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Journal articles on the topic 'Hippocampus (H)'

Author: Grafiati

Published: 3 June 2025

Last updated: 31 July 2025

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1

Swan, Jeanette H., Mary C. Evans, and Brian S. Meldrum. "Long-Term Development of Selective Neuronal Loss and the Mechanism of Protection by 2-Amino-7-Phosphonoheptanoate in a Rat Model of Incomplete Forebrain Ischaemia." Journal of Cerebral Blood Flow & Metabolism 8, no. 1 (1988): 64–78. http://dx.doi.org/10.1038/jcbfm.1988.9.

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Excitatory neurotransmission at the N-methyl-D-aspartate (NMDA) receptor is selectively blocked by 2-amino-7-phosphonoheptanoate acid (2-APH). Acute focal microinjection of 2-APH into the rat hippocampus partially protects against cytopathology developing in selectively vulnerable neurons after 30 min of ischaemia and 2 h of reperfusion. We show that this protective action of 2-APH does not involve alterations in local cerebral blood flow (CBF). Intermediate cytopathology and long-term neuronal survival has been assessed in rats receiving focal injections of (±) 2-APH. 20 μg in 1 μl, into one

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Umeoka, Shuichi C., Hans O. Lüders, John P. Turnbull, Mohamad Z. Koubeissi, and Robert J. Maciunas. "Requirement of longitudinal synchrony of epileptiform discharges in the hippocampus for seizure generation: a pilot study." Journal of Neurosurgery 116, no. 3 (2012): 513–24. http://dx.doi.org/10.3171/2011.10.jns11261.

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Object The goal in this study was to assess the role of longitudinal hippocampal circuits in the generation of interictal and ictal activity in temporal lobe epilepsy (TLE) and to evaluate the effects of multiple hippocampal transections (MHT). Methods In 6 patients with TLE, the authors evaluated the synchrony of hippocampal interictal and ictal epileptiform discharges by using a cross-correlation analysis, and the effect of MHT on hippocampal interictal spikes was studied. Five of the 6 patients were studied with depth electrodes, and epilepsy surgery was performed in 4 patients (anterior te

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Pignataro, Giuseppe, Samaneh Maysami, Francesca E. Studer, Andrew Wilz, Roger P. Simon, and Detlev Boison. "Downregulation of Hippocampal Adenosine Kinase after Focal Ischemia as Potential Endogenous Neuroprotective Mechanism." Journal of Cerebral Blood Flow & Metabolism 28, no. 1 (2007): 17–23. http://dx.doi.org/10.1038/sj.jcbfm.9600499.

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The rate of ischemic brain injury varies with the brain region, requiring only hours in striatum but days in hippocampus. Such maturation implies the existence of endogenous neuroprotective mechanisms. Adenosine is an endogenous neuroprotectant regulated by adenosine kinase (ADK). To investigate, whether adenosine might play a role in protecting the hippocampus after focal ischemia, we subjected transgenic mice, which overexpress ADK in hippocampal neurons (Adk-tg mice) to transient middle cerebral artery occlusion (MCAO). Although the hippocampus of wild-type (wt) mice was consistently spared

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Stephenson, G., and J. Funder. "Hippocampal and renal type I receptors are differentially regulated." American Journal of Physiology-Endocrinology and Metabolism 252, no. 4 (1987): E525—E529. http://dx.doi.org/10.1152/ajpendo.1987.252.4.e525.

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Previously, we have shown that renal mineralocorticoid receptors and hippocampal "corticosterone-perferring" sites have identical intrinsic steroid specificity in vitro. Others have shown that the aldosterone binding species in kidney and hippocampus have identical trypsin fragmentation patterns on isoelectric focusing. To further explore possible areas of identity, we determined levels of type I receptors in hippocampus, renal outer medulla cortex, and renal inner medulla papilla from 22 min to 16 days after adrenalectomy. Available type I sites in kidney fractions increased postadrenalectomy

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Wang, Hong, Rong Jiang, Qin He, et al. "Expression Pattern of Peroxisome Proliferator-Activated Receptors in Rat Hippocampus following Cerebral Ischemia and Reperfusion Injury." PPAR Research 2012 (2012): 1–10. http://dx.doi.org/10.1155/2012/596394.

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The present study was designed to investigate the pattern of time-dependent expression of peroxisome proliferator-activated receptors (PPARα,β, andγ) after global cerebral ischemia and reperfusion (I/R) damage in the rat hippocampus. Male Sprague Dawley (SD) rats were subjected to global cerebral I/R. The rat hippocampi were isolated to detect the expression of PPARs mRNA and protein levels at 30 min–30 d after I/R by RT-PCR and Western blot analysis, respectively. The expression levels of PPARs mRNA and protein in the rat hippocampus significantly increased and peaked at 24 h for PPARαandγ(at

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Radovanovic, Ljiljana, Andrea Novakovic, Jelena Petrovic, and Jasna Saponjic. "Different Alterations of Hippocampal and Reticulo-Thalamic GABAergic Parvalbumin-Expressing Interneurons Underlie Different States of Unconsciousness." International Journal of Molecular Sciences 24, no. 7 (2023): 6769. http://dx.doi.org/10.3390/ijms24076769.

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We traced the changes in GABAergic parvalbumin (PV)-expressing interneurons of the hippocampus and reticulo-thalamic nucleus (RT) as possible underlying mechanisms of the different local cortical and hippocampal electroencephalographic (EEG) microstructures during the non-rapid-eye movement (NREM) sleep compared with anesthesia-induced unconsciousness by two anesthetics with different main mechanisms of action (ketamine/diazepam versus propofol). After 3 h of recording their sleep, the rats were divided into two experimental groups: one half received ketamine/diazepam anesthesia and the other

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Goekint, Maaike, Inge Bos, Elsa Heyman, Romain Meeusen, Yvette Michotte, and Sophie Sarre. "Acute running stimulates hippocampal dopaminergic neurotransmission in rats, but has no influence on brain-derived neurotrophic factor." Journal of Applied Physiology 112, no. 4 (2012): 535–41. http://dx.doi.org/10.1152/japplphysiol.00306.2011.

