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CA1 Field of Hippocampus

The CA1 field of the hippocampus is a critical region invloved in memory formation and spatial navigation.
This field receives input from the entorhinal cortex and is known for its role in long-term potentiation, a key mechanism of learning and memory.
Researchers can leverage PubCompare.ai's cutting-edge tools to optimize their CA1 field research, identifying the best protocols and products from the literature, preprints, and patents.
PubCompare.ai's AI-driven platform saves time and maximizes outcomes, allowing scientists to accelerate discoveries in this important area of neuroscience.

Most cited protocols related to «CA1 Field of Hippocampus»

1
Rolipram Modulates Sleep Deprivation-Induced Memory
C57BL/6J male mice (2–5 months of age) were housed individually on a 12 hr/12 hr light/dark schedule with lights on at 7 A.M. (ZT0) and handled for 6 days. Mice were sleep-deprived (SD) in their home cages for 5 hours by gentle handling beginning at ZT5 or left undisturbed (non-sleep-deprived mice, NSD). For contextual fear conditioning experiments, animals were placed in a novel chamber for 3 minutes, and received a 2-second, 1.5 mA footshock after 2.5 minutes. Half of the mice were deprived of sleep for 5 hours post-training. Mice received intra-peritoneal injections of rolipram (ROL; 1 mg/kg) or vehicle (2% DMSO in 0.9% saline) immediately and 2.5 hours post-training. Testing of contextual memory was performed 24 hours after training in the trained context and 48 hours after training in a novel chamber.
Electrophysiological recordings were carried out as previously reported28 (link). 1-train LTP was induced by a single 100 Hz, 1-second duration train of stimuli. 4-train LTP consisted of 4 trains applied with a 5-minute inter-train interval; for massed 4-train LTP a 5-second inter-train interval was used. Theta-burst stimulation (TBS) consisted of 40-ms duration, 100 Hz bursts delivered at 5 Hz for 3 seconds (15 bursts of 4 pulses per burst, for a total of 60 pulses). Chemical LTP was induced by treatment of slices for 15 minutes with 5µM forskolin (FSK) in 0.1% ethanol, or a combination of 50µM forskolin and 30µM 3-isobutyl-1-methylxanthine (IBMX, in water). Rolipram (0.1µM in 0.1% DMSO) was applied for 60 minutes, beginning 30 minutes before tetanization.
cAMP assays on CA1 regions of hippocampal slices 10 minutes after treatment for 15 minutes with forskolin (50µM), forskolin + IBMX (30µM), or vehicle (0.1% EtOH) were performed by radioimmunoassay according to kit instructions. cAMP-specific PDE activity assays29 (link) and Western blots for PDE4A530 (link) were performed as previously described.
Full Methods and any associated references are available in the online version of the paper at www.nature.com/nature.
Vecsey C.G., Baillie G.S., Jaganath D., Havekes R., Daniels A., Wimmer M., Huang T., Brown K.M., Li X.Y., Descalzi G., Kim S.S., Chen T., Shang Y.Z., Zhuo M., Houslay M.D, & Abel T. (2009). Sleep deprivation impairs cAMP signaling in the hippocampus. Nature, 461(7267), 1122-1125.
