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803 results for “hippocampal”
Data from: Hippocampal neurogenesis regulates forgetting during adulthood and infancy
Throughout life, new neurons are continuously added to the dentate gyrus. As this continuous addition remodels hippocampal circuits, computational models predict that neurogenesis leads to degradation or forgetting of established memories. Consistent with this, increasing neurogenesis after the formation of a memory was sufficient to induce forgetting in adult mice. By contrast, during infancy, when hippocampal neurogenesis levels are high and freshly-generated memories tend to be rapidly forgotten (infantile amnesia), decreasing neurogenesis after memory formation mitigated forgetting. In precocial species, including guinea pigs and degus, the majority of granule cells are generated prenatally. Consistent with reduced levels of postnatal hippocampal neurogenesis, infant guinea pigs and degus did not exhibit forgetting. However, increasing neurogenesis after memory formation induced infantile amnesia in these species.
Data from: Blood-brain barrier deterioration and hippocampal gene expression in polymicrobial sepsis: an evaluation of endothelial MyD88 and the vagus nerve
Systemic infection can initiate or exacerbate central nervous system (CNS) pathology, even in the absence of overt invasion of bacteria into the CNS. Recent epidemiological studies have demonstrated that human survivors of sepsis have an increased risk of long-term neurocognitive decline. There is thus a need for improved understanding of the physiological mechanisms whereby acute sepsis affects the CNS. In particular, MyD88-dependent activation of brain microvascular endothelial cells and a resulting loss of blood-brain barrier integrity have been proposed to play an important role in the effects of systemic inflammation on the CNS. Signaling through the vagus nerve has also been considered to be an important component of CNS responses to systemic infection. Here, we demonstrate that blood-brain barrier permeabilization and hippocampal transcriptional responses during polymicrobial sepsis occur even in the absence of MyD88-dependent signaling in cerebrovascular endothelial cells. We further demonstrate that these transcriptional responses can occur without vagus nerve input. These results suggest that redundant signals mediate CNS responses in sepsis. Either endothelial or vagus nerve activation may be individually sufficient to transmit systemic inflammation to the central nervous system. Transcriptional activation in the forebrain in sepsis may be mediated by MyD88-independent endothelial mechanisms or by non-vagal neuronal pathways.
Data from: Environmental enrichment normalizes hippocampal timing coding in a malformed hippocampus
Neurodevelopmental insults leading to malformations of cortical development (MCD) are a common cause of psychiatric disorders, learning impairments and epilepsy. In the methylazoxymethanol (MAM) model of MCDs, animals have impairments in spatial cognition that, remarkably, are improved by post-weaning environmental enrichment (EE). To establish how EE impacts network-level mechanisms of spatial cognition, hippocampal in vivo single unit recordings were performed in freely moving animals in an open arena. We took a generalized linear modeling approach to extract fine spike timing (FST) characteristics and related these to place cell fidelity used as a surrogate of spatial cognition. We find that MAM disrupts FST and place-modulated rate coding in hippocampal CA1 and that EE improves many FST parameters towards normal. Moreover, FST parameters predict spatial coherence of neurons, suggesting that mechanisms determining altered FST are responsible for impaired cognition in MCDs. This suggests that FST parameters could represent a therapeutic target to improve cognition even in the context of a brain that develops with a structural abnormality.