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Hippocampal brain-derived neurotrophic factor (BDNF) protein is increased with exercise in rats. Monoamines seem to play a role in the regulation of BDNF, and monoamine neurotransmission is known to increase with exercise. The purpose of this study was to examine the influence of acute exercise on monoaminergic neurotransmission and BDNF protein concentrations. Hippocampal microdialysis was performed in rats that were subjected to 60 min of treadmill running at 20 m/min or rest. Two hours postexercise, the rats were killed, and the hippocampus was dissected. In experiments without microdialysi

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Arboit, Alberto, Karla Krautwald, and Frank Angenstein. "The cholinergic system modulates negative BOLD responses in the prefrontal cortex once electrical perforant pathway stimulation triggers neuronal afterdischarges in the hippocampus." Journal of Cerebral Blood Flow & Metabolism 42, no. 2 (2021): 364–80. http://dx.doi.org/10.1177/0271678x211049820.

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Repeated high-frequency pulse-burst stimulations of the rat perforant pathway elicited positive BOLD responses in the right hippocampus, septum and prefrontal cortex. However, when the first stimulation period also triggered neuronal afterdischarges in the hippocampus, then a delayed negative BOLD response in the prefrontal cortex was generated. While neuronal activity and cerebral blood volume (CBV) increased in the hippocampus during the period of hippocampal neuronal afterdischarges (h-nAD), CBV decreased in the prefrontal cortex, although neuronal activity did not decrease. Only after term

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Kowalska, Danuta. "Effects of the anterior temporal lobe lesions, separate or combined with hippocampal damage, on spatial delayed responses guided by auditory stimulus." Acta Neurobiologiae Experimentalis 59, no. 4 (1999): 303–13. http://dx.doi.org/10.55782/ane-1999-1315.

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Seventeen dogs were trained in a three-choice auditory spatial delayed response task, guided by auditory stimulus, at a l0 s delay to a criterion of 90% correct responses in 90 consecutive trials. Four dogs then received bilateral anterior temporal lobe lesions (AT), 6 dogs received hippocampal lesions (H), and 7 dogs served as controls (C). Group C reached postoperative criterion immediately while groups AT and H needed additional training. When subsequently tested at longer delays and with distractions, the group H animals performed more poorly than either the AT or C animals. Further, the g

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Long, Qianfa, Dinesh Upadhya, Bharathi Hattiangady, et al. "Intranasal MSC-derived A1-exosomes ease inflammation, and prevent abnormal neurogenesis and memory dysfunction after status epilepticus." Proceedings of the National Academy of Sciences 114, no. 17 (2017): E3536—E3545. http://dx.doi.org/10.1073/pnas.1703920114.

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Status epilepticus (SE), a medical emergency that is typically terminated through antiepileptic drug treatment, leads to hippocampus dysfunction typified by neurodegeneration, inflammation, altered neurogenesis, as well as cognitive and memory deficits. Here, we examined the effects of intranasal (IN) administration of extracellular vesicles (EVs) secreted from human bone marrow-derived mesenchymal stem cells (MSCs) on SE-induced adverse changes. The EVs used in this study are referred to as A1-exosomes because of their robust antiinflammatory properties. We subjected young mice to pilocarpine

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Xia, Ying, Peng Zhao, Jin Xue, et al. "Na+ Channel Expression and Neuronal Function in the Na+/H+ Exchanger 1 Null Mutant Mouse." Journal of Neurophysiology 89, no. 1 (2003): 229–36. http://dx.doi.org/10.1152/jn.00488.2002.

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Mice lacking Na+/H+ exchanger 1 (NHE1) suffer from recurrent seizures and die early postnatally. Although the mechanisms for seizures are not well established, our previous electrophysiological work has shown that neuronal excitability and Na+ current density are increased in hippocampal CA1 neurons of these mutant mice. However, it is unknown whether this increased density is related to altered expression or functional regulation of Na+ channels. In this work, we asked three questions: is the increased excitability limited to CA1 neurons, is the increased Na+ current density related to an inc

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Ruiter, Marvin, Christine Lützkendorf, Jian Liang та Corette J. Wierenga. "Amyloid-β Oligomers Induce Only Mild Changes to Inhibitory Bouton Dynamics". Journal of Alzheimer's Disease Reports 5, № 1 (2021): 153–60. http://dx.doi.org/10.3233/adr-200291.

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The amyloid-β protein precursor is highly expressed in a subset of inhibitory neuron in the hippocampus, and inhibitory neurons have been suggested to play an important role in early Alzheimer’s disease plaque load. Here we investigated bouton dynamics in axons of hippocampal interneurons in two independent amyloidosis models. Short-term (24 h) amyloid-β (Aβ)-oligomer application to organotypic hippocampal slices slightly increased inhibitory bouton dynamics, but bouton density and dynamics were unchanged in hippocampus slices of young-adult AppNL - F - G-mice, in which Aβ levels are chronical

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Schröder, Jane K., Laila Abdel-Hafiz, Amira A. H. Ali, et al. "Effects of the Light/Dark Phase and Constant Light on Spatial Working Memory and Spine Plasticity in the Mouse Hippocampus." Cells 12, no. 13 (2023): 1758. http://dx.doi.org/10.3390/cells12131758.

