We have used flow cytometry to investigate whether MyD88, an adaptor protein that transmits signals from TLRs and receptors for IL-1 and IL-18, regulates leukocyte infiltration into the stab-injured entorhinal cortex (EC) and into sites of axonal degeneration in the denervated hippocampus. 
Astroglial loss/damage was observed in the entorhinal cortex and the CA1 region at 4 weeks and 8 weeks after SE, respectively. These astroglial responses in the hippocampo-entorhinal cortex were accompanied by hyperexcitability of the CA1 region (impairment of paired-pulse inhibition and increase in excitability ratio). Unlike the dentate gyrus and the entorhinal cortex, CA1 astroglial damage was protected by conventional anti-epileptic drugs. alpha-Aminoadipic acid (a specific astroglial toxin) infusion into the entorhinal cortex induced astroglial damage and changed the electrophysiological properties in the CA1 region. Astroglial regeneration in the dentate gyrus and the stratum oriens of the CA1 region was found to originate from gliogenesis, while that in the entorhinal cortex and stratum radiatum of the CA1 region originated from in situ proliferation.
Notably, newborn neurons with a mature neuronal phenotype are found in the olfactory tubercles, anterior olfactory nuclei, tenia tecta, islands of Calleja, amygdala, and lateral entorhinal cortex.
One day after the injection we found a pattern of cell loss (hilus, parts of CA3, CA1 and layer III of the medial entorhinal cortex) reminiscent of that seen in models of temporal lobe epilepsy.
Among the other olfactory structures, only the entorhinal cortex and the tenia tecta are connected with both the CoA and the MeA.
Gene expression profiles were assessed in the hippocampus, entorhinal cortex, superior-frontal gyrus, and postcentral gyrus across the lifespan of 55 cognitively intact individuals aged 20-99 years. For example, comparing equally powered groups, 5,029 probe sets were significantly altered with age in the superior-frontal gyrus, compared with 1,110 in the entorhinal cortex.
Mature stellate cells of the rat medial entorhinal cortex (EC), layer II, exhibit subthreshold membrane potential oscillations (MPO) at theta frequencies (4-12 Hz) in vitro.
Grid cells in the medial entorhinal cortex and place cells in the hippocampus are thought to participate in the formation of a dynamic representation of the animal's current location, and these cells are presumably critical for storing the representation in memory. To traverse the environment, animals must be able to translate coordinate information from spatial maps in the entorhinal cortex and hippocampus into body-centered representations that can be used to direct locomotion.
At baseline, both the amnestic MCI and mild AD groups differed from the controls in hippocampal and entorhinal cortex volume, but not from each other. Longitudinal analyses showed that the rate of atrophy of the entorhinal cortex and hippocampus for the stable controls differed significantly from MCI participants who converted to AD and the AD groups.
Whole brain volume (WBV) and volumes of the entorhinal cortex (ERC), hippocampus, and three subregions of the hippocampus (head; HH, body; HB and tail; HT) were compared.
The SC pathway transmits information to area CA1 that originates in entorhinal cortex and is processed by the dentate gyrus and area CA3. CA1 also receives direct excitatory input from entorhinal cortex via the perforant path (PP), but the role of this cortical input is less certain.
Chronic recordings in the medial entorhinal cortex of behaving rats have found grid cells, neurons that fire when the rat is in a hexagonal array of locations. Differences in h current could underlie differences in membrane potential oscillation properties and contribute to grid cell periodicity along the dorsal-ventral axis of medial entorhinal cortex..
Hippocampal neurons of intact animals responded to high-frequency (tetanic) stimulation of entorhinal cortex of ipsilateral cerebral hemisphere by tetanic and posttetanic potentiation of a different intensity and duration, which was accompanied by posttetanic depression.
The entorhinal cortex (EC) projects via the perforant pathway to all subfields in the hippocampal formation. A neuroanatomical tracer (biotinylated dextran amine, BDA) was stereotaxically injected in the medial or lateral entorhinal cortex, thus selectively labeling either perforant pathway component. Thus, the medial and lateral subdivisions of the entorhinal cortex similarly tune the firing of principal neurons in the subiculum by way of parvalbumin positive interneurons in their respective terminal zones..
Independently, the degree of microvacuolation was graded in the entorhinal cortex and the amygdala of the same cases. In contrast, in AD/LBD microvacuolation correlated with LB density in the entorhinal cortex and amygdala.
Using whole-cell patch-recording techniques in a rat entorhinal cortex (EC) slice preparation, we tested whether EC layer III neurons display persistent firing due to mGluR activation, independently of cholinergic activation.
AIMS: To investigate whether subjects with dementia with Lewy bodies (DLB), Alzheimer's disease (AD) and Parkinson's disease with dementia (PDD) have reduced entorhinal cortex (EC) volumes compared to controls and cognitively intact Parkinson's disease (PD) subjects.
BACKGROUND: Neuritic plaques (NPs) and neurofibrillary tangles (NFTs) in the brain, especially in the hippocampus, entorhinal cortex, and isocortex, are hallmark lesions of Alzheimer disease and dementia in the elderly.
The volumes of the hippocampus and entorhinal cortex (EC) were manually outlined from anatomical MR images.
The entorhinal cortex (EC) receives afferent projections from the main olfactory bulb; this constitutes an olfactory pathway to the hippocampus.
