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147 results for “CA1”
Hippocampal CA1 pyramidal cell membrane voltage recorded in response to noise stimuli at two temperatures.
<p>Electrophysiological recording of the membrane voltage (whole-cell patch-clamp) of three hippocampal CA1 pyramidal cells. Cells are stimulated with a current step chosen to ensure a firing rate around 5-10Hz (amplitude of the current step is given in the filenames) and a noise stimulus with zero mean (Ornstein-Uhlenbeck process with 4ms timescale). Each CSV file contains three columns, the timepoints (saved at 10000Hz), the noise stimulus, and the voltage trace recorded in response to the given noise stimulus. Voltages are recorded at low temperatures (around 32 degrees Celsius) and at high temperatures (around 37 degrees Celsius for cell 1, around 40 degrees Celsius for cells 2 and 3), exact temperatures are given in the filenames. The file metadata.csv contains additional information.</p>
Adenosine deficiency facilitates CA1 synaptic hyperexcitability in the presymptomatic phase of a mouse KI model of Alzheimer disease.
<p><span>All data points, statistical models and raw western blot images from "Adenosine deficiency facilitates CA1 synaptic hyperexcitability in the presymptomatic phase of a mouse KI model of Alzheimer disease" are available. </span></p>
Lateralization of CA1 assemblies in the absence of CA3 input
<p>Raw data (sorted spikes, local field potentials, behavior) for the paper "Lateralization of CA1 assemblies in the absence of CA3 input" Guan et al., <em>Nat Commun</em>, (2021). Each zip file contain data recorded from single mouse. Mice HX384, HX385, HX388, HX443 constitute the 'control' group. Mice HX1582, HX1584, HX386, HX387, HX400 constitute the 'mutants' (CA3-TeTX) group.</p>
Data from: Distinct catecholaminergic pathways projecting to hippocampal CA1 transmit contrasting signals during navigation in familiar and novel environments
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Data set of CA1 pyramidal cell models using an intact whole hippocampus preparation
<p>The frequency-current (f-I) profiles of pyramidal cells are presented. Each .abf file contains the f-I curve data for the respective cell (as labelled PYR1, PYR2, PYR3 and PYR4 for Pyramidal cell 1, Pyramidal cell 2, Pyramidal cell 3 and Pyramidal cell 4). That is, they contain the cell's response to the application of a series of depolarizing current steps of 1 s duration while the cells are held in current clamp, as well as the current clamp data itself. Each recording is 2 s total. Amplitudes of the input were increased incrementally with step sizes of 10 pA for PYR1, PYR3, and PYR4, and a step size of 25 pA for PYR 2. PYR1 first spikes on the 5th of 30 steps with 38.7 pA of depolarizing input. PYR2 first spikes on the 3rd of 13 steps with 1.2 pA of input. PYR3 first spikes on the 7th of 34 steps with 62.0 pA of input, and PYR4 first spikes on the 7th of 30 steps with 12.1 pA of input.</p>
Data set of CA1 pyramidal cell recordings using an intact whole hippocampus preparation, including recordings of rebound firing (V2)
<p>The frequency-current (f-I) profiles and an example of rebound firing of pyramidal cells are presented. Four .abf files contain the f-I curve data for the respective cell (as labelled PYR1, PYR2, PYR3 and PYR4 for Pyramidal cell 1, Pyramidal cell 2, Pyramidal cell 3 and Pyramidal cell 4). That is, they contain the cell's response to the application of a series of depolarizing current steps of 1 s duration while the cells are held in current clamp, as well as the current clamp data itself. Each recording is 2 s total. Amplitudes of the input were increased incrementally with step sizes of 10 pA for PYR1, PYR3, and PYR4, and a step size of 25 pA for PYR 2. PYR1 first spikes on the 5th of 30 steps with 38.7 pA of depolarizing input. PYR2 first spikes on the 3rd of 13 steps with 1.2 pA of input. PYR3 first spikes on the 7th of 34 steps with 62.0 pA of input, and PYR4 first spikes on the 7th of 30 steps with 