Publication 2009
1-Methyl-3-isobutylxanthine Aftercare Animals Biological Assay CA1 Field of Hippocampus Colforsin Ethanol Fear Injections, Intraperitoneal Light Males Memory methylxanthine Mice, House Mice, Inbred C57BL Neoplasm Metastasis Normal Saline Pulses Radioimmunoassay Rolipram Sleep Sulfoxide, Dimethyl Western Blot
2
Manual Hippocampal Subfield Segmentation

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Publication 2010
Arteries Body Regions CA1 Field of Hippocampus CA3 Field of Hippocampus Cyst Decompression Sickness Entorhinal Area Gyrus, Dentate Head Hippocampal Formation Human Body Parahippocampal Gyrus Seahorses Subiculum Tail
3
Spatial Memory and Prefrontal-Hippocampal Synchrony
We generated Df(16)A+/− mice and their wild-type littermates on a pure (>99.9%) C57BL/6J background (The Jackson Laboratory) as previously described13 (link),14 (link). All mice were 3–6 months old at the time of the experiments. Animals were implanted with recording electrodes in the medial prefrontal cortex and the dorsal CA1 region of the hippocampus (Supplementary Fig. 7). After they had recovered from surgery for a week, we put the animals on a restricted diet until their weight reached 85% of their pre-surgical weight. They were then trained on a discrete non-match-to-sample spatial working memory task in a T-maze, until they reached criterion performance. During performance of the task, neural data (putative spikes and field potentials) were acquired using a 16-channel headstage and a Cheetah32 data acquisition system (Neuralynx). Each animal’s position in the maze was monitored using two light-emitting diodes mounted on the headstage. To extract putative spikes, neural signals were band-pass filtered between 0.6 and 6 kHz and waveforms that passed a threshold were digitized at 30 kHz. Waveforms were then sorted into single-unit clusters using SPIKESORT3D (version 2.3, Neuralynx). To extract field potential activity, the same signals were band-pass filtered between 1 and 1,000 Hz and digitized at 2 kHz. Further analysis of neural and behavioural data was performed using custom written MATLAB (version 7.6, MathWorks) scripts. We measured synchrony between hippocampal and prefrontal neural activity using two approaches. First, we examined the degree to which the firing of prefrontal neurons was modulated by the phase of the theta oscillation in the hippocampus. Second, we quantified the coherence between field potentials recorded in the two structures. All procedures were conducted in accordance with US National Institutes of Health regulations and approved by the Columbia University and New York State Psychiatric Institute Institutional Animal Care and Use Committees.
Sigurdsson T., Stark K.L., Karayiorgou M., Gogos J.A, & Gordon J.A. (2010). Impaired hippocampal–prefrontal synchrony in a genetic mouse model of schizophrenia. Nature, 464(7289), 763-767.
Publication 2010
Animals CA1 Field of Hippocampus Dietary Restriction Institutional Animal Care and Use Committees Light MAZE protocol Memory, Short-Term Mus Nervousness Neurons Operative Surgical Procedures Prefrontal Cortex Seahorses Task Performance
4
Optogenetic Interrogation of Hippocampal Neurons

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Publication 2014
Animals CA1 Field of Hippocampus Calmodulin-Dependent Protein Kinase II Cardiac Arrest Cells GABA-A Receptor High-Frequency Oscillation Ventilation Interneurons Light Mus Opsins Pulses Pyramidal Cells Rattus norvegicus Short Interspersed Nucleotide Elements Silicon Urethane Vision
5
Extracellular Unit Recordings and Intracellular Neuronal Responses to Transcranial Electric Stimulation
Extracellular signals were amplified (×1000) and wide-band pass filtered (1 Hz–5 kHz). Intracellular signals were buffered (×1) and amplified by a DC amplifier (Axoprobe 1A; Axon Instruments). Signals were continuously acquired at 20 kHz on one or two synchronized 64 channel DataMax systems (16 bit resolution; RC Electronics, Santa Barbara, CA). All analyses were conducted off-line. The stimulation signal was directly fed from the stimulator output (STG1008 Stimulus Generator; Multi Channel Systems, Germany) to one of the recording channels. The peak-to-peak amplitude of the stimulator output is referred to as the stimulation intensity. All intensity values are given as peak-to-peak amplitudes. For LFP display and analysis, the volume-conducted stimulus (TES) artifact was removed as follows. The TES-related component of the LFP was estimated using least-square fit between the stimulation signal and the LFP. Time delay parameter and the scaling factor of the fit were adjusted dynamically in 10-second windows, sliding in 7-second steps. By subtracting the best-fit component from the LFP a continuous artifact-free signal was constructed (SI Fig. 4). Spectrograms of the LFP trace (Fig. 6A) were computed using windows of 4-second lengths, sliding in 1-second steps.