The Schaffer collateral (SC) input from CA3 axons onto the more proximal dendrites of CA1 is part of the trisynaptic circuit, which originates in Layer II of the entorhinal cortex (EC).
RESULTS: In entorhinal cortex, only Eph A5 mRNA and protein expressed, which significantly decreased on Day 7 after pilocarpine induced status epilepticus(P<0.01),and resumed to normal levels on Day 30 (P>0.05). CONCLUSION: The down-regulation of Eph A5 mRNA and protein in entorhinal cortex and dentate gyrus, and ephrin A3 mRNA in dentate gyrus after status epilepticus may be part of the endogenous molecular mechanism of mossy fiber sprouting to the inner molecular layer of dentate gyrus..
Verbal reports of memories of these specific episodes at the time of free recall were preceded by selective reactivation of the same hippocampal and entorhinal cortex neurons.
To further understand how P4 modulates synaptic plasticity, we used entorhinal cortex lesions (ECL) which induce E2-dependent neurite sprouting in the hippocampus.
Finally, we demonstrate the performance of the system by mapping the excitatory and inhibitory connections of entorhinal cortex layer II stellate neurons and present an approach for the analysis of photo-induced synaptic responses in high spontaneous activity..
The entorhinal cortex is commonly perceived as a major input and output structure of the hippocampal formation, entertaining the role of the nodal point of cortico-hippocampal circuits. Superficial layers receive convergent cortical information, which is relayed to structures in the hippocampus, and hippocampal output reaches deep layers of entorhinal cortex, that project back to the cortex. Therefore, an integrative approach on the entorhinal cortex, that takes into account recent additions to our knowledge database on entorhinal connectivity, is timely. We argue that layers in entorhinal cortex show different functional characteristics most likely not on the basis of strikingly different inputs or outputs, but much more likely on the basis of differences in intrinsic organization, combined with very specific sets of inputs. Here, we aim to summarize recent anatomical data supporting the notion that the traditional description of the entorhinal cortex as a layered input-output structure for the hippocampal formation does not give the deserved credit to what this structure might be contributing to the overall functions of cortico-hippocampal networks..
Dopaminergic projections to the superficial layers of the lateral entorhinal cortex can modulate the strength of olfactory inputs to the region. We have found that low concentrations of dopamine facilitate field EPSPs in the entorhinal cortex, and that higher concentrations of dopamine suppress synaptic responses.
In this study, we investigate the latency and selectivity of visually responsive neurons recorded from microelectrodes in the parahippocampal cortex, entorhinal cortex, hippocampus, and amygdala of human subjects during a visual object presentation task. Regional analysis showed significant correlations between latency and selectivity within the parahippocampal cortex, entorhinal cortex, and hippocampus, but not within the amygdala.
Densities of neuritic plaques (NPs) and of neurofibrillary tangles (NFTs) were assessed in several neocortical regions and in the hippocampus, entorhinal cortex, and amygdala. RESULTS: There were differences among the five groups for NP ratings in the entorhinal cortex (p = 0.003), amygdala (p = 0.009), and overall NP (p = 0.014) as well as counts of NPs in all regions examined (p values ranging from 0.009 to 0.04).
The present series of studies set out to investigate the functional role of the observed increases in 5-HT in the medial prefrontal cortex (mPFC), the entorhinal cortex (EC), and the occipital cortex (OccC) in the mediation of cocaine-induced conditioned place preference (CPP) and hyperactivity.
We included cortical regions as well as limbic area's (hippocampus, entorhinal cortex) basal ganglia (putamen, caudate nucleus), thalamus and cingulated gyrus.
Investigation at the molecular level revealed impaired juxtaparanodal clustering of Caspr2 and Kv1.1/1.2 in the hippocampus, entorhinal cortex, cerebellum and olfactory bulb, with diffusion into the internode.
METHODS: 23 patients with (AD and 23 sex, age, and educational background-matched normal controls (NC group) underwent three-dimensional MRI to measure the hippocampus, amygdala, entorhinal cortex (EC), perirhinal cortex (PC), cornu temporale, and uncus distance in the baseline survey. RESULTS: The baseline survey showed that the levels of uncus distance and total temporal horn volume of the ADS patients were 11 +/- 4 and 1.21 +/- 1.00 respectively, both significantly higher than those of the NC group (7 +/- 3 and 0.59 +/- 0.54 respectively, P < 0.01, P < 0.05), and the levels of total entorhinal cortex volume, total perirhinal cortex volume, and total hippocampus volume were 2.52 +/- 0.86, 2.19 +/- 0.62, and 3.23 +/- 0.75 respectively, all significantly lower than those of the BC group (3.67 +/- 0.54, 3.39 +/- 0.51, and 3.98 0.38, all P < 0.01). The levels of uncus distance and total temporal horn volume of the AD patients during the follow-up survey were 11 +/- 4 and 1.21 +/- 1.00 respectively, both significantly higher than those of the NC group (7 +/- 3 and 0.59 +/- 0.54 respectively, both P < 0.05); and the total entorhinal cortex volume, total perirhinal cortex volume, and total hippocampus volume of the AD patients during the followup survey were. CONCLUSION: The AD patients have more remarkable atrophy of entorhinal cortex, perirhinal cortex, and have obvious extension of cornu temporale and uncus distance in comparison with the normal controls.