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Circadian rhythms in behavior and physiology such as rest/activity and hormones are driven by an internal clock and persist in the absence of rhythmic environmental cues. However, the period and phase of the internal clock are entrained by the environmental light/dark cycle. Consequently, aberrant lighting conditions, which are increasing in modern society, have a strong impact on rhythmic body and brain functions. Mice were exposed to three different lighting conditions, 12 h light/12 h dark cycle (LD), constant darkness (DD), and constant light (LL), to study the effects of the light/dark cy

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Shen, Fengming, Juan Wang, Feng Gao, Jingji Wang, and Guoqi Zhu. "Ginsenoside Rg1 Prevents Cognitive Impairment and Hippocampal Neuronal Apoptosis in Experimental Vascular Dementia Mice by Promoting GPR30 Expression." Neural Plasticity 2021 (December 3, 2021): 1–11. http://dx.doi.org/10.1155/2021/2412220.

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This study is aimed at investigating the potential roles of G protein-coupled estrogen receptor 1 (GPER, also known as GPR30) in the preventive effect of ginsenoside Rg1 against cognitive impairment and hippocampal cell apoptosis in experimental vascular dementia (VD) in mice. The effects of bilateral common carotid artery stenosis (BCAS) on GPR30 expression at mRNA level were evaluated. Thereafter, the BCAS mouse model was utilized to evaluate the protection of Rg1 (0.1, 1, 10 mg/kg, 14 days, ip). Spatial memory was evaluated by water Morris Maze 7 days post BCAS. After behavioral tests, neur

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Merino, José Joaquín, Vilma Muñetón-Gomez, César Muñetón-Gómez, María Ángeles Pérez-Izquierdo, María Loscertales, and Adolfo Toledano Gasca. "Hippocampal CCR5/RANTES Elevations in a Rodent Model of Post-Traumatic Stress Disorder: Maraviroc (a CCR5 Antagonist) Increases Corticosterone Levels and Enhances Fear Memory Consolidation." Biomolecules 10, no. 2 (2020): 212. http://dx.doi.org/10.3390/biom10020212.

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Background: Contextual fear conditioning (CFC) is a rodent model that induces a high and long-lasting level of conditioning associated with traumatic memory formation; this behavioral paradigm resembles many characteristics of posttraumatic stress disorder (PSTD). Chemokines (chemotactic cytokines) play a known role in neuronal migration and neurodegeneration but their role in cognition is not totally elucidated. Aim: We ascertain whether CCR5/RANTES beta chemokines (hippocampus/prefrontal cortex) could play a role in fear memory consolidation (CFC paradigm). We also evaluated whether chronic

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Murthy, S. R. K., E. Thouennon, W. S. Li, et al. "Carboxypeptidase E Protects Hippocampal Neurons During Stress in Male Mice by Up-regulating Pro-survival BCL2 Protein Expression." Endocrinology 154, no. 9 (2013): 3284–93. http://dx.doi.org/10.1210/en.2013-1118.

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Prolonged chronic stress causing elevated plasma glucocorticoids leads to neurodegeneration. Adaptation to stress (allostasis) through neuroprotective mechanisms can delay this process. Studies on hippocampal neurons have identified carboxypeptidase E (CPE) as a novel neuroprotective protein that acts extracellularly, independent of its enzymatic activity, although the mechanism of action is unclear. Here, we aim to determine if CPE plays a neuroprotective role in allostasis in mouse hippocampus during chronic restraint stress (CRS), and the molecular mechanisms involved. Quantitative RT-PCR/i

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Osacka, Jana, Alexander Kiss, Zuzana Bacova, and Andrej Tillinger. "Effects of antipsychotics, haloperidol and olanzapine, on the expression of apoptosis-related genes in mouse mHippoE-2 cells and rat hippocampus." Endocrine Regulations 57, no. 1 (2023): 152–61. http://dx.doi.org/10.2478/enr-2023-0019.

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Abstract Objective. Modified levels of pro- (caspase3, Bax) and anti-apoptotic (Bcl-2) regulatory proteins have been detected in certain brain areas of schizophrenic patients indicating a possible dysregulation of apoptosis. In the present study, effects of antipsychotics, haloperidol (HAL) and olanzapine (OLA), on the gene expression of caspase3 (casp3), Bax and Bcl-2 were studied in vitro in mouse hippocampal mHippoE-2 cell line and in vivo in the hippocampus of MK-801 animal schizophrenia model with the aim to provide evidence that antipsychotics may affect the activity of apoptosis-related

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Y.W., Len, Christianus A., Worachananant S., Muta Harah Z, and Chong C.M. "Estimation of live food consumption for Hippocampus barbouri and Hippocampus kuda." International Journal of Aquatic Research and Environmental Studies 1, no. 1 (2021): 23–35. https://doi.org/10.70102/ijares/v1i1/3.

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Seahorse is found worldwide in marine habitats such as the seagrass beds, coral reefs, mangroves and estuaries. Hippocampus barbouri and Hippocampus kuda are among the most traded seahorse species. In recent year, worldwide attention strongly support the establishment of seahorse aquaculture as to provide an alternative source of seahorse. However, the main bottleneck in succeeding seahorse aquaculture were problems faced in the culture of early stage juvenile, specifically the diet. The selection of suitable diet will contribute to the breeding success and larval rearing of seahorse. In this

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Hartmann, Alice, Aline Fassini, América Scopinho, et al. "Role of the endocannabinoid system in the dorsal hippocampus in the cardiovascular changes and delayed anxiety-like effect induced by acute restraint stress in rats." Journal of Psychopharmacology 33, no. 5 (2019): 606–14. http://dx.doi.org/10.1177/0269881119827799.