Unit activity was detected from the high-pass filtered (>0.8 kHz) trace and single units were semi-automatically isolated using Klusta-Kwik© (Harris et al., 2000 (link)), followed by a manual refinement using a custom-made software (Hazan et al., 2006 (link)), which utilized spike waveforms, auto-correlograms and cross-correlograms. To ensure that only high quality units were used in the analyses, we set two criteria for spike inclusion. First, the amplitude of the spike should be >60 µV. This value is based on our previous observations that smaller amplitude spikes result in clusters bordered closely by other clusters (at least in the hippocampal CA1 region; Henze et al., 2000 (link)). Second, the peak-to-peak spike amplitude (p2p) should exceed 3.6 times the temporally local background noise, determined according to the standard deviation of the signal in the immediate vicinity of each spike (between 0.8-0.4 msec before and 0.4–0.8 msec after the extracellular trough), and scaled by the natural logarithm of the number of samples across which the standard deviation was computed. This definition of spike signal/noise, SNR = p2p / SD(noise) / ln(n), is independent of the number of samples used to compute the noise and is asymptotically 1 for band pass-filtered white noise (SI Fig. 1). Although these strict criteria likely eliminated several true spikes, it reduced the likelihood of obtaining false positive results. A cluster was classified as ‘multiunit’ if the autocorrelogram lacked a clear refractory period. Multiunit clusters recorded from the same electrode (e.g., the shank of the probe) were merged into a single multiunit cluster to avoid potential oversampling by neighboring recording sites. Short latency (< 5 msec) temporal interactions with other isolated neurons were used to identify single neurons as putative excitatory or inhibitory cells (Bartho et al., 2004 (link); Isomura et al., 2006 (link); Fujisawa et al., 2008 (link); Sirota et al., 2008 (link)). The significance of monosynaptic connections was evaluated according to the global and point-wise significance values obtained by jittering (n=500) the cross-correlograms between single unit pairs. Cross-correlograms with significant peaks < 5 msec of the reference neuron spikes were regarded as monosynaptically connected (Fujisawa et al., 2008 (link)).
TES stimulation was applied multiple times (minimum of 5 trials) for a given stimulation protocol, that varied in intensity, frequency (0.8 to 1.7 Hz) and duration (15 cycles to 60 cycles; 1 minute long for few acute experiments) across sessions. Each stimulation trial was followed by a stimulation-free period (> 40 sec, except for short duration stimulation trials, for which it was 10 sec). The signal was a sinusoid waveform. In most sessions, stimulation was applied through 3 stimulating electrodes (3-poles), such that the same polarity was applied to both hemispheres (side) versus the opposite polarity applied to the center (frontal) electrode (Fig. 1Aa, d). This configuration yielded synchronous electric fields in both hemispheres. In a few experiments, bipolar stimulation was used (Fig. 1Ab–c). Trials using the same stimulation protocol were combined for statistical analysis.
To assess the effect of stimulation on unit firing, each spike was assigned to the instantaneous phase of the reference TES signal obtained by Hilbert transformation. The significance of phase-modulation was evaluated using Kuiper’s test of random deviation from uniformity on circular data (Fisher, 1993 ). This omnibus test was preferred over the more standard Rayleigh test, since our findings (such as bimodal phase preference) precluded having a predefined assumption regarding the modality of the TES-induced phase entrainment and thus the application of conventional (unimodal) phase entrainment measures (e.g., Rayleigh statistic). Since omnibus tests require a sufficiently large sample of data, we applied 2 criteria a) a minimum number of spikes (at least 250 per stimulation protocol) and b) a minimum number of trials (at least 5) for a given stimulation intensity, frequency and configuration. Because both multi- and single units had different number of spikes and both were tested against the same uniformity hypothesis, we examined whether the number of spikes biased our results. A fixed number of spikes (n=600, n=1000) was randomly chosen from a given TES session and tested against uniformity. Such sub-sampling did not show any particular trend substantially different from the case when all spikes were included. Probabilities <0.01 were regarded as significant.