Hypothesized baseline predictors for follow-up conversion to AD (entire sample: 39/148 converters) were cognitive test performance, informant report of functional impairment, apolipoprotein E genotype, olfactory identification deficit, and magnetic resonance imaging (MRI) hippocampal and entorhinal cortex volumes. RESULTS: In the 3-year follow-up patient sample (33/126 converters), five of eight hypothesized predictors were selected by backward and stepwise logistic regression: Pfeffer Functional Activities Questionnaire (FAQ; informant report of functioning), University of Pennsylvania Smell Identification Test (UPSIT; olfactory identification), Selective Reminding Test (SRT) immediate recall (verbal memory), MRI hippocampal volume, and MRI entorhinal cortex volume.
Brain sections were collected from the medial prefrontal cortex (mPFC), dorsolateral frontal cortex (DFC), caudate putamen, nucleus accumbens, hippocampal CA1 and CA3 regions, and entorhinal cortex and processed for in-vitro receptor autoradiography.
We have used functional pharmacological approaches to examine whether NMDA receptors at excitatory synapses in the rat entorhinal cortex are mobile at either postsynaptic sites or in presynaptic terminals.
Discrete bilateral ablations to the entorhinal cortex impaired retention but had no effect on new learning.
RESULTS: Values of binding potential for hippocampus (1.2), entorhinal cortex (1.1), septum (1.1), medial prefrontal cortex (1.0), amygdala (0.8), raphe nuclei (0.6), paraventricular hypothalamic nucleus (0.5) and raphe obscurus (0.5) were comparable to those previously measured with PET in cats, non-human primates or humans. Test-retest variability was in the order of 10% in the larger brain regions (hippocampus, medial prefrontal and entorhinal cortex) and less than 20% in small nuclei such as the septum and the paraventricular hypothalamic, basolateral amygdaloid and raphe nuclei.
During the early developmental stage, a neural circuit is established between the entorhinal cortex (EC) and the hippocampal dentate gyrus (DG) via the perforant pathway.
METHODS AND RESULTS: In this study, we immunohistochemically documented the evolution of AD-related transgene expression, amyloid deposition, tau phosphorylation, astrogliosis, and microglial activation throughout the hippocampus, entorhinal cortex, primary motor cortex, and amygdala over a 26-month period in male 3xTg-AD mice.
OBJECTIVE: To examine the effects of age, sex, race/ethnicity, and vascular disease history on measures of brain morphology, including relative brain volume, ventricular volume, hippocampus and entorhinal cortex volumes, and white matter hyperintensity (WMH) burden, in a large community-based cohort of racially/ethnically diverse older adults without dementia. MAIN OUTCOME MEASURES: Relative brain volume (total brain volume/intracranial volume), ventricular volume, and hippocampus and entorhinal cortex volumes were derived manually on high-resolution MR images.
Here we used Pavlovian fear conditioning in rats to explore whether the entorhinal cortex and fornix, which are the major cortical and subcortical interfaces of the hippocampus, are also involved in the context-dependence of extinction. In contrast, rats with neurotoxic lesions in the entorhinal cortex or electrolytic lesions in the fornix did not exhibit a renewal of fear when tested outside the extinction context. Impairments in freezing behavior to the auditory CS were not able to account for the observed results, insofar as rats with either entorhinal cortex or fornix lesions exhibited normal freezing behavior during the conditioning session.
The hippocampus and entorhinal cortex have been linked to both memory functions and to spatial cognition, but it has been unclear how these ideas relate to each other. An important part of spatial cognition is the ability to keep track of a reference location using self-motion cues (sometimes referred to as path integration), and it has been suggested that the hippocampus or entorhinal cortex is essential for this ability. Patients with hippocampal lesions or larger lesions that also included entorhinal cortex were led on paths while blindfolded (up to 15 m in length) and were asked to actively maintain the path in mind. Thus, in humans, the hippocampus and entorhinal cortex are not essential for path integration..
This study aimed to investigate the atrophy of the posterior cingulate cortex (PCC) and medical temporal lobe (MTL) structures (i.e., the entorhinal cortex (ERC) and hippocampus) and the regional disruption of the cingulum bundle in mild cognitive impairment (MCI) and Alzheimer's disease (AD) patients.
Whereas the entorhinal cortex (EC) receives profuse serotonergic innervations from the raphe nuclei in the brain stem and is critically involved in the generation of temporal lobe epilepsy, the function of serotonin (5-hydroxytryptamine, 5-HT) in the EC and particularly its roles in temporal lobe epilepsy are still elusive.
The medial entorhinal cortex (EC) is a part of the neural network for the representation of self-location in the rat.
Compared with the swimming only group and holding-box group, agmatine levels were significantly increased in the CA1 and dentate gyrus subregions of the hippocampus, the entorhinal cortex and the vestibular nucleus in the water-maze training group.
BACKGROUND: MRI studies have demonstrated differential rates of atrophy in the entorhinal cortex and hippocampus during the prodromal phase of Alzheimer disease (AD). Post hoc comparisons demonstrated greater rates of atrophy for converters vs nonconverters for six ROIs: hippocampus, entorhinal cortex, temporal pole, middle temporal gyrus, fusiform gyrus, and inferior temporal gyrus.
