scholarly journals Emergence of preconfigured and plastic time-compressed sequences in early postnatal development

Science ◽  
2019 ◽  
Vol 363 (6423) ◽  
pp. 168-173 ◽  
Author(s):  
U. Farooq ◽  
G. Dragoi
Keyword(s):  
Hippocampal Neurons ◽  
Memory Formation ◽  
Sequential Patterns ◽  
Early Postnatal Development ◽  
Neuronal Ensembles ◽  
Electrophysiological Activity ◽  
Age Dependent ◽  
Large Ensembles ◽  
Eye Opening ◽  
The Brain

When and how hippocampal neuronal ensembles first organize to support encoding and consolidation of memory episodes, a critical cognitive function of the brain, are unknown. We recorded electrophysiological activity from large ensembles of hippocampal neurons starting on the first day after eye opening as naïve rats navigated linear environments and slept. We found a gradual age-dependent, navigational experience–independent assembly of preconfigured trajectory-like sequences from persistent, location-depicting ensembles during postnatal week 3. Adult-like compressed binding of adjacent locations into trajectories during navigation and their navigational experience–dependent replay during sleep emerged in concert from spontaneous preconfigured sequences only during early postnatal week 4. Our findings reveal ethologically relevant distinct phases in the development of hippocampal preconfigured and experience-dependent sequential patterns thought to be important for episodic memory formation.

scholarly journals Memory formation: from network structure to neural dynamics

2010 ◽  
Vol 368 (1918) ◽  
pp. 2251-2267 ◽  
Author(s):  
Sarah Feldt ◽  
Jane X. Wang ◽  
Vaughn L. Hetrick ◽  
Joshua D. Berke ◽  
Michal Żochowski
Keyword(s):  
Brain Function ◽  
Cognitive Process ◽  
Neural Correlates ◽  
Memory Formation ◽  
Neural Dynamics ◽  
Formation Processes ◽  
Neuronal Dynamics ◽  
Neuronal Ensembles ◽  
Derived Data ◽  
The Brain

Understanding the neural correlates of brain function is an extremely challenging task, since any cognitive process is distributed over a complex and evolving network of neurons that comprise the brain. In order to quantify observed changes in neuronal dynamics during hippocampal memory formation, we present metrics designed to detect directional interactions and the formation of functional neuronal ensembles. We apply these metrics to both experimental and model-derived data in an attempt to link anatomical network changes with observed changes in neuronal dynamics during hippocampal memory formation processes. We show that the developed model provides a consistent explanation of the anatomical network modifications that underlie the activity changes observed in the experimental data.

Complexity Measures of Brain Electrophysiological Activity

2010 ◽  
Vol 24 (2) ◽  
pp. 131-135 ◽  
Author(s):  
Włodzimierz Klonowski ◽  
Pawel Stepien ◽  
Robert Stepien
Keyword(s):  
Brain Activity ◽  
Deterministic Chaos ◽  
Epileptic Seizures ◽  
Eeg Signal ◽  
Eeg Signals ◽  
Complexity Measures ◽  
Electrophysiological Activity ◽  
Signal Complexity ◽  
Physiological Sleep ◽  
The Brain

Over 20 years ago, Watt and Hameroff (1987 ) suggested that consciousness may be described as a manifestation of deterministic chaos in the brain/mind. To analyze EEG-signal complexity, we used Higuchi’s fractal dimension in time domain and symbolic analysis methods. Our results of analysis of EEG-signals under anesthesia, during physiological sleep, and during epileptic seizures lead to a conclusion similar to that of Watt and Hameroff: Brain activity, measured by complexity of the EEG-signal, diminishes (becomes less chaotic) when consciousness is being “switched off”. So, consciousness may be described as a manifestation of deterministic chaos in the brain/mind.