For the color-coded population display, the spike count of each unit was normalized by subtracting the mean spike count of that unit from the spike count of each bin and dividing by the standard deviation (20° phase bins across one period of TES signal). To examine the relationship between spikes and the intrinsic slow oscillation, the peak spectral power of LFP (peakF) within the 0.4–10 Hz frequency range was computed in 3.2-second windows. The original LFP signal was band-pass filtered around peakF, between [0.75×peakF 1.25×peakF] Hz, using 2nd order, Butterworth Filter (a built-in Matlab function). The phase of the band-pass filtered LFP was then derived by Hilbert transformation. Phase-modulation of units by the slow oscillation was evaluated by Rayleigh circular statistics, since the unimodal phase modulation by the intrinsic slow oscillation could be safely assumed from previous experimental evidence (Steriade et al., 1993 (link)). For the display of cycle-by-cycle unit firing, peri-event time histograms of spike times around the first/last troughs of the reference TES signal were constructed.
For the analysis of the intracellular signal (<1,250 Hz, low-pass), the signal was band-passed filtered (0.5–10 Hz) to remove the action potentials. The relationship between the filtered intracellular potential (Vi) and the phase of the slow oscillation or TES was assessed using joint probability density. This measure allows the assessment of the correlation between network or TES effects and Vi across (20°) phase bins (Isomura et al., 2006 (link)). To compensate for the added effect of the TES-induced field on Vi, TES was repeated after the pipette was withdrawn from the neuron. The obtained extracellular average polarization for each phase bin of TES signal was subtracted from the Vi to arrive at a field-corrected joint density (Fig. 1D).
To evaluate the state-dependence of stimulation, the Chi-square test was performed, comparing the distribution of P-values, the significance of phase modulation (Kuiper’s test), of each unit. Either two or three P-value categories were constructed: not-significant (nS, P>0.05), significant (S, P<0.005
Ozen S., Sirota A., Belluscio M.A., Anastassiou C.A., Stark E., Koch C, & Buzsáki G. (2010). Transcranial Electric Stimulation Entrains Cortical Neuronal Populations in Rats. The Journal of Neuroscience, 30(34), 11476-11485.
Publication 2010
Action Potentials Axon CA1 Field of Hippocampus Cells Electricity Joints Neurons Protoplasm Psychological Inhibition Sinusoidal Beds

Most recents protocols related to «CA1 Field of Hippocampus»

1
Doublet Removal for Single-Cell Analysis
We annotated each nucleus with a doublet score – the nucleus’ probability of being a doublet, related to the fraction of artificially generated doublet neighbors (using an in-house optimization of DoubletFinder107 with the following parameters: PCs = 1-45, pN = 0.25, pK = 150/(#cells), pANN = False and sct = False). This score would later be considered for the removal of doublets. We first used a high-resolution clustering (1.3 for the hippocampus and 1.5 for the VAT, see description under Dimensionality reduction and clustering). We excluded clusters that had more than 50% of cells that had over a high doublet score (0.35 for the hippocampus and 0.4 for the adipose tissue). Second, cells from other clusters that had over a high doublet score were excluded. In the VAT: 10,625 doublets were removed and 275,336 nuclei remained in the dataset. In the hippocampus: we excluded from the analysis cells from clusters classified as endothelial cells or OPCs, since the doublet detection failed for these cell types. For OPCs, these specifically include cells differentiating from oligodendrocytes. At the end of this stage in the hippocampus dataset, 38,060 doublets were removed and 269,503 nuclei remained in the data set (for n = 28 mice, across all mouse genotype and diet groups). The downstream analysis of sub-clustering of specific cell types included a second inspection for doublets.