The entorhinal cortex plays an important role in spatial memory and episodic memory functions. These functions may result from cellular mechanisms for integration of the afferent input to entorhinal cortex. This article reviews physiological data on persistent spiking and membrane potential oscillations in entorhinal cortex then presents models showing how both these cellular mechanisms could contribute to properties observed during unit recording, including grid cell firing, and how they could underlie behavioural functions including path integration.
The entorhinal cortex receives a large projection from the piriform cortex, and synaptic plasticity in this pathway may affect olfactory processing. In vitro whole cell recordings have been used here to investigate postsynaptic signalling mechanisms that mediate the induction of long-term synaptic depression (LTD) in layer II entorhinal cortex cells. Activation of protein phosphatases following calcium influx therefore contributes to induction of LTD in layer II of the entorhinal cortex..
For each hemisphere, normalized correlation coefficients were computed between pairs of time-course signals extracted from five regions involved in MTLE epileptogenic networks (Brodmann area 38, amygdala, entorhinal cortex (EC), anterior hippocampus (AntHip), and posterior hippocampus (PostHip)).
These deficits are associated with significant changes in brain nerve growth factor (NGF) and brain derived neurotrophic factor (BDNF), particularly in the hippocampus and entorhinal cortex.
In the VCX and the region containing the entorhinal cortex and amygdala (ECX), BDNF protein levels were increased 12 h after the phase advance, while BDNF mRNA levels were increased significantly in the VCX and slightly in the ECX after 4 h.
The effects of entorhinal cortex (EC) stimulation on the activity of identified medial prefrontal cortex (mPFC) pyramidal neurons were examined using single-unit extracellular recordings and sharp-electrode intracellular recordings in anesthetized rats.
CONCLUSIONS: A number of neuroimaging candidate markers are promising, such as hippocampus and entorhinal cortex volumes, basal forebrain nuclei, cortical thickness, deformation-based and voxel-based morphometry, structural and effective connectivity by using diffusion tensor imaging, tractography, and functional magnetic resonance imaging.
In the parahippocampal region, increased putrescine level with age was observed in the entorhinal cortex, and age did not alter the spermidine levels.
We report that dual immunohistochemical staining for c-Fos and CTb revealed an increase in the percentage of c-Fos-immunopositive basolateral amygdaloid complex-projecting neurons in open-field-exposed rats compared with HA and control rats in the ipsilateral CA1 region of the ventral hippocampus, subiculum and lateral entorhinal cortex.
The medial entorhinal cortex is likewise attracting increasing interest, insofar as evidence accumulates that this area also contributes to spatial information processing. These findings suggest complementary contributions of the hippocampus and medial entorhinal cortex in support of episodic memory, wherein hippocampal networks encode sequences of events that compose temporally and spatially extended episodes, whereas medial entorhinal networks disambiguate overlapping episodes by binding sequential events into distinct memories..
The entorhinal cortex (EC) is a nodal and independent mnemonic element of the medial temporal lobe memory circuit as it forms a bidirectional interface between the neocortex and hippocampus.
The present study was aimed to investigate whether this type of maternal malnutrition could result in modification of plastic capabilities of the entorhinal cortex (EC) in the adult progeny.
We find that dementia in PD is significantly associated with alphaSyn in the anterior cingulate gyrus, superior frontal gyrus, temporal cortex, entorhinal cortex, amygdaloid complex and CA2 sector of the hippocampus. Abeta in the anterior cingulate gyrus, entorhinal cortex, amygdaloid complex and nucleus basalis of Meynert is also associated with dementia as is tau in the CA2 sector of the hippocampus.
In some areas, such as the entorhinal cortex, it is present as the only ER, whereas in other regions, such as the bed nucleus of the stria terminalis and preoptic area, it can be found co-expressed with ERalpha, often within the same neurones.
We tested the hypothesis by mapping, throughout hippocampal subfield CA1, field potentials evoked by stimulation of different sites in lateral entorhinal cortex in awake rats, thereby establishing the topography of electrophysiological transmission between the entorhinal cortex and CA1.
In limbic seizures, neuronal excitation is conveyed from the entorhinal cortex directly to CA1 and subicular regions. This phenomenon is associated with a reduced ability of CA3 to respond to entorhinal cortex inputs.
Results show a clear dominance of activations around the collateral sulcus, corresponding to parahippocampal and entorhinal cortex activities.
In the present study, anticonvulsant efficacy against soman intoxication (1.3 x LD50) was examined in rats with either lesion of the perirhinal cortex, posterior piriform cortex, entorhinal cortex, hippocampal region, or amygdala. The results showed that prevention of convulsions or increased latency to onset of convulsions was ensured in rats with perirhinal or piriform cortical lesions, whereas anticonvulsant effects were not achieved in rats with damage to the entorhinal cortex, hippocampal region, or amygdala.
Compared to the sham and control cage groups, rats exposed to a GSM signal at 6 W/Kg showed decreased CO activity in some areas of the prefrontal and frontal cortex (infralimbic cortex, prelimbic cortex, primary motor cortex, secondary motor cortex, anterior cingulate cortex areas 1 and 2 (Cg1 and Cg2)), the septum (dorsal and ventral parts of the lateral septal nucleus), the hippocampus (dorsal field CA1, CA2 and CA3 of the hippocampus and dental gyrus) and the posterior cortex (retrosplenial agranular cortex, primary and secondary visual cortex, perirhinal cortex and lateral entorhinal cortex).