Effects of Aqueous Extract of Red Acalypha (Acalypha Wilkesiana) on Hippocampal Morphology and Memory in Sprague-Dawley Rats
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The correlation between hippocampal ferroptosis and emotional disorders induced by neuropathic pain in CCI rats
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Association of CSF biomarkers with hippocampal-dependent memory in preclinical Alzheimer disease
<p><b>Objective: </b>To determine if memory tasks with demonstrated sensitivity to hippocampal function can detect variance related to preclinical Alzheimer's disease (AD) biomarkers, we examined associations between performance in three memory tasks and CSF Ab<sub>42</sub>/Ab<sub>40 </sub>and p-tau<sub>181</sub> in cognitively unimpaired older adults (CU).</p> <p><b>Methods: </b>CU enrolled in the Stanford Aging and Memory Study (N=153; age 68.78 ± 5.81 yrs; 94 female) completed a lumbar puncture and memory assessments. CSF Ab<sub>42</sub>,<sub> </sub>Ab<sub>40</sub>, and phosopho-tau<sub>181</sub> (p-tau<sub>181</sub>) were measured with the automated Lumipulse G system in a single-batch analysis. Episodic memory was assayed using a delayed recall composite, paired associate (word-picture) cued recall, and a mnemonic discrimination task that involves discrimination between studied 'target' objects, novel 'foil' objects, and perceptually similar 'lure' objects. Analyses examined cross-sectional relationships between memory performance, age, and CSF measures, controlling for sex and education.</p> <p><span><b>Results: </b>Age and lower Ab<sub>42</sub>/Ab<sub>40 </sub>were independently associated with elevated p-tau<sub>181</sub>. Age, Ab<sub>42</sub>/Ab<sub>40,</sub> and p-tau<sub>181</sub> were each associated with a) poorer associative memory and b) diminished improvement in mnemonic discrimination performance across levels of decreased task difficulty (i.e., target-lure similarity). P-tau mediated the effect of Ab<sub>42</sub>/Ab<sub>40 </sub>on memory. Relationships between CSF proteins and delayed recall were similar but non-significant. CSF Ab<sub>42 </sub>was not significantly associated with p-tau<sub>181 </sub>or memory. </span></p> <p><b>Conclusions: </b>Tests designed to tax hippocampal function are sensitive to subtle individual differences in memory among CU, and correlate with early AD-associated biomarker changes in CSF. These tests may offer utility for identifying cognitively unimpaired older adults with preclinical AD pathology.<b> </b></p>
Dataset related to article Super-resolution study of PIAS SUMO E3-ligases in hippocampal and cortical neurons
<p>Immagini ottenute con la sim e il confocale dei neuroni ippocampali e corticali presenti nelle immagini. Grafici relativi ai coefficenti di localizzazione</p>
Data for: Hippocampal place codes are gated by behavioral engagement
<p><span>As animals explore an environment, the hippocampus is thought to automatically form and maintain a place code by combining sensory and self-motion signals. Instead, we observed an extensive degradation of the place code when mice voluntarily disengaged from a virtual-navigation task, remarkably even as they continued to traverse the identical environment. Internal states therefore can strongly gate spatial maps and reorganize hippocampal activity even without sensory and self-motion changes.</span></p>
Effect of 3D Synthetic Microscaffold Nichoid on the Morphology of Cultured Hippocampal Neurons and Astrocytes
<p>The dataset contains the raw data and images of the paper.</p>
Raw data for: Okada et al., Photopharmacological modulation of hippocampal local field potential by caged-glutamate with MicroLED probe
<p>Matlab data of LFPs (sampling rate, 1k/sec; microV)</p>
Hippocampal contextualization of social rewards in mice
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Data from: Algal toxin impairs sea lion memory and hippocampal connectivity, with implications for strandings
Domoic acid (DA) is a naturally occurring neurotoxin known to harm marine animals. DA-producing algal blooms are increasing in size and frequency. Although chronic exposure is known to produce brain lesions, the influence of DA toxicosis on behavior in wild animals is unknown. We showed, in a large sample of wild sea lions, that spatial memory deficits are predicted by the extent of right dorsal hippocampal lesions related to natural exposure to DA and that exposure also disrupts hippocampal-thalamic brain networks. Because sea lions are dynamic foragers that rely on flexible navigation, impaired spatial memory may affect survival in the wild.
Data from: Impaired hippocampal place cell dynamics in a mouse model of the 22q11.2 deletion
Hippocampal place cells represent the cellular substrate of episodic memory. Place cell ensembles reorganize to support learning but must also maintain stable representations to facilitate memory recall. Despite extensive research, the learning-related role of place cell dynamics in health and disease remains elusive. Using chronic two-photon Ca2+ imaging in hippocampal area CA1 of wild-type and Df(16)A+/− mice, an animal model of 22q11.2 deletion syndrome, one of the most common genetic risk factors for cognitive dysfunction and schizophrenia, we found that goal-oriented learning in wild-type mice was supported by stable spatial maps and robust remapping of place fields toward the goal location. Df(16)A+/− mice showed a significant learning deficit accompanied by reduced spatial map stability and the absence of goal-directed place cell reorganization. These results expand our understanding of the hippocampal ensemble dynamics supporting cognitive flexibility and demonstrate their importance in a model of 22q11.2-associated cognitive dysfunction.