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Background: The dorsal hippocampus has a central role in modulating cardiovascular responses and behavioral adaptation to stress. The dorsal hippocampus also plays a key role in stress-associated mental disorders. The endocannabinoid system is widely expressed in the dorsal hippocampus and modulates defensive behaviors under stressful conditions. The endocannabinoid anandamide activates cannabinoid type 1 receptors and is metabolized by the fatty acid amide hydrolase enzyme. Aims: We sought to verify whether cannabinoid type 1 receptors modulate stress-induced cardiovascular changes, and if ph

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Grissom, Elin M., та Jill M. Daniel. "Evidence for Ligand-Independent Activation of Hippocampal Estrogen Receptor-α by IGF-1 in Hippocampus of Ovariectomized Rats". Endocrinology 157, № 8 (2016): 3149–56. http://dx.doi.org/10.1210/en.2016-1197.

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In the absence of ovarian estrogens, increased levels of estrogen receptor (ER)α in the hippocampus are associated with improvements in cognition. In vitro evidence indicates that under conditions of low estrogen, growth factors, including Insulin-Like Growth Factor 1 (IGF-1), can activate ERα and regulate ERα-mediated transcription through mechanisms that likely involve modification of phosphorylation sites on the receptor. The goal of the current work was to investigate a role for IGF-1 in ligand-independent activation of ERα in the hippocampus of female rats. Ovariectomized rats received a

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Ikeda, Muneki, Yasushi Hojo, Yoshimasa Komatsuzaki, et al. "Hippocampal spine changes across the sleep–wake cycle: corticosterone and kinases." Journal of Endocrinology 226, no. 2 (2015): M13—M27. http://dx.doi.org/10.1530/joe-15-0078.

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The corticosterone (CORT) level changes along the circadian rhythm. Hippocampus is sensitive to CORT, since glucocorticoid receptors are highly expressed. In rat hippocampus fixed in a living state every 3 h, we found that the dendritic spine density of CA1 pyramidal neurons increased upon waking (within 3 h), as compared with the spine density in the sleep state. Particularly, the large-head spines increased. The observed change in the spine density may be due to the change in the hippocampal CORT level, since the CORT level at awake state (∼30 nM) in cerebrospinal fluid was higher than that

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Ohtsuki, T., M. Matsumoto, K. Kitagawa, et al. "Delayed neuronal death in ischemic hippocampus involves stimulation of protein tyrosine phosphorylation." American Journal of Physiology-Cell Physiology 271, no. 4 (1996): C1085—C1097. http://dx.doi.org/10.1152/ajpcell.1996.271.4.c1085.

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Glutamate triggers neuronal degeneration after ischemia-reperfusion in the brain. However, the details of intracellular signal transduction that propagates cell death remain unknown. The present work investigated whether protein tyrosine phosphorylation mediates neuronal death in the ischemic brain. Transient forebrain ischemia for 5-10 min in Mongolian gerbils or intoxication with the glutamate analogue kainic acid (12 mg/kg) in Sprague-Dawley rats caused neuronal death selectively in the hippocampus 2-4 days or 1 day later, respectively. Under these conditions, 160-, 115-, 105-, 92-, and 85-

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Álvarez-Croda, Dulce-Mariely, Juan Santiago-García, Jesús S. Medel-Matus та ін. "Hippocampal distribution of IL-1β and IL-1RI following lithium-pilocarpine-induced status epilepticus in the developing rat". Anais da Academia Brasileira de Ciências 88, suppl 1 (2016): 653–63. http://dx.doi.org/10.1590/0001-3765201620150296.

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The contribution of Interleukin-1β (IL-1β) to neuronal injury induced by status epilepticus (SE) in the immature brain remains unclear. The goal of this study was to determine the hippocampal expression of IL-1β and its type 1 receptor (IL-1RI) following SE induced by the lithium-pilocarpine model in fourteen-days-old rat pups; control animals were given an equal volume of saline instead of the convulsant. IL-1β and IL-1RI mRNA hippocampal levels were assessed by qRT-PCR 6 and 24 h after SE or control conditions. IL-1β and IL-1RI expression was detected in the dorsal hippocampus by immunohisto

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Huang, Pen-Sen, Ping-Yen Tsai, Ling-Yu Yang, et al. "3,6′-Dithiopomalidomide Ameliorates Hippocampal Neurodegeneration, Microgliosis and Astrogliosis and Improves Cognitive Behaviors in Rats with a Moderate Traumatic Brain Injury." International Journal of Molecular Sciences 22, no. 15 (2021): 8276. http://dx.doi.org/10.3390/ijms22158276.

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Traumatic brain injury (TBI) is a leading cause of disability and mortality worldwide. It can instigate immediate cell death, followed by a time-dependent secondary injury that results from disproportionate microglial and astrocyte activation, excessive inflammation and oxidative stress in brain tissue, culminating in both short- and long-term cognitive dysfunction and behavioral deficits. Within the brain, the hippocampus is particularly vulnerable to a TBI. We studied a new pomalidomide (Pom) analog, namely, 3,6′-dithioPom (DP), and Pom as immunomodulatory imide drugs (IMiD) for mitigating T

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Stanley, David A., Sachin S. Talathi, Mansi B. Parekh, et al. "Phase shift in the 24-hour rhythm of hippocampal EEG spiking activity in a rat model of temporal lobe epilepsy." Journal of Neurophysiology 110, no. 5 (2013): 1070–86. http://dx.doi.org/10.1152/jn.00911.2012.

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For over a century epileptic seizures have been known to cluster at specific times of the day. Recent studies have suggested that the circadian regulatory system may become permanently altered in epilepsy, but little is known about how this affects neural activity and the daily pattern of seizures. To investigate, we tracked long-term changes in the rate of spontaneous hippocampal EEG spikes (SPKs) in a rat model of temporal lobe epilepsy. In healthy animals, SPKs oscillated with near 24-h period; however, after injury by status epilepticus, a persistent phase shift of ∼12 h emerged in animals

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Choo, C. K., and H. C. Liew. "Spatial distribution, substrate assemblages and size composition of sea horses (Family Syngnathidae) in the coastal waters of Peninsular Malaysia." Journal of the Marine Biological Association of the United Kingdom 83, no. 2 (2003): 271–76. http://dx.doi.org/10.1017/s0025315403007069h.