Deletion of murine tau gene increases tau aggregation in a human mutant tau transgenic mouse model

2010 ◽  
Vol 38 (4) ◽  
pp. 1001-1005 ◽  
Author(s):  
Kunie Ando ◽  
Karelle Leroy ◽  
Céline Heraud ◽  
Anna Kabova ◽  
Zehra Yilmaz ◽  
...  
Keyword(s):  
Mouse Model ◽  
Transgenic Mouse ◽  
Double Mutant ◽  
Transgenic Mouse Model ◽  
Tau Proteins ◽  
Dependent Manner ◽  
Age Dependent ◽  
Ad Alzheimer’S Disease ◽  
Tau Aggregation ◽  
The Brain

We have reported previously a tau transgenic mouse model (Tg30tau) overexpressing human 4R1N double-mutant tau (P301S and G272V) and that develops AD (Alzheimer's disease)-like NFTs (neurofibrillary tangles) in an age-dependent manner. Since murine tau might interfere with the toxic effects of human mutant tau, we set out to analyse the phenotype of our Tg30tau model in the absence of endogenous murine tau with the aim to reproduce more faithfully a model of human tauopathy. By crossing the Tg30tau line with TauKO (tau-knockout) mice, we have obtained a new mouse line called Tg30×TauKO that expresses only exogenous human double-mutant 4R1N tau. Whereas Tg30×TauKO mice express fewer tau proteins compared with Tg30tau, they exhibit augmented sarkosyl-insoluble tau in the brain and an increased number of Gallyas-positive NFTs in the hippocampus. Taken together, exclusion of murine tau causes accelerated tau aggregation during aging of this mutant tau transgenic model.

scholarly journals Comparison of age‐dependent alterations in thioredoxin 2 and thioredoxin reductase 2 expressions in hippocampi between mice and rats

2021 ◽  
Vol 37 (1) ◽  
Author(s):  
Yeon Ho Yoo ◽  
Dae Won Kim ◽  
Bai Hui Chen ◽  
Hyejin Sim ◽  
Bora Kim ◽  
...  
Keyword(s):  
Thioredoxin Reductase ◽  
Pyramidal Cells ◽  
Brain Regions ◽  
Young Age ◽  
Cresyl Violet ◽  
Western Blots ◽  
Protein Levels ◽  
Cresyl Violet Staining ◽  
Age Dependent ◽  
The Brain

Abstract Background Aging is one of major causes triggering neurophysiological changes in many brain substructures, including the hippocampus, which has a major role in learning and memory. Thioredoxin (Trx) is a class of small redox proteins. Among the Trx family, Trx2 plays an important role in the regulation of mitochondrial membrane potential and is controlled by TrxR2. Hitherto, age-dependent alterations in Trx2 and TrxR2 in aged hippocampi have been poorly investigated. Therefore, the aim of this study was to examine changes in Trx2 and TrxR2 in mouse and rat hippocampi by age and to compare their differences between mice and rats. Results Trx2 and TrxR2 levels using Western blots in mice were the highest at young age and gradually reduced with time, showing that no significant differences in the levels were found between the two subfields. In rats, however, their expression levels were the lowest at young age and gradually increased with time. Nevertheless, there were no differences in cellular distribution and morphology in their hippocampi when it was observed by cresyl violet staining. In addition, both Trx2 and TrxR2 immunoreactivities in the CA1-3 fields were mainly shown in pyramidal cells (principal cells), showing that their immunoreactivities were altered like changes in their protein levels. Conclusions Our current findings suggest that Trx2 and TrxR2 expressions in the brain may be different according to brain regions, age and species. Therefore, further studies are needed to examine the reasons of the differences of Trx2 and TrxR2 expressions in the hippocampus between mice and rats.

scholarly journals Post-status epilepticus treatment with the Fyn inhibitor, saracatinib, improves cognitive function in mice

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Xin-Ming Luo ◽  
Jing Zhao ◽  
Wen-Yue Wu ◽  
Jie Fu ◽  
Zheng-Yu Li ◽  
...  
Keyword(s):  
Status Epilepticus ◽  
Cognitive Function ◽  
Cognitive Deficits ◽  
Tyrosine Kinases ◽  
Hippocampal Neurons ◽  
Water Maze ◽  
Behavioral Tests ◽  
Life Threatening ◽  
The Brain ◽  
Normal Object

