TDC.

We examined visual recognition memory and executive functioning (spatial working memory [SWM], spatial planning, rule learning, and attention shifting) in 12-year-olds (n = 150) who participated in the Bucharest Early Intervention Project, a randomized controlled trial of foster care for institutionally reared children. Similar to prior reports at 8 years of age, institutionally reared children showed significant deficits in visual recognition memory and SWM. Deficits in attention shifting and rule learning were also apparent at this time point. These data suggest that early experiences continue to shape the development of memory, learning, and executive functioning processes in preadolescence, which may explain broader cognitive and learning difficulties commonly associated with severe early life neglect.

The consolidation of spatial memory depends on the reactivation (‘replay’) of hippocampal place cells that were active during recent behaviour. Such reactivation is observed during sharp-wave ripples (SWRs)—synchronous oscillatory electrical events that occur during non-rapid-eye-movement (non-REM) sleep 1 – 8 and whose disruption impairs spatial memory 3 , 5 , 6 , 8 . Although the hippocampus also encodes a wide range of non-spatial forms of declarative memory, it is not yet known whether SWRs are necessary for such memories. Moreover, although SWRs can arise from either the CA3 or the CA2 region of the hippocampus 7 , 9 , the relative importance of SWRs from these regions for memory consolidation is unknown. Here we examine the role of SWRs during the consolidation of social memory—the ability of an animal to recognize and remember a member of the same species—focusing on CA2 because of its essential role in social memory 10 – 12 . We find that ensembles of CA2 pyramidal neurons that are active during social exploration of previously unknown conspecifics are reactivated during SWRs. Notably, disruption or enhancement of CA2 SWRs suppresses or prolongs social memory, respectively. Thus, SWR-mediated reactivation of hippocampal firing related to recent experience appears to be a general mechanism for binding spatial, temporal and sensory information into high-order memory representations, including social memory. Social memory is consolidated in the brain through the reactivation of neuronal firing by sharp-wave ripples in the CA2 region of the hippocampus, in a similar way to the consolidation of spatial memory.