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Four species of sea horses (Syngnathidae: Hippocampus) were found in Peninsular Malaysia during a survey conducted between April and August 2001. These were Hippocampus trimaculatus, H. spinosissimus, H. kuda and H. kelloggi. All four species were found in the Straits of Malacca; two species (H. trimaculatus and H. spinosissimus) in the east coast of Peninsular Malaysia in the South China Sea; and three species: H. trimaculatus, H. spinosissimus and H. kuda in the south coast, Straits of Johor. There were habitat and depth separations by species. Hippocampus trimaculatus, which was found throu

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Strauch, Christina, and Denise Manahan-Vaughan. "Orchestration of Hippocampal Information Encoding by the Piriform Cortex." Cerebral Cortex 30, no. 1 (2019): 135–47. http://dx.doi.org/10.1093/cercor/bhz077.

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Abstract The hippocampus utilizes olfactospatial information to encode sensory experience by means of synaptic plasticity. Odor exposure is also a potent impetus for hippocampus-dependent memory retrieval. Here, we explored to what extent the piriform cortex directly impacts upon hippocampal information processing and storage. In behaving rats, test-pulse stimulation of the anterior piriform cortex (aPC) evoked field potentials in the dentate gyrus (DG). Patterned stimulation of the aPC triggered both long-term potentiation (LTP &gt; 24 h) and short-term depression (STD), in a frequency-de

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D'Antuono, Margherita, Ruba Benini, Giuseppe Biagini, et al. "Limbic Network Interactions Leading to Hyperexcitability in a Model of Temporal Lobe Epilepsy." Journal of Neurophysiology 87, no. 1 (2002): 634–39. http://dx.doi.org/10.1152/jn.00351.2001.

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In mouse brain slices that contain reciprocally connected hippocampus and entorhinal cortex (EC) networks, CA3 outputs control the EC propensity to generate experimentally induced ictal-like discharges resembling electrographic seizures. Neuronal damage in limbic areas, such as CA3 and dentate hilus, occurs in patients with temporal lobe epilepsy and in animal models (e.g., pilocarpine- or kainate-treated rodents) mimicking this epileptic disorder. Hence, hippocampal damage in epileptic mice may lead to decreased CA3 output function that in turn would allow EC networks to generate ictal-like e

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Jiao, Yuan, Hongwu Fan, Kexin Wang, and Shan Lu. "Sevoflurane Impairs Short-Term Memory by Affecting PSD-95 and AMPA Receptor in the Hippocampus of a Mouse Model." Behavioural Neurology 2019 (October 21, 2019): 1–11. http://dx.doi.org/10.1155/2019/1068260.

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Objective. To explore the effects of sevoflurane on the latency and error times of the passive avoidance and levels of PSD-95 and AMPA receptors in the hippocampus. We evaluated the effects of sevoflurane on short-term memory in adult mice and explored the possible mechanism. Methods. 144 Kunming mice (2-3 months, 30-35 g) were randomly divided into two groups A (n=64) and B (n=80) and received the dark-avoidance (DA) and step-down avoidance (SA) tests, respectively. The groups DA and SA were further divided into control (inhaled 40% O2 2 h) and sevoflurane (3.3% sevoflurane and 40% O2 2 h) su

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Miller, A. H., R. L. Spencer, M. Stein, and B. S. McEwen. "Adrenal steroid receptor binding in spleen and thymus after stress or dexamethasone." American Journal of Physiology-Endocrinology and Metabolism 259, no. 3 (1990): E405. http://dx.doi.org/10.1152/ajpendo.1990.259.3.e405.

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Type I and II adrenal steroid receptor binding was measured in spleen and thymus of adrenalectomized (ADX) rats and intact rats at basal levels of corticosterone after 1 h of restraint stress or after exogenous administration of dexamethasone (DEX). Concurrent receptor determinations were made in the hippocampus and pituitary. Receptor binding measures in immune tissues and pituitary were less responsive to varying levels of endogenous hormones than binding measures in hippocampus. Compared with ADX rats, type I binding in spleen and pituitary of intact rats at basal levels of corticosterone w

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Spahic, Harisa, Pritika Parmar, Sarah Miller, et al. "Dysregulation of ErbB4 Signaling Pathway in the Dorsal Hippocampus after Neonatal Hypoxia-Ischemia and Late Deficits in PV+ Interneurons, Synaptic Plasticity and Working Memory." International Journal of Molecular Sciences 24, no. 1 (2022): 508. http://dx.doi.org/10.3390/ijms24010508.

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Neonatal hypoxic-ischemic (HI) injury leads to deficits in hippocampal parvalbumin (PV)+ interneurons (INs) and working memory. Therapeutic hypothermia (TH) does not prevent these deficits. ErbB4 supports maturation and maintenance of PV+ IN. Thus, we hypothesized that neonatal HI leads to persistent deficits in PV+ INs, working memory and synaptic plasticity associated with ErbB4 dysregulation despite TH. P10 HI-injured mice were randomized to normothermia (NT, 36 °C) or TH (31 °C) for 4 h and compared to sham. Hippocampi were studied for α-fodrin, glial fibrillary acidic protein (GFAP), and

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Snyder, Brina, Hua-Kang Wu, Brianna Tillman, and Thomas F. Floyd. "Aged Mouse Hippocampus Exhibits Signs of Chronic Hypoxia and an Impaired HIF-Controlled Response to Acute Hypoxic Exposures." Cells 11, no. 3 (2022): 423. http://dx.doi.org/10.3390/cells11030423.