The entorhinal cortex is perhaps the area of the brain in which neurofibrillary tangles and amyloid plaques are first detectable in old age with or without mild cognitive impairment, and very particularly in Alzheimer's disease. Lesions or biochemical impairments of the entorhinal cortex hinder extinction. Microinfusion experiments have shown that glutamate NMDA receptors, calcium and calmodulin-dependent protein kinase II, and protein synthesis in the entorhinal cortex are involved in and required for extinction. Aging also hinders extinction; it is possible that its effect may be in part mediated by the entorhinal cortex..
Very high binding site density is also seen in the cerebral cortex with highest binding density in pyriform, insular and entorhinal cortex.
Limbic connectivity was statistically inferred by correlating mean thickness of the entorhinal cortex (EC) with thickness at each vertex across the entire neocortex.
The MF form a distinct type of synapses, rich in zinc, that appear to duplicate, in terms of the information they convey, what CA3 cells already receive from entorhinal cortex layer II cells, which project both to the DG and to CA3. First, neurophysiological recordings indicate that the very sparse dentate activity is concentrated on cells that display multiple but disorderly place fields, unlike both the single fields typical of CA3 and the multiple regular grid-aligned fields of medial entorhinal cortex.
The nonhuman primate entorhinal cortex is the primary interface for information flow between the neocortex and the hippocampal formation. Based on previous retrograde tracer studies, neocortical afferents to the macaque monkey entorhinal cortex originate largely in polysensory cortical association areas. However, the topographical and laminar distributions of cortical inputs to the entorhinal cortex have not yet been comprehensively described. The present study examines the regional and laminar termination of projections within the entorhinal cortex arising from different cortical areas. The study is based on a library of 51 (3)H-amino acid injections that involve most of the afferent regions of the entorhinal cortex. Some areas, such as the medial portion of orbitofrontal area 13 and parahippocampal areas TF and TH, project widely within the entorhinal cortex. The lateral orbitofrontal, insular, anterior cingulate, and perirhinal cortices, for example, project only to rostral levels of the entorhinal cortex. The upper bank of the superior temporal sulcus projects mainly to intermediate levels of the entorhinal cortex, and the parietal and retrosplenial cortices project to caudal levels. The projections from some of these cortical regions preferentially terminate in the superficial layers (I-III) of the entorhinal cortex, whereas others project more heavily to the deep layers (V-VI).
Alzheimer's type pathology was restricted to a few diffuse beta-amyloid plaques in the entorhinal cortex and rare tangles in the hippocampus.
We compared the volumes of regional lobar gray matter (GM) and medial temporal lobe structures, including the hippocampus, entorhinal cortex (ERC), fusiform and parahippocampal gyri, and metabolite ratios from the posterior cingulate in individuals who had a Clinical Demetia Rating (CDR) of 0.5, but who did not meet MCI criteria (preMCI, N=17), patients with mild cognitive impairment (MCI, N=13), and cognitively normal controls (N=18).
METHODS: Interictal EEG activity in mesial temporal lobe (MTL) structures (hippocampus, entorhinal cortex and amygdala) was obtained from intracerebral recordings performed in 21 patients with drug-resistant mesial temporal lobe epilepsy (MTLE group).
Voxel-based morphometry of the FFD-normalized magnetic resonance images from PFBT survivors and sibling controls detected reduced gray matter density in the thalamus and entorhinal cortex and reduced white matter density in the internal capsule, hypothalamus, corpus callosum, and cuneus of the occipital lobe in the PFBT survivors.
METHODS: Immunohistochemical staining of GAD 65/67 was performed in the orbitofrontal, anterior cingulate and dorsolateral prefrontal cortex (DLC), the entorhinal cortex (EC), the hippocampal formation, and the medial dorsal and lateral dorsal thalamic nuclei, with consecutive determination of GAD-immunoreactive (-ir) neuropil relative density.
entorhinal cortex, subiculum, CA1, CA1-CA2 transition zone, CA3-4 and dentate gyrus (CA3&DG) and total hippocampal volume were determined using a manual marking strategy.
Analyses of fMRI data revealed differential MTL activation in the left hippocampus and entorhinal cortex with a response profile across conditions that paralleled the behavioral results; the identified region responded selectively to those conditions that contained semantic novelty.
Tau and phospho-tau correlated inversely with hippocampal volumes and left entorhinal cortex volume in the whole study group.
It was restricted to the dentate gyrus and entorhinal cortex in approximately 75% of cases; approximately 25% showed more widespread TDP-43 pathology in frontal and temporal cortices, resembling the FTLD-U subtype associated with progranulin mutations.
conjoint CBF and entorhinal cortex lesions), indicative of a dramatic impact on cognitive function when there is coexisting, rather than isolated, damage in these two brain regions.
However, related structures such as the entorhinal cortex have not been systematically examined. This research study aimed to examine possible abnormalities in the volume of the entorhinal cortex (ERC) in TRD patients.