12.1 pA of input. In the .abf file labelled PYR5_rebound, an example of rebound firing of a pyramidal cell following hyperpolarizing input is given. While the cell was held at -52 mV in current clamp, as series of 1 s hyperpolarizing steps (10 steps, 25 pA increments) were used to record the post- hyperpolarization rebound spiking. For the figure showing this rebound spiking (Figure 1), the first two hyperpolarizing steps and the respective firing are shown. For visualization purposes, the spike artifact in the current clamp input trace was removed and replaced with the mean current in the Figure. </p>
Data set of CA1 pyramidal cell models using an intact whole hippocampus preparationV2
<p>The frequency-current (f-I) profiles and an example of rebound firing of pyramidal cells are presented. Four .abf files contain the f-I curve data for the respective cell (as labelled PYR1, PYR2, PYR3 and PYR4 for Pyramidal cell 1, Pyramidal cell 2, Pyramidal cell 3 and Pyramidal cell 4). That is, they contain the cell's response to the application of a series of depolarizing current steps of 1 s duration while the cells are held in current clamp, as well as the current clamp data itself. Each recording is 2 s total. Amplitudes of the input were increased incrementally with step sizes of 10 pA for PYR1, PYR3, and PYR4, and a step size of 25 pA for PYR 2. PYR1 first spikes on the 5th of 30 steps with 38.7 pA of depolarizing input. PYR2 first spikes on the 3rd of 13 steps with 1.2 pA of input. PYR3 first spikes on the 7th of 34 steps with 62.0 pA of input, and PYR4 first spikes on the 7th of 30 steps with 12.1 pA of input. In the .abf file labelled PYR5_rebound, an example of rebound firing of a pyramidal cell following hyperpolarizing input is given. While the cell was held at -52 mV in current clamp, as series of 1 s hyperpolarizing steps (10 steps, 25 pA increments) were used to record the post- hyperpolarization rebound spiking. For the figure showing this rebound spiking (Figure 1), the first two hyperpolarizing steps and the respective firing are shown. For visualization purposes, the spike artifact in the current clamp input trace was removed and replaced with the mean current in the Figure.</p>
Action potential dependent sIPSCs from juvenile (P21-30) C57BL/6J male mice from CA1 pyramidal neurons receiving input from PV+ interneurons
<p>species : Mus musculus</p> <p>sex : male</p> <p>strain : C57BL/6J</p> <p>age : post-natal day 21-30</p> <p>Voltage-clamp recordings of GABAA spontaneous inhibitory post-synaptic currents (sIPSCs) were obtained from juvenile (P21-30) C57BL/6J male mice and recorded from hippocampal CA1 pyramidal neurons receiving input from parvalbumin positive (PV+) interneurons. The dataset contains 614 individual events recorded from 3 different neurons (expC1-C3).</p>
Action potential dependent sIPSCs from juvenile (P21-30) C57BL/6J male mice CA1 pyramidal neurons receiving input from PV+ and CCK+ interneurons
<p>species : Mus musculus</p> <p>sex : male</p> <p>strain : C57BL/6J</p> <p>age : post-natal day 21-30</p> <p>Voltage-clamp recordings of GABAA spontaneous inhibitory post-synaptic currents (sIPSCs) were obtained from juvenile (P21-30) C57BL/6J male mice and recorded from hippocampal CA1 pyramidal neurons receiving input from parvalbumin positive and cholecystokinin positive (CCK+) interneurons. The dataset contains 2130 individual events recorded from 3 different neurons (expD1-D3).</p>
Action potential dependent sIPSCs from 3-4 months old C57BL/6J X SJL female mice hippocampus CA1 pyramidal cell
<p>species : Mus musculus</p> <p>sex : female</p> <p>strain : C57BL/6J X SJL</p> <p>age : 3 - 4 months</p> <p>Voltage-clamp recordings of GABAA spontaneous inhibitory post-synaptic currents (sIPSCs) were obtained from 3-4 months old C57BL/6J X SJL female mice . The dataset contains 701 individual events recorded from 7 different neurons (expB1-B7).</p>
OGD triggered Zn2+ rises and Ca2+ deregulation events in CA1 and CA3 hippocampal pyramidal neurons of MT-III and ZnT3 knockout mice.