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Altered hypoxia-inducible factor-alpha (HIF-α) activity may have significant consequences in the hippocampus, which mediates declarative memory, has limited vascularization, and is vulnerable to hypoxic insults. Previous studies have reported that neurovascular coupling is reduced in aged brains and that diseases which cause hypoxia increase with age, which may render the hippocampus susceptible to acute hypoxia. Most studies have investigated the actions of HIF-α in aging cortical structures, but few have focused on the role of HIF-α within aged hippocampus. This study tests the hypothesis th

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Park, Hee-Jung, Myeong-Hyun Nam, Ji-Hoon Park, et al. "Comparison of Malondialdehyde, Acetylcholinesterase, and Apoptosis-Related Markers in the Cortex and Hippocampus of Cognitively Dysfunctional Mice Induced by Scopolamine." Biomedicines 12, no. 11 (2024): 2475. http://dx.doi.org/10.3390/biomedicines12112475.

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Objectives: Until now, many researchers have conducted evaluations on hippocampi for analyses of cognitive dysfunction models using scopolamine. However, depending on the purposes of these analyses, there are differences in the experimental results for the hippocampi and cortexes. Therefore, this study intends to compare various analyses of cognitive dysfunction after scopolamine administration with each other in hippocampi and cortexes. Methods: Scopolamine was administered at three dosages in mice: 0.5, 1, and 3 mg/kg. And this study evaluates the differences in cognitive function and the ex

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Rezai, Ali R., Manish Ranjan, Pierre-François D’Haese, et al. "Noninvasive hippocampal blood−brain barrier opening in Alzheimer’s disease with focused ultrasound." Proceedings of the National Academy of Sciences 117, no. 17 (2020): 9180–82. http://dx.doi.org/10.1073/pnas.2002571117.

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The blood–brain barrier (BBB) presents a significant challenge for treating brain disorders. The hippocampus is a key target for novel therapeutics, playing an important role in Alzheimer’s disease (AD), epilepsy, and depression. Preclinical studies have shown that magnetic resonance (MR)-guided low-intensity focused ultrasound (FUS) can reversibly open the BBB and facilitate delivery of targeted brain therapeutics. We report initial clinical trial results evaluating the safety, feasibility, and reversibility of BBB opening with FUS treatment of the hippocampus and entorhinal cortex (EC) in pa

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Li, Xiao-Min, Fan Su, Mu-Huo Ji, et al. "Disruption of Hippocampal Neuregulin 1–ErbB4 Signaling Contributes to the Hippocampus-dependent Cognitive Impairment Induced by Isoflurane in Aged Mice." Anesthesiology 121, no. 1 (2014): 79–88. http://dx.doi.org/10.1097/aln.0000000000000191.

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Abstract Background: A prolonged isoflurane exposure may lead to cognitive decline in rodents. Neuregulin 1 (NRG1)–ErbB4 signaling plays a key role in the modulation of hippocampal synaptic plasticity through regulating the neurotransmission. The authors hypothesized that hippocampal NRG1–ErbB4 signaling is involved in isoflurane-induced cognitive impairments in aged mice. Methods: Fourteen-month-old C57BL/6 mice were randomized to receive 100% O2 exposure, vehicle injection after 100% O2 exposure, vehicle injection after exposure to isoflurane carried by 100% O2, NRG1-β1 injection after expos

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Welsh, Frank A., and Valerie A. Harris. "Postischemic Hypothermia Fails to Reduce Ischemic Injury in Gerbil Hippocampus." Journal of Cerebral Blood Flow & Metabolism 11, no. 4 (1991): 617–20. http://dx.doi.org/10.1038/jcbfm.1991.112.

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The objective of this study was to determine whether postischemic hypothermia diminishes ischemic injury in gerbil hippocampus. Cerebral ischemia was produced by occluding both carotid arteries for 5 min, while maintaining the temperature of the cranium and rectum at 38°C. Upon recirculation, the animals were divided into three groups: Normothermic (38°C), moderately hypothermic (33°C), and deeply hypothermic (23°C). In the normothermic group, cranial and rectal temperatures were maintained at 38°C for 30 min and 2 h, respectively, prior to the removal of the temperature probes. In the moderat

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Jung, Hyo Young, Woosuk Kim, Kyu Ri Hahn, et al. "Pyridoxine Deficiency Exacerbates Neuronal Damage after Ischemia by Increasing Oxidative Stress and Reduces Proliferating Cells and Neuroblasts in the Gerbil Hippocampus." International Journal of Molecular Sciences 21, no. 15 (2020): 5551. http://dx.doi.org/10.3390/ijms21155551.

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We investigated the effects of pyridoxine deficiency on ischemic neuronal death in the hippocampus of gerbil (n = 5 per group). Serum pyridoxal 5′-phosphate levels were significantly decreased in Pyridoxine-deficient diet (PDD)-fed gerbils, while homocysteine levels were significantly increased in sham- and ischemia-operated gerbils. PDD-fed gerbil showed a reduction in neuronal nuclei (NeuN)-immunoreactive neurons in the medial part of the hippocampal CA1 region three days after. Reactive astrocytosis and microgliosis were found in PDD-fed gerbils, and transient ischemia caused the aggregatio

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Arabian, Maedeh, Nahid Aboutaleb, Mansoureh Soleimani, et al. "Preconditioning with morphine protects hippocampal CA1 neurons from ischemia–reperfusion injury via activation of the mTOR pathway." Canadian Journal of Physiology and Pharmacology 96, no. 1 (2018): 80–87. http://dx.doi.org/10.1139/cjpp-2017-0245.