Suzzi S., Croese T., Ravid A., Gold O., Clark A.R., Medina S., Kitsberg D., Adam M., Vernon K.A., Kohnert E., Shapira I., Malitsky S., Itkin M., Brandis A., Mehlman T., Salame T.M., Colaiuta S.P., Cahalon L., Slyper M., Greka A., Habib N, & Schwartz M. (2023). N-acetylneuraminic acid links immune exhaustion and accelerated memory deficit in diet-induced obese Alzheimer’s disease mouse model. Nature Communications, 14, 1293.
Publication 2023
CA1 Field of Hippocampus CA3 Field of Hippocampus Cell Nucleus Cells Diet Endothelial Cells Genotype Mus Oligodendroglia Seahorses Tissue, Adipose
2
Hippocampal GFAP Immunohistochemistry in Rats
The Cornu Ammonis (CA) 1 and CA 3 regions of hippocampus were selected for the investigations of hippocampus. The brains of rats were removed and stored for 3 days in 10% formaldehyde in 0.1 M phosphate-buffer saline. The histopathological examinations were performed according to previous descriptions.32 (link) GFAP immunohistochemistry was performed by primary antibodies against GFAP (Abcam, Inc., Mass, USA; 1/1000) for 24 hours. Olympus BX51 microscope was used for obtaining the histopathological images. GFAP immunostaining index was calculated as follows: GFAP-positive cells were counted at 40× magnification in randomized sections (3-4) for each rat. An imaging system (Image-Pro Express 1.4.5, Media Cybernetics, Inc. USA) was used for the assessments.8 (link),33 (link)
Doğan M., Albayrak Y, & Erbaş O. (2023). Torasemide Improves the Propionic Acid-Induced Autism in Rats: A Histopathological and Imaging Study. Alpha Psychiatry, 24(1), 22-31.
Publication 2023
Antibodies Brain Buffers CA1 Field of Hippocampus CA3 Field of Hippocampus Cells Formaldehyde Glial Fibrillary Acidic Protein Immunohistochemistry Microscopy Phosphates Physical Examination Saline Solution Seahorses
3
Neurophysiological Investigations of Hippocampal LTP
Neurophysiological studies were conducted in rats 7 days post-injury as described50 (link). Briefly, brains were rapidly dissected in ice-cold artificial cerebrospinal fluid (ACSF; 75 mM sucrose, 87 mM NaCl, 2.5 mM KCl, 1.25 mM NaH2PO4, 25 mM NaHCO3, 7 mM MgCl2, 0.5 mM CaCl2 and 10 mM glucose). Transverse hippocampal slices (350 μ) were sectioned using a vibratome (Leica Microsystems Inc., VT1000S) in NMDG cutting/recovery solution (N-methyl D-glucamine (100 mM), KCl (2.5 mM), NaH2PO4 (1.2 mM), NaHCO3 (30 mM), HEPES (20 mM), MgS04 (1 0 mM), CaCl2 (0.5 mM), and glucose (25 mM) at 30 °C (pH 7.3–7.4). After 2 min, slices were transferred to HEPES holding solution NaCl (92 mM), KCl (2.5 mM), NaH2CO3 (30 mM), NaH2PO4 (1 mM), HEPES (20 mM), D-Glucose (25 mM), MgCl2 (1 mM), CaCl2 (1 mM) for 1 h at 30 °C. Slices were allowed to incubate for 30 min in recording solution of oxygenated Kreb’s (125 mM NaCl, 2.5 mM KCl, 1.25 mM NaH2PO4, 25 mM NaHCO3, 1.1 mM MgCl2, 2 mM CaCl2 and 25 mM glucose) prior to recording.