<p>The posted data provide the control characterization of the oxygen glucose deprivation (OGD) triggered occurrences of cytosolic Zn<sup>2+</sup> rises and terminal Ca<sup>2+</sup> deregulation events in individual CA1 and CA3 pyramidal neurons in acute hippocampal slices of the MT-III knockout mice ( <strong>004649 - 129S7-Mt3<sup>tm1Rpa</sup>/J</strong>, Jackson Laboratory) and ZnT3 knockout mice ( <strong>005064 -</strong> <strong>B6;129-Slc30a3<sup>tm1Rpa</sup>/J</strong>, Jackson Laboratory).</p>
Mouse CA1 Calcium Imaging and Behavioural Dataset in 3x3 Geometric Morph Paradigm
<p>The following dataset was collected by Dr. J. Quinn Lee, Dr. Alexandra T. Keinath, and Erica Cianfarano in the laboratory of Dr. Mark P. Brandon. All methods and details are described in the original research article reporting these data published in <em>Neuron</em>: Lee, Keinath, Cianfarano, and Brandon (2025) Identifying representational structure in CA1 to benchmark theoretical models of cognitive mapping. Any use of the following dataset must cite the original publication in Neuron. The code base to reproduce all analyses and figures can be found at: <a href="https://github.com/jquinnlee/georepca1">https://github.com/jquinnlee/georepca1</a></p> <p dir="auto">The dataset (Python joblib files or MATLAB .mat files in the zipped "data" folder) are given names of animal IDs from the original study that can be downloaded from Zenodo and contain the following fields in each file:</p> <p dir="auto">SFPs: spatial footprints (also known as ROI) for every registered cell, centered over each cell. Shape - Dimx, dimy, number of SFPs (ROIs), number of days. If cell is not registered it will be nan along dimx and dimy for a given day.</p> <p dir="auto">blocked: location of blocked (occluded) partitions in 3x3 design of environment. Location of partitions are shown in paper, but are organized in the following way – [[0, 1, 2], [3, 4, 5], [6, 7, 8]]. If no partitions are blocked, value is -1.</p> <p dir="auto">centroids: centroid of spatial footprint. Shape – number of cells, x-y location, number of days.</p> <p dir="auto">envs: environment shape identified with string name</p> <p dir="auto">maps: three types of maps generated from the dataset. “sampling” is the occupancy of animal in each spatial bin, shape – xbins, ybins, number of days. “smoothed” is the event rate map smoothed with 2.5 cm gaussian kernel, shape – xbins, ybins, number of cells, number of days. “unsmoothed” is the same event rate map data without smoothing.</p> <p dir="auto">position: x-y position data for all days. List shape number of days, with shape on each day indicating x-y position in first dimension, and number of temporal bins / frames in second dimension.</p> <p dir="auto">trace: rise-extracted calcium traces, where “1” indicates a significant event. See paper for details on processing pipeline. If cell is not registered on given day, will appear as nan the same shape.</p> <p dir="auto">Precomputed results can also be downloaded in the zipped "results" folder to avoid recomputing main results from scratch using the Github code base linked above.</p>
Data From: Fear conditioning potentiates the Hippocampal CA1 commissural pathway In vivo and increases awake phase sleep
<p>The hippocampus is essential for spatial learning and memory. To assess learning we used contextual fear conditioning (cFC), where animals learn to associate a place with aversive events like foot-shocks. Candidate memory mechanisms for cFC are long-term potentiation and long-term depression, but there is little direct evidence of them operating in the hippocampus in vivo following cFC. Also, little is known about the behavioral state changes induced by cFC. To address these issues, we recorded local field potentials in freely behaving mice by stimulating in the left dorsal CA1 region and recording in the right dorsal CA1 region. Synaptic strength in the commissural pathway was monitored by measuring field excitatory postsynaptic potentials (fEPSPs) before and after cFC. After cFC, the commissural pathway's synaptic strength was potentiated. Although recordings occurred during the wake phase of the light/dark cycle, the mice slept more in the post-conditioning period than in the pre-conditioning period. Relative to awake periods, in non-rapid eye movement (NREM) sleep the fEPSPs were larger in both pre- and post-conditioning periods. We also found a significant negative correlation between the animal's speed and fEPSP size. Therefore, to avoid confounds in the fEFSP potentiation estimates, we controlled for speed-related and sleep-related fEPSP changes and still found that cFC induced long-term potentiation, but no significant long-term depression. Synaptic strength changes were not found in the control group that simply explored the fear-conditioning chamber, indicating that exploration of the novel place did not produce the measurable effects caused by cFC. These results show that following cFC, the CA1 commissural pathway is potentiated, likely contributing to the functional integration of the left and right hippocampi in fear memory consolidation. In addition, the cFC paradigm produces significant changes in an animal's behavioral state, which are observable as proximal changes in sleep patterns.</p>