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The signaling pathway of chronic morphine treatment to prevent neuronal damage following transient cerebral ischemia is not clear. In this study, we examined the role of mammalian target of rapamycin (mTOR) to identify the neuroprotective effects of chronic morphine preconditioning on the hippocampus following ischemia–reperfusion (I/R) injury. Morphine was administered for 5 days, twice a day, before inducing I/R injury. The possible role of mTOR was evaluated by the injection of rapamycin (5 mg/kg body weight, by intraperitoneal injection) before I/R was induced. The passive avoidance test w

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Fang, Kun, Dong Liu, Salil S. Pathak, et al. "Disruption of Circadian Rhythms by Ambient Light during Neurodevelopment Leads to Autistic-like Molecular and Behavioral Alterations in Adult Mice." Cells 10, no. 12 (2021): 3314. http://dx.doi.org/10.3390/cells10123314.

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Although circadian rhythms are thought to be essential for maintaining body health, the effects of chronic circadian disruption during neurodevelopment remain elusive. Here, using the “Short Day” (SD) mouse model, in which an 8 h/8 h light/dark (LD) cycle was applied from embryonic day 1 to postnatal day 42, we investigated the molecular and behavioral changes after circadian disruption in mice. Adult SD mice fully entrained to the 8 h/8 h LD cycle, and the circadian oscillations of the clock proteins, PERIOD1 and PERIOD2, were disrupted in the suprachiasmatic nucleus and the hippocampus of th

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Zhang, Jiancheng, Youge Qu, Lijia Chang, Yaoyu Pu, and Kenji Hashimoto. "(R)-Ketamine Rapidly Ameliorates the Decreased Spine Density in the Medial Prefrontal Cortex and Hippocampus of Susceptible Mice After Chronic Social Defeat Stress." International Journal of Neuropsychopharmacology 22, no. 10 (2019): 675–79. http://dx.doi.org/10.1093/ijnp/pyz048.

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Abstract Background A recent study demonstrated that spine formation rates by ketamine in the prefrontal cortex (PFC) were not altered at 3–6 h following a single injection, but were markedly altered at 12–24 h. Here, we investigated the acute (3 h post-treatment) effects of (R)-ketamine in the decreased spine density in the medial PFC (mPFC) and hippocampus in susceptible mice after chronic social defeat stress (CSDS). Methods (R)-ketamine (10 mg/kg) or saline was administered intraperitoneally to CSDS-susceptible mice. Dendritic spine density in the mPFC and hippocampus was measured 3 h afte

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Power, John M., Lucien T. Thompson, James R. Moyer, and John F. Disterhoft. "Enhanced Synaptic Transmission in CA1 Hippocampus After Eyeblink Conditioning." Journal of Neurophysiology 78, no. 2 (1997): 1184–87. http://dx.doi.org/10.1152/jn.1997.78.2.1184.

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Power, John M., Lucien T. Thompson, James R. Moyer, Jr., and John F. Disterhoft. Enhanced synaptic transmission in CA1 hippocampus after eyeblink conditioning. J. Neurophysiol. 78: 1184–1187, 1997. CA1 field potentials evoked by Schaffer collateral stimulation of hippocampal slices from trace-conditioned rabbits were compared with those from naive and pseudoconditioned controls. Conditioned rabbits received 80 trace conditioning trials daily until reaching a criterion of 80% conditioned responses in a session. Hippocampal slices were prepared 1 or 24 h after reaching criterion (for trace-condi

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More, Jamileth, María Mercedes Casas, Gina Sánchez, Cecilia Hidalgo, and Paola Haeger. "Contextual Fear Memory Formation and Destabilization Induce Hippocampal RyR2 Calcium Channel Upregulation." Neural Plasticity 2018 (July 5, 2018): 1–11. http://dx.doi.org/10.1155/2018/5056181.

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Hippocampus-dependent spatial and aversive memory processes entail Ca2+ signals generated by ryanodine receptor (RyR) Ca2+ channels residing in the endoplasmic reticulum membrane. Rodents exposed to different spatial memory tasks exhibit significant hippocampal RyR upregulation. Contextual fear conditioning generates robust hippocampal memories through an associative learning process, but the effects of contextual fear memory acquisition, consolidation, or extinction on hippocampal RyR protein levels remain unreported. Accordingly, here we investigated if exposure of male rats to contextual fe

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Lippmann, Kristina, Lyn Kamintsky, Soo Young Kim, et al. "Epileptiform activity and spreading depolarization in the blood–brain barrier-disrupted peri-infarct hippocampus are associated with impaired GABAergic inhibition and synaptic plasticity." Journal of Cerebral Blood Flow & Metabolism 37, no. 5 (2016): 1803–19. http://dx.doi.org/10.1177/0271678x16652631.

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Peri-infarct opening of the blood–brain barrier may be associated with spreading depolarizations, seizures, and epileptogenesis as well as cognitive dysfunction. We aimed to investigate the mechanisms underlying neural network pathophysiology in the blood–brain barrier-dysfunctional hippocampus. Photothrombotic stroke within the rat neocortex was associated with increased intracranial pressure, vasogenic edema, and peri-ischemic blood–brain barrier dysfunction that included the ipsilateral hippocampus. Intrahippocampal recordings revealed electrographic seizures within the first week in two-th

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Pereira, Danilo, Renan Frittoli, Paulo Julio, Lilian Costallat, Leticia Rittner, and Simone Appenzeller. "LONGITUDINAL NEUROCHEMICAL CHANGES IN THE HIPPOCAMPUS ASSOCIATED WITH MOOD AND COGNITIVE IMPAIRMENT IN SYSTEMIC LUPUS ERYTHEMATOSUS." Journal of Rheumatology 52, Suppl 1 (2025): 6–7. https://doi.org/10.3899/jrheum.2025-0390.o004.