Previous rat gene expression analysis using microarrays indicated prominent activation of the classical complement pathway which peaked at 1 week after SE in CA3 and entorhinal cortex.
We measured cortical thickness and volume in MTL subregions (hippocampal CA fields 1, 2 and 3; dentate gyrus; entorhinal cortex; subiculum; perirhinal cortex; parahippocampal cortex; and fusiform gyrus) using a high-resolution in-plane (0.4x0.4 mm) MRI sequence in 30 cognitively normal volunteers (14 APOE-4 carriers, 16 non-carriers, mean age 57 years). APOE-4 carriers had reduced cortical thickness compared with non-carriers in entorhinal cortex (ERC) and the subiculum (Sub), but not in the main hippocampal body or perirhinal cortex.
It has previously been reported that dopamine (DA) responses observed in the core and dorsomedial shell parts of the nucleus accumbens (Nacc) in latent inhibition (LI) are dependent on the left entorhinal cortex (ENT).
On the one hand, it is a critical link in providing the entorhinal cortex and hippocampal formation with cortical input, while on the other hand it receives output from these structures and projects widely by disseminating the medial temporal lobe output to the cortex.
Whereas brain responses to stimulus intensity in the olfactory modality involved a wide neural network including cerebellum, entorhinal cortex, visual areas, and frontal regions, contrasting high and low CO2 concentrations revealed activation in a less complex network including various sub-regions of the cingulate cortex.
Here we show that phase precession is expressed independently of the hippocampus in spatially modulated grid cells in layer II of medial entorhinal cortex, one synapse upstream of the hippocampus. The results point to possible mechanisms for grid formation and raise the possibility that hippocampal phase precession is inherited from entorhinal cortex..
The major input to the hippocampus arrives from the entorhinal cortex (EC) to the dentate gyrus (DG) through the perforant path.
In contrast to synaptic p-tau, which was highest in the entorhinal cortex and hippocampus (P = 0.004), synaptic Abeta fluorescence was significantly lower in the entorhinal cortex and hippocampus relative to neocortical regions (P = 0.0003). Synaptic Abeta and p-tau fluorescence was significantly correlated (r = 0.683, P < 0.004), and dual-labeling experiments demonstrated that 24.1% of Abeta-positive terminals were also positive for p-tau, with the highest fraction of dual labeling (39.3%) in the earliest affected region, the entorhinal cortex.
Met-enkephalin levels in neuronal projections from the entorhinal cortex and dentate gyrus (brain regions important for memory that are affected in early stages of AD) were increased in hAPP mice, as were preproenkephalin mRNA levels.
Following a six month treatment of an 8 month old cohort, immunohistochemical analysis of coronal sections reveals that plaque burdens were reduced in the cingulate cortex, hippocampus, and entorhinal cortex by 54%, 43%, and 51%, respectively. Congo red plaque burdens were decreased in the cingulate cortex, hippocampus, and entorhinal cortex by 53%, 53%, and 58%, respectively as well.
We therefore investigated both resonant and nonresonant neurons of rat entorhinal cortex.
Structural imaging, historically used to exclude an intracerebral lesion as a cause for dementia, is increasingly playing a role in "ruling in" diagnoses, with atrophy of the hippocampus and entorhinal cortex an early and sensitive marker for AD, and cortical and subcortical infarcts and white matter lesions characteristic of VaD.
Evidence has accumulated that the entorhinal cortex (EC) is involved in memory operations underlying formation of a long-term memory.
We here investigated the effects of neonatal lesions of the entorhinal cortex (EC) in rats on maze learning and on structural alterations of its main projection region, the hippocampus, as well as other regions with anatomical connections to the EC that are involved in maze learning.
Glutamic acid391 tau truncation was prominent in the entorhinal cortex, whereas D421 truncation was prominent in the subiculum, suggesting that NFTs composed of either D421- or E391-truncated tau may be formed mutually exclusively in these areas.
NFTs in the entorhinal cortex were stained with both RD3 and RD4, but NFTs in the premotor cortex were stained with only RD4.
In order to understand how plasticity is related to neurodegeneration, we studied synaptic proteins with quantitative immunohistochemistry in the entorhinal cortex from Alzheimer patients and age-matched controls. Therefore, increased PSD-95 immunoreactivity in the entorhinal cortex might result from compensatory mechanisms, as in the SH-SY5Y clone, whereas increased Alzheimer-like Tau phosphorylation is not related to PSD-95 expression, as suggested by the OA-treated cell models..
This activity is initiated not in the hippocampus but in the subiculum, an output region that projects to the entorhinal cortex.
In order to demonstrate changes in the protein expression profile we analyzed DARPP-32 levels in the striatum, prefrontal cortex (PFC), hippocampus and entorhinal cortex of Wistar rats after step-down IA learning.
Recent studies emphasize the importance of the entorhinal cortex in spatial representation and navigation. Furthermore, evidence is accumulating to show that spatial processing depends on interactions between the entorhinal cortex and the hippocampus. To investigate these interactions, we examined the effects of entorhinal cortex lesions on the activity of hippocampal CA1 place cells. Rats received bilateral radiofrequency lesions of the entorhinal cortex or sham lesions before place cell recording. entorhinal cortex lesions did not abolish place cell spatial firing but reduced noticeably discharge rate and field size. These findings indicate that the entorhinal cortex is necessary for the stability of hippocampal representations across exposures to a familiar environment. Consistent with the recent discovery of grid cells in the medial entorhinal cortex, our results suggest that the entorhinal cortex contributes to providing a spatial framework that would enable the hippocampus to maintain stable environment-specific representations..