Recordings were performed using a Multiclamp 700A amplifier with a Digidata 1322 and pClamp 10 software (Axon, Molecular devices, LLC). Field excitatory postsynaptic potentials (fEPSP) from CA1 were evoked by square current pulses (0.1 ms) at 0.033 Hz with a bipolar stimulation electrode (FHC, Bowdoinham, ME). Stimulus intensity was defined using a stimulus intensity required to induce 50% of the maximum EPSP slope using the input–output curves. The sample intensity was used for PPR recordings across different intervals. A stable baseline was recorded for at least 10 min prior to high frequency stimulation (HFS, 4 trains, 100 Hz, 1 s duration, separated by 20 s). Post-tetanic potentiation (PTP) was analyzed by taking the average of the slopes from the traces recorded during the first 2 min after HFS. LTP was assessed for at least 45–50 min following HFS. The PPR values were calculated by dividing the second fEPSP slope by the first fEPSP slope (fEPSP2/fEPSP1). All recordings were performed in the absence of any drug treatment and only 1 or 2 slices were recorded from each individual rat. Data were analyzed with Clampfit 10 software (Axon, Molecular devices, LLC).
Umfress A., Chakraborti A., Priya Sudarsana Devi S., Adams R., Epstein D., Massicano A., Sorace A., Singh S., Iqbal Hossian M., Andrabi S.A., Crossman D.K., Kumar N., Shahid Mukhtar M., Luo H., Simpson C., Abell K., Stokes M., Wiederhold T., Rosen C., Lu H., Natarajan A, & Bibb J.A. (2023). Cdk5 mediates rotational force-induced brain injury. Scientific Reports, 13, 3394.
Publication 2023
Axon Bicarbonate, Sodium Brain CA1 Field of Hippocampus Cerebrospinal Fluid Cold Temperature Excitatory Postsynaptic Potentials Glucose HEPES Injuries Magnesium Chloride Medical Devices Pharmaceutical Preparations Pulses Sodium Chloride Sucrose Tetanus
4
Automated Hippocampal Subfield Segmentation
Automated segmentation of hippocampal subfields (ASHS) was implemented in the entire DELCODE cohort using the Penn ABC-3T ASHS Atlas for T2-weighted MRI [9 (link), 18 (link), 19 (link)]. Using this atlas, hippocampal subfields (subiculum, dentate gyrus, Cornu Ammonis 1, 2, and 3, hippocampal tail) and parahippocampal regions (entorhinal cortex, Brodmann areas 35 and 36, parahippocampal cortex) were segmented in correspondence with the manual segmentation protocol by Berron et al. [9 (link)].
Each created segmentation mask underwent thorough quality assurance by an experienced rater. Quality ratings were performed separately for each hemisphere and for hippocampal and parahippocampal regions. In the present study, only participants whose segmentation masks passed the quality assurance for both hippocampal and parahippocampal regions in both hemispheres were included.
The quality assurance routine first included a visual inspection of all segmentation masks on five coronal and two sagittal snapshots. If there were no indications of segmentation errors, the respective mask was included for analyses. If it became apparent that segmentation failed, the respective segmentation mask was excluded from analyses. If the snapshots showed indications of possible segmentation errors, the respective segmentation mask was inspected in its entire three-dimensional extent. Here, any segmentation error that was visible on more than two consecutive slices on T2w MRI (i.e., extending more than 3 mm longitudinally) led to manual editing or exclusion of the segmentation mask. Errors affecting the outer boundaries of the segmented structures were edited in accordance with the manual segmentation rules by Berron et al. [9 (link)]. Errors that affected internal boundaries between subregions were not edited and led to exclusion of the respective segmentation mask. The rater was blinded to the diagnosis and amyloid status of the participants.