Abstract Background Status epilepticus (SE) is a life-threatening neurological disorder. The hippocampus, as an important area of the brain that regulates cognitive function, is usually damaged after SE, and cognitive deficits often result from hippocampal neurons lost after SE. Fyn, a non-receptor Src family of tyrosine kinases, is potentially associated with the onset of seizure. Saracatinib, a Fyn inhibitor, suppresses epileptogenesis and reduces epileptiform spikes. However, whether saracatinib inhibits cognitive deficits after SE is still unknown. Methods In the present study, a pilocarpine-induced SE mouse model was used to answer this question by using the Morris water maze and normal object recognition behavioral tests. Results We found that saracatinib inhibited the loss in cognitive function following SE. Furthermore, we found that the number of hippocampal neurons in the saracatinib treatment group was increased, when compared to the SE group. Conclusions These results showed that saracatinib can improve cognitive functions by reducing the loss of hippocampal neurons after SE, suggesting that Fyn dysfunction is involved in cognitive deficits after SE, and that the inhibition of Fyn is a possible treatment to improve cognitive function in SE patients.

scholarly journals Latent learning drives sleep-dependent plasticity in distinct CA1 subpopulations

2020 ◽  
Author(s):  
Wei Guo ◽  
Jie J. Zhang ◽  
Jonathan P. Newman ◽  
Matthew A. Wilson
Keyword(s):  
Hippocampal Neurons ◽  
Dimensional Manifold ◽  
Latent Learning ◽  
Neural Ensembles ◽  
Correlated Activity ◽  
Place Fields ◽  
Internal States ◽  
Low Dimensional ◽  
Low Dimensional Manifold ◽  
The Brain

AbstractLatent learning allows the brain the transform experiences into cognitive maps, a form of implicit memory, without reinforced training. Its mechanism is unclear. We tracked the internal states of the hippocampal neural ensembles and discovered that during latent learning of a spatial map, the state space evolved into a low-dimensional manifold that topologically resembled the physical environment. This process requires repeated experiences and sleep in-between. Further investigations revealed that a subset of hippocampal neurons, instead of rapidly forming place fields in a novel environment, remained weakly tuned but gradually developed correlated activity with other neurons. These ‘weakly spatial’ neurons bond activity of neurons with stronger spatial tuning, linking discrete place fields into a map that supports flexible navigation.

scholarly journals Aspartoacylase Supports Oxidative Energy Metabolism during Myelination

2012 ◽  
Vol 32 (9) ◽  
pp. 1725-1736 ◽  
Author(s):  
Jeremy S Francis ◽  
Louise Strande ◽  
Vladamir Markov ◽  
Paola Leone
Keyword(s):  
Energy Metabolism ◽  
Postnatal Development ◽  
Strong Association ◽  
Canavan Disease ◽  
Lipid Synthesis ◽  
Systematic Analysis ◽  
Early Postnatal Development ◽  
Neuronal Viability ◽  
Oxidative Energy Metabolism ◽  
The Brain

The inherited leukodystrophy Canavan disease arises due to a loss of the ability to catabolize N-acetylaspartic acid (NAA) in the brain and constitutes a major point of focus for efforts to define NAA function. Accumulation of noncatabolized NAA is diagnostic for Canavan disease, but contrasts with the abnormally low NAA associated with compromised neuronal integrity in a broad spectrum of other clinical conditions. Experimental evidence for NAA function supports a role in white matter lipid synthesis, but does not explain how both elevated and lowered NAA can be associated with pathology in the brain. We have undertaken a systematic analysis of postnatal development in a mouse model of Canavan disease that delineates development and pathology by identifying markers of oxidative stress preceding oligodendrocyte loss and dysmyelination. These data suggest a role for NAA in the maintenance of metabolic integrity in oligodendrocytes that may be of relevance to the strong association between NAA and neuronal viability. N-acetylaspartic acid is proposed here to support lipid synthesis and energy metabolism via the provision of substrate for both cellular processes during early postnatal development.