Data from: Weak sinusoidal electric fields entrain spontaneous Ca transients in the dendritic tufts of CA1 pyramidal cells in rat hippocampal slice preparations
Neurons might interact via electric fields and this notion has been referred to as ephaptic interaction. It has been shown that various types of ion channels are distributed along the dendrites and are capable of supporting generation of dendritic spikes. We hypothesized that generation of dendritic spikes play important roles in the ephaptic interactions either by amplifying the impact of electric fields or by providing current source to generate electric fields. To test if dendritic activities can be modulated by electric fields, we developed a method to monitor local Ca-transients in the dendrites of a neuronal population in acute rat hippocampal slices by applying spinning-disk confocal microscopy and multi-cell dye loading technique. In a condition in which the dendrites of CA1 pyramidal neurons show spontaneous Ca-transients due to added 50 μM 4-aminopyridine to the bathing medium and adjusted extracellular potassium concentration, we examined the impact of sinusoidal electric fields on the Ca-transients. We have found that spontaneously occurring fast-Ca-transients in the tufts of the apical dendrites of CA1 pyramidal neurons can be blocked by applying 1 μM tetrodotoxin, and that the timing of the transients become entrained to sub-threshold 1-4 Hz electric fields with an intensity as weak as 0.84 mV/mm applied parallel to the somato-dendritic axis of the neurons. The extent of entrainment increases with intensity below 5 mV/mm, but does not increase further over the range of 5-20 mV/mm. These results suggest that population of pyramidal cells might be able to detect electric fields with biologically relevant intensity by modulating the timing of dendritic spikes.
Time-course adaptive changes in hippocampal transcriptome and synaptic function induced by simulated microgravity associated with cognition
<p>Introduction: The investigation of cognitive function in microgravity, both short-term and long-term, remains largely descriptive. And the underlying mechanisms of the changes over time remain unclear. Methods: Behavioral tests, electrophysiological recording, and RNA sequencing were used to observe differences in behavior, synaptic plasticity, and gene expression. Results: Initially, we measured the performance of spatial cognition exposed to long-term simulated microgravity (SM). Both working memory and advanced cognitive abilities were enhanced. Somewhat surprisingly, the synaptic plasticity of the hippocampal CA3-CA1 synapse was impaired. To gain insight into the mechanism of changing regularity over time, transcriptome sequencing in the hippocampus was performed. The analysis identified 20 differentially expressed genes (DEGs) in the hippocampus after short-term modeling, 19 of which were up-regulated. Gene ontology (GO) analysis showed that these up-regulated genes were mainly enriched in synaptic-related processes, such as <em>Stxbp5l</em> and <em>Epha6</em>. This might be related to the enhancement of working memory performance under short-term SM exposure. Under exposure to long-term SM, 7 DEGs were identified in the hippocampus, all of which were up-regulated and related to oxidative stress and metabolism, such as <em>Depp1</em> and <em>Lrg1</em>. Compensatory effects occurred with increased modeling time. Discussion: To sum up, our current research indicates that the cognitive function under SM exposure is consistently maintained or potentially even being enhanced over both short and long durations. The underlying mechanisms are intricate and potentially linked to the differential expression of hippocampal-associated genes and alterations in synaptic function, with these effects being time-dependent. The present study will lay the experimental and theoretical foundation of the multi-level mechanism of cognitive function under space flight.</p>
Hippocampal Oscillations During Exploration
ClinicalTrials.gov study NCT07224191. IPD Sharing: YES. Countries: 1. Publications: 0.
Hippocampal Network Changes Following Mindfulness Training in Tobacco Vaping Adolescents in an Open-label, Pilot Study
ClinicalTrials.gov study NCT06503159. IPD Sharing: NO. Countries: 1. Publications: 0.
The Effects of Added Sugar Intake on Brain Blood Flow and Hippocampal Function in Midlife Adults
ClinicalTrials.gov study NCT05211726. IPD Sharing: NO. Countries: 1. Publications: 0.
Hippocampal Stimulation in Chronic Low Back Pain
ClinicalTrials.gov study NCT04888494. IPD Sharing: YES. Countries: 1. Publications: 0.
Attenuation of Corticosteroid Induced Hippocampal Changes
ClinicalTrials.gov study NCT01656187. IPD Sharing: NO. Countries: 1. Publications: 0.
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These curated guides explain access requirements, typical timelines, costs, and reuse considerations for widely used research datasets.
Allen Brain Atlas
Allen Brain Atlas is an Allen Institute collection of brain map atlases, datasets, APIs, and analysis tools covering mouse, human, and non-human primate brain resources.
Annotated Behaviour and Observability Dataset (ABODe)
ABODe is a University of Edinburgh DataShare dataset for behavior classification in group-housed mice using home-cage video, identities, bounding boxes, ground-plate positions, and annotator labels.
DANDI Archive for NWB datasets
DANDI is a BRAIN Initiative archive for publishing and sharing neurophysiology data, including electrophysiology, optophysiology, and behavioral data packaged as NWB and related standards.
International Brain Laboratory public data
The International Brain Laboratory public data releases expose standardized mouse decision-making experiments, including Neuropixels recordings, widefield calcium imaging, behavior, and session metadata accessed through the ONE API.
OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.