Yildirim Z., Delen F., Berron D., Baumeister H., Ziegler G., Schütze H., Glanz W., Dobisch L., Peters O., Freiesleben S.D., Schneider L.S., Priller J., Spruth E.J., Schneider A., Fliessbach K., Wiltfang J., Schott B.H., Meiberth D., Buerger K., Janowitz D., Perneczky R., Rauchmann B.S., Teipel S., Kilimann I., Laske C., Munk M.H., Spottke A., Roy N., Heneka M., Brosseron F., Wagner M., Roeske S., Ramirez A., Ewers M., Dechent P., Hetzer S., Scheffler K., Kleineidam L., Wolfsgruber S., Yakupov R., Schmid M., Berger M., Gurvit H., Jessen F, & Duzel E. (2023). Brain reserve contributes to distinguishing preclinical Alzheimer’s stages 1 and 2. Alzheimer's Research & Therapy, 15, 43.
Publication 2023
Amyloid Proteins Brodmann Area 35 CA1 Field of Hippocampus Cortex, Cerebral Diagnosis Entorhinal Area Gyrus, Dentate Subiculum Tail
5
Alzheimer's Model Mice Treated with Thioredoxin-1
Male FAD4T APP/PS1 mice and WT littermates, 2 months old, were
purchased from GemPharmtech (Nanjing, China) and used in this experiment. Mice
were housed in cages and maintained on a 12 h light–dark cycle and had free
access to water and food. Mice were divided randomly into four groups:
WT + AAV-Vector (n = 6), WT + AAV-Trx-1 (n = 6), APP/PS1 + AAV-Vector (n = 5),
and APP/PS1+ AAV-Trx-1 groups (n = 5). The adeno-associated virus (AAV-Vector or
AAV-Trx-1, Hanbio, Shanghai, China) were stereotaxically injected into the
hippocampal cornu ammonis 1 (CA1) of mice. After recovery from the surgery, the
animals were kept for virus expression for about 4 weeks before they were used
in the experiments. Mice were subjected to Morris Water Maze (MWM) test when
they were 5 months old. The experimental procedures were carried out according
to guidelines for the use of Experimental Animal Ethics Committee of Jiaxing
University Medical College.
Jia J., Yin J., Zhang Y., Xu G., Wang M., Jiang H., Li L., Zeng X, & Zhu D. (2023). Thioredoxin-1 Promotes Mitochondrial Biogenesis Through Regulating AMPK/Sirt1/PGC1α Pathway in Alzheimer's Disease. ASN NEURO, 15, 17590914231159226.
Publication 2023
CA1 Field of Hippocampus Cloning Vectors Dependovirus Ethics Committees Food Males Mice, House Morris Water Maze Test Operative Surgical Procedures TXN protein, human Virus

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More about "CA1 Field of Hippocampus"

The CA1 region of the hippocampus is a critical area in the brain that plays a vital role in memory formation and spatial navigation.
This field, also known as the Ammon's horn or the hippocampus proper, receives input from the entorhinal cortex and is known for its involvement in long-term potentiation (LTP), a key mechanism underlying learning and memory.
Researchers can leverage cutting-edge tools like PubCompare.ai to optimize their CA1 field investigations.
This AI-driven platform helps scientists identify the best research protocols from the literature, preprints, and patents, saving time and maximizing research outcomes.
The platform's machine learning algorithms analyze a vast amount of scientific data to pinpoint the optimal experimental procedures and products, allowing researchers to accelerate their discoveries in this important area of neuroscience.
To study the CA1 field, researchers may employ various techniques and software, such as the FD Rapid GolgiStain Kit for visualizing neuronal morphology, Image-Pro Plus 6.0 or Image-Pro Plus for image analysis, Stereo Investigator software for stereological assessments, and stereotaxic apparatuses for precise surgical procedures.
In addition, tools like the In Situ Cell Death Detection Kit can be used to investigate cell death and apoptosis, while the VT1000S microtome and GlutaMAX supplements can aid in sample preparation and neuronal culture maintenance.
Electrophysiological recordings can be performed using the Multiclamp 700B amplifier, and imaging studies can be conducted with the LSM 700 confocal microscope.
By leveraging these cutting-edge tools and techniques, researchers can deepen their understanding of the CA1 field's role in memory, learning, and spatial navigation, ultimately leading to groundbreaking discoveries in the field of neuroscience.