ca-ca1
<p>数据库</p>
Denervated mouse CA1 pyramidal neurons express homeostatic synaptic plasticity following entorhinal cortex lesion
<p><span>Structural, functional, and molecular reorganization of denervated neural networks is often observed in neurological conditions. The loss of input is accompanied by homeostatic synaptic adaptations, which can affect the reorganization process. A major challenge of denervation-induced homeostatic plasticity operating in complex neural networks is the specialization of neuronal inputs. It remains unclear whether neurons respond similarly to the loss of distinct inputs. Here, we used <em>in</em> <em>vitro</em> entorhinal cortex lesion (ECL) and Schaffer collateral lesion (SCL) in mouse organotypic entorhino-hippocampal tissue cultures to study denervation-induced plasticity of CA1 pyramidal neurons. We observed microglia accumulation, presynaptic bouton degeneration, and a reduction in dendritic spine numbers in the denervated layers three days after SCL and ECL. Transcriptome analysis of the CA1 region revealed complex changes in differential gene expression following SCL and ECL compared to non-lesioned controls with a specific enrichment of differentially expressed synapse-related genes observed after ECL. Consistent with this finding, denervation-induced homeostatic plasticity of excitatory synapses was observed three days after ECL but not after SCL. Chemogenetic silencing of the EC but not CA3 confirmed the pathway-specific induction of homeostatic synaptic plasticity in CA1. Additionally, increased RNA oxidation was observed after SCL and ECL. These results reveal important commonalities and differences between distinct pathway lesions and demonstrate a pathway-specific induction of denervation-induced homeostatic synaptic plasticity. </span></p>
Local activation of CA1 pyramidal cells induces theta phase precession
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Data From: Fear conditioning potentiates the Hippocampal CA1 commissural pathway In vivo and increases awake phase sleep
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Denervated mouse CA1 pyramidal neurons express homeostatic synaptic plasticity following entorhinal cortex lesion
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CA1 20-40 Hz oscillatory dynamics reflect trial-specific information processing supporting nonspatial sequence memory
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Data from: Developmental changes in hippocampal CA1 single neuron firing and theta activity during associative learning
Hippocampal development is thought to play a crucial role in the emergence of many forms of learning and memory, but ontogenetic changes in hippocampal activity during learning have not been examined thoroughly. We examined the ontogeny of hippocampal function by recording theta and single neuron activity from the dorsal hippocampal CA1 area while rat pups were trained in associative learning. Three different age groups [postnatal days (P)17-19, P21-23, and P24-26] were trained over six sessions using a tone conditioned stimulus (CS) and a periorbital stimulation unconditioned stimulus (US). Learning increased as a function of age, with the P21-23 and P24-26 groups learning faster than the P17-19 group. Age- and learning-related changes in both theta and single neuron activity were observed. CA1 pyramidal cells in the older age groups showed greater task-related activity than the P17-19 group during CS-US paired sessions. The proportion of trials with a significant theta (4–10 Hz) power change, the theta/delta ratio, and theta peak frequency also increased in an age-dependent manner. Finally, spike/theta phase-locking during the CS showed an age-related increase. The findings indicate substantial developmental changes in dorsal hippocampal function that may play a role in the ontogeny of learning and memory.
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Allen Brain Atlas
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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
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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.
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