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O004 / #223Topic:AS05 - CNS LupusSCIENTIFIC HYBRID SESSION: CLINICAL TRACK PRESENTATIONS - OUTSTANDING ABSTRACT PRESENTATIONS23-05-2025 9:00 AM - 10:00 AMBackground/PurposeSystemic lupus erythematosus (SLE) is an autoimmune disease with multiorgan involvement. The hippocampus is one of the most thoroughly investigated structures in the brain and hippocampal atrophy was found in SLE patients. Proton magnetic resonance spectroscopy (¹H-MRS) has proved to be a noninvasive tool for detecting neuronal metabolic dysfunction in neurological diseases. The purpose of this study was to investigate the p

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Yook, Jang Soo, Randeep Rakwal, Junko Shibato, et al. "Leptin in hippocampus mediates benefits of mild exercise by an antioxidant on neurogenesis and memory." Proceedings of the National Academy of Sciences 116, no. 22 (2019): 10988–93. http://dx.doi.org/10.1073/pnas.1815197116.

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Regular exercise and dietary supplements with antioxidants each have the potential to improve cognitive function and attenuate cognitive decline, and, in some cases, they enhance each other. Our current results reveal that low-intensity exercise (mild exercise, ME) and the natural antioxidant carotenoid astaxanthin (AX) each have equivalent beneficial effects on hippocampal neurogenesis and memory function. We found that the enhancement by ME combined with AX in potentiating hippocampus-based plasticity and cognition is mediated by leptin (LEP) made and acting in the hippocampus. In assessing

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Perng, Vivian, Chong Li, Carolyn R. Klocke, et al. "Iron Deficiency and Iron Excess Differently Affect Dendritic Architecture of Pyramidal Neurons in the Hippocampus of Piglets." Journal of Nutrition 151, no. 1 (2020): 235–44. http://dx.doi.org/10.1093/jn/nxaa326.

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ABSTRACT Background Both iron deficiency and overload may adversely affect neurodevelopment. Objectives The study assessed how changes in early-life iron status affect iron homeostasis and cytoarchitecture of hippocampal neurons in a piglet model. Methods On postnatal day (PD) 1, 30 Hampshire × Yorkshire crossbreed piglets (n = 15/sex) were stratified by sex and litter and randomly assigned to experimental groups receiving low (L-Fe), adequate (A-Fe), or high (H-Fe) levels of iron supplement during the pre- (PD1–21) and postweaning periods (PD22–35). Pigs in the L-Fe, A-Fe, and H-Fe groups ora

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Xu, Bin, Limin Lang, Shize Li, et al. "Corticosterone Excess-Mediated Mitochondrial Damage Induces Hippocampal Neuronal Autophagy in Mice Following Cold Exposure." Animals 9, no. 9 (2019): 682. http://dx.doi.org/10.3390/ani9090682.

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Cold stress can induce autophagy mediated by excess corticosterone (CORT) in the hippocampus, but the internal mechanism induced by cold stress is not clear. In vivo, male and female C57BL/6 mice were stimulated in 4 °C, 3 h per day for 1 week to build the model of cold sress. In vitro, hippocampal neuronal cell line (HT22) cells were incubated with or without mifepristone (RU486) for 1 h, then treated with 400 μM cortisol (CORT) for 3 h. In vivo, autophagy was measured by western blotting. In vitro, monodansylcadaverine staining, western blotting, flow cytometry, transmission electron microsc

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LEE, HIE RIN, and KEELY M. BUMSTED O’BRIEN. "Morphological and behavioral limit of visual resolution in temperate (Hippocampus abdominalis) and tropical (Hippocampus taeniopterus) seahorses." Visual Neuroscience 28, no. 4 (2011): 351–60. http://dx.doi.org/10.1017/s0952523811000149.

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AbstractSeahorses are visually guided feeders that prey upon small fast-moving crustaceans. Seahorse habitats range from clear tropical to turbid temperate waters. How are seahorse retinae specialized to mediate vision in these diverse environments? Most species of seahorse have a specialization in their retina associated with acute vision, the fovea. The purpose of this study was to characterize the fovea of temperate Hippocampus abdominalis and tropical H. taeniopterus seahorses and to investigate their theoretical and behavioral limits of visual resolution. Their foveae were identified and

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Svensson, Maria, Thord Hallin, Jonas Broms, Joakim Ekstrand, and Anders Tingström. "Spatial memory impairment in Morris water maze after electroconvulsive seizures." Acta Neuropsychiatrica 29, no. 1 (2016): 17–26. http://dx.doi.org/10.1017/neu.2016.22.

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ObjectiveElectroconvulsive therapy (ECT) is one of the most efficient treatments for severe major depression, but some patients suffer from retrograde memory loss after treatment. Electroconvulsive seizures (ECS), an animal model of ECT, have repeatedly been shown to increase hippocampal neurogenesis, and multiple ECS treatments cause retrograde amnesia in hippocampus-dependent memory tasks. Since recent studies propose that addition of newborn hippocampal neurons might degrade existing memories, we investigated whether the memory impairment after multiple ECS treatments is a cumulative effect

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Stroev, Sergey, Ekaterina Tjulkova, Michail Samoilov, and Markku Pelto-Huikko. "One- and three-time mild hypobaric hypoxia modifies expression of mitochondrial thioredoxin-2 in hippocampus of rat." Acta Neurobiologiae Experimentalis 71, no. 2 (2011): 244–55. http://dx.doi.org/10.55782/ane-2011-1844.

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Our previous study demonstrated that preconditioning by 3-times repetitive mild hypoxia significantly augmented expression of mitochondrial thioredoxin-2 (Trx-2) at 3 h after subsequent acute severe hypoxia in rat hippocampus. However, it was unclear whether this augmentation was due to build up of Trx-2 by mild hypoxia before severe hypoxia or by modification of reaction to severe hypoxia itself. To answer on this question we study the expression level during and after preconditioning without subsequent severe hypoxia. Trx-2 expression was studied by immunocytochemistry 3 h and 24 h after fir

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