The neural pathway from the perirhinal cortex to the entorhinal cortex (EC) is considered one of the main routes into the entorhinal-hippocampal network.
Methods: Hippocampal subregions (CA1, CA3, and dentate gyrus [ DG]) and entorhinal cortex were dissected at different time-points.
On day 6, regenerated fibers were seen to navigate from the entorhinal cortex into the hippocampus.
nNOS-immunoreactive (nNOS-IR) and Nissl-stained neurons were counted in entorhinal cortex, hippocampal CA1, CA2, CA3, and CA4 subfields, and subiculum.
Previous work has established that stellate cells of the medial entorhinal cortex produce prominent intrinsic subthreshold oscillations in the voltage response concentrated within the theta range (3-7 Hz). It has been speculated that these oscillations play an important role in vivo in establishing network behavior both in the entorhinal cortex and hippocampus.
OBJECTIVES:: Magnetic resonance (MRI) studies rely on sulcal boundaries to delineate the human entorhinal cortex (EC) and typically show that EC size is reduced in Alzheimer's disease (AD) and a predictor of future dementia.
Densities of postmortem neuritic plaques (NPs) and neurofibrillary tangles (NFTs) were measured in the cerebral cortex, hippocampus, and entorhinal cortex.
We investigated the role of neuronal RAGE in Abeta-induced synaptic dysfunction in the entorhinal cortex, an area of the brain important in memory processes that is affected early in AD. Together, our results indicate that Abeta impairs LTP in the entorhinal cortex through neuronal RAGE-mediated activation of p38 MAPK..
There is a second pathway to CA1 from the entorhinal cortex.
In the MTL, PER provides input to the hippocampal formation directly and via the entorhinal cortex (EC), whereas in the VVS, PER is considered to be at the top of the visual processing hierarchy of object information.
However, CA1 LTP and the accompanying memory processes can be dissociated, and in addition plastic events in several other brain regions(amygdala, entorhinal cortex, parietal cortex) are also necessary for memory formation of the one-trial task, and perhaps of many others..
Remarkably, however, Asp664-cleaved AbetaPP was prominent in neuronal somata and in processes in entorhinal cortex and hippocampus of non-diseased human brains at ages <45 years.
The entorhinal cortex (EC) plays an important role in temporal lobe epilepsy.
Compared with controls, AD cases had significantly lower expression of 70% of the nuclear genes encoding subunits of the mitochondrial electron transport chain in posterior cingulate cortex, 65% of those in the middle temporal gyrus, 61% of those in hippocampal CA1, 23% of those in entorhinal cortex, 16% of those in visual cortex, and 5% of those in the superior frontal gyrus.
The aim of the present study was to investigate the duration-dependent dendritic changes in CA1, CA3 and entorhinal cortex (EC) of hippocampus and layer II of prefrontal cortex (PFC) with spatial memory functions in rats on exposure to different duration of HH.
Subregional analyses of the hippocampus suggest CA1-dependent memory processes rely heavily upon interactions between the CA1 subregion and entorhinal cortex.
In this chapter, we focus on a protocol based on organotypic slice cultures of mouse entorhinal cortex and hippocampus that can be employed to study axonal regeneration and collateral sprouting in the central nervous system in vitro.
(J Neurophysiol 96: 3305-3313, 2006), observed a novel form of spike timing dependent plasticity (iSTDP) in GABAergic synaptic couplings in layer II of the entorhinal cortex.
We demonstrated that the variation of pERK immunopositive cell density in the visual cortex was significantly reduced by normalizing the values to the density in the nonvisual area in the entorhinal cortex, thus enabling us to detect differences between animals under different visual conditions with higher sensitivity.
OBJECTIVE: In our previous study, a lesion in the entorhinal cortex was found to significantly attenuate the elevation of adrenocorticotropic hormone (ACTH) in plasma during immobilization stress. The aim of the present study was to investigate whether the entorhinal cortex exerts a modulatory effect on circadian ACTH and corticosterone release. MATERIALS AND METHODS: Ibotenic acid (15 microg/microl) was stereotaxically bilaterally injected into the entorhinal cortex of rats. RESULTS: Compared with sham-operated control rats, rats with entorhinal cortex lesions produced by ibotenic acid showed either significantly elevated plasma ACTH or plasma corticosterone levels at 0800 h, but no difference at 1300 h or 1800 h. CONCLUSION: The results of the present study indicate that the entorhinal cortex plays a certain role in the regulation by the central nervous system of the circadian rhythm of the hypothalamic-pituitary-adrenal (HPA) axis..
Anatomical evidence suggests an interplay between the dorsal CA1 of the hippocampus (CA1), the basolateral amygdala (BLA) and the entorhinal cortex (EC), but their specific interactions in the context of emotional memory remain obscure.
These regions include the entorhinal cortex, hippocampus, middle temporal gyrus, posterior cingulate cortex, superior frontal gyrus, and primary visual cortex.
The shape characteristics of the late response, its polarity, and its latent period relative to the early population spike suggest that stimulation of Shäffer collaterals gives rise, in CA1, to a wave of excitation which passes through the entorhinal cortex and returns to CA1 directly via fibers of the perforant path.
This dose of GBP also produced significant (P<0.001) decreases in BOLD signal intensity in the amygdala and the entorhinal cortex.
In contrast, the entorhinal cortex issued projections to the amygdala from its deep layers, suggesting feedback communication, and received reciprocal amygdalar projections most densely in layers II-III, which project to the hippocampus.
METHODS: Auditory sensory gating has been recorded from the hippocampus and entorhinal cortex (EC) in anesthetized rats.
Principal neurons in layer III of the rat lateral entorhinal cortex (LEC) generate a self-sustained plateau potential and persistent spiking following the application of a brief suprathreshold excitatory stimulus delivered in the presence of the muscarinic receptor agonist carbachol.
This integration occurs by the convergence of highly processed sensory information onto neural systems in entorhinal cortex and hippocampus.
BACKGROUND: The entorhinal cortex is located in the medial temporal lobe and is involved in memory and learning. OBJECTIVES: To explore entorhinal cortex volumes in a large sample of patients with schizophrenia recruited from the geographically defined catchment area of South Verona (i.e. RESULTS: A significant group effect was found for total entorhinal cortex but not for hippocampus, with patients suffering from schizophrenia having smaller entorhinal volumes compared to normal subjects (F=6.24, p=0.01), particularly on the right side (F=9.76, p=0.002). Also, the laterality index for entorhinal cortex was higher in normal individuals than in patients with schizophrenia (F=5.45, p=0.02). Future longitudinal MRI studies including high-risk subjects and drug-free, first-episode patients are crucial to further understand whether entorhinal cortex shrinkage is already present at the onset of the illness or appears as a consequence of the illness..
Accurate automatic identification of cortex and thickness estimation is frustrated by the presence of dura adjacent to regions such as the entorhinal cortex.
Using a persistent firing buffer mechanism in layer II of entorhinal cortex, simulated episodic learning involves dentate gyrus, layer III of entorhinal cortex, and hippocampal regions CA3 and CA1.
We studied variations in the concentration of Na, K, Ca, and Mg in the hippocampus of rats with damaged entorhinal cortex. The concentration of Mg, Na, K, and Ca remained practically unchanged, while the content of Zn and Cu increased during learning and memory retrieval in animals with damaged entorhinal cortex.
In this study we report that in the presence of normal buffer, epileptiform discharges occur spontaneously (duration = 2.60 +/- 0.49 s) or can be induced by electrical stimuli (duration = 2.50 +/- 0.62 s) in the entorhinal cortex (EC) of brain slices obtained from pilocarpine-treated rats but not in those from age-matched, nonepileptic control (NEC) animals.
The parallel, entorhinal cortex projections to different hippocampal regions potentially support separate mnemonic functions. Thus, functional entorhinal cortex coupling with CA1 activity became more direct with additional training, so producing a trisynaptic circuit bypass.
Activations in regions of perirhinal and entorhinal cortex were associated with configural learning of repeated contexts independent from explicit memory for those contexts.
We here investigated the effects of neonatal entorhinal cortex (EC) lesions on adult rat behavior before and after repeated high-dose treatment with the NMDA antagonist dizocilpine, in order to combine these etiopathogenetical factors in an animal model.
It contains parallel excitatory pathways referred to as the trisynaptic pathway (which carries information as follows: entorhinal cortex --> dentate gyrus --> CA3 --> CA1 --> entorhinal cortex) and the monosynaptic pathway (entorhinal cortex --> CA1 --> entorhinal cortex).
Place-specific firing in the hippocampus is determined by path integration-based spatial representations in the grid-cell network of the medial entorhinal cortex. To test this possibility, we made selective lesions in layer III of medial entorhinal cortex by local infusion of the neurotoxin gamma-acetylenic GABA.
The earliest neuroanatomical changes in amnestic mild cognitive impairment (aMCI) involve the hippocampus and entorhinal cortex, structures implicated in the integration and learning of associative information.
METHODS: We describe the methodology and diagnostic value of manual volumetry of the hippocampus and entorhinal cortex, automated voxel-based morphometry, cortical thickness measurement, basal forebrain volumetry and deformation-based morphometry, implementing multivariate statistics and machine learning algorithms to improve group separation and prediction of AD in at-risk groups.
Measures of whole brain, ventricular, hippocampal, and entorhinal cortex volumes were acquired. CONCLUSION: In moderate stages of amnestic mild cognitive impairment, common cognitive tests provide better predictive accuracy than measures of whole brain, ventricular, entorhinal cortex, or hippocampal volumes for assessing progression to Alzheimer disease..
We found that GCPII levels measured by [ (125)I]DCIT quantitative autoradiography were significantly lower in the PFC and entorhinal cortex in patients with schizophrenia compared to age-matched controls.
We suggest that slow oscillation of the neocortex, which was discovered by Mircea Steriade, temporally coordinates the self-organized oscillations in the neocortex, entorhinal cortex, subiculum and hippocampus.
We also tested the impact of cd39-deletion in a model of ischemia, in an entorhinal cortex lesion and in the facial nucleus after facial nerve lesion.