Mutant Presenilin 2 Transgenic Mouse: Effect on an Age-Dependent Increase of Amyloid β-Protein 42 in the Brain

2002 ◽  
Vol 71 (1) ◽  
pp. 313-322 ◽  
Author(s):  
Fumitaka Oyama ◽  
Naoya Sawamura ◽  
Kimio Kobayashi ◽  
Maho Morishima-Kawashima ◽  
Takashi Kuramochi ◽  
...  
Keyword(s):  
Transgenic Mouse ◽  
Amyloid Β ◽  
Amyloid Β Protein ◽  
Β Protein ◽  
Age Dependent ◽  
Presenilin 2 ◽  
The Brain

Age-Dependent Changes in the Plasma and Brain Pharmacokinetics of Amyloid-β Peptides and Insulin

2021 ◽  
pp. 1-14
Author(s):  
Andrew L. Zhou ◽  
Nidhi Sharda ◽  
Vidur V. Sarma ◽  
Kristen M. Ahlschwede ◽  
Geoffry L. Curran ◽  
...  
Keyword(s):  
Neurodegenerative Disorder ◽  
Single Photon ◽  
Photon Emission ◽  
Amyloid Β ◽  
Emission Computed Tomography ◽  
Systemic Injection ◽  
Age Related ◽  
Age Dependent ◽  
Plasma Pharmacokinetics ◽  
The Brain

Background: Age is the most common risk factor for Alzheimer’s disease (AD), a neurodegenerative disorder characterized by the hallmarks of toxic amyloid-β (Aβ) plaques and hyperphosphorylated tau tangles. Moreover, sub-physiological brain insulin levels have emerged as a pathological manifestation of AD. Objective: Identify age-related changes in the plasma disposition and blood-brain barrier (BBB) trafficking of Aβ peptides and insulin in mice. Methods: Upon systemic injection of 125I-Aβ 40, 125I-Aβ 42, or 125I-insulin, the plasma pharmacokinetics and brain influx were assessed in wild-type (WT) or AD transgenic (APP/PS1) mice at various ages. Additionally, publicly available single-cell RNA-Seq data [GSE129788] was employed to investigate pathways regulating BBB transport in WT mice at different ages. Results: The brain influx of 125I-Aβ 40, estimated as the permeability-surface area product, decreased with age, accompanied by an increase in plasma AUC. In contrast, the brain influx of 125I-Aβ 42 increased with age, accompanied by a decrease in plasma AUC. The age-dependent changes observed in WT mice were accelerated in APP/PS1 mice. As seen with 125I-Aβ 40, the brain influx of 125I-insulin decreased with age in WT mice, accompanied by an increase in plasma AUC. This finding was further supported by dynamic single-photon emission computed tomography (SPECT/CT) imaging studies. RAGE and PI3K/AKT signaling pathways at the BBB, which are implicated in Aβ and insulin transcytosis, respectively, were upregulated with age in WT mice, indicating BBB insulin resistance. Conclusion: Aging differentially affects the plasma pharmacokinetics and brain influx of Aβ isoforms and insulin in a manner that could potentially augment AD risk.

scholarly journals Differences in lipidome and metabolome organization of prefrontal cortex among human populations

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Anna Tkachev ◽  
Vita Stepanova ◽  
Lei Zhang ◽  
Ekaterina Khrameeva ◽  
Dmitry Zubkov ◽  
...  
Keyword(s):  
Han Chinese ◽  
Human Populations ◽  
Cortical Region ◽  
Molecular Phenotype ◽  
Logistic Regression Models ◽  
Prefrontal Cortical ◽  
Age Dependent ◽  
Polar Low ◽  
The Brain ◽  
Two Populations

AbstractHuman populations, despite their overwhelming similarity, contain some distinct phenotypic, genetic, epigenetic, and gene expression features. In this study, we explore population differences at yet another level of molecular phenotype: the abundance of non-polar and polar low molecular weight compounds, lipids and metabolites in the prefrontal cortical region of the brain. We assessed the abundance of 1,670 lipids and 258 metabolites in 146 Han Chinese, 97 Western European, and 60 African American individuals of varying ages, covering most of the lifespan. The statistical analysis and logistic regression models both demonstrated extensive lipid and metabolic divergence of the Han Chinese individuals from the other two populations. This divergence was age-dependent, peaking in young adults, and involved metabolites and lipids clustering in specific metabolic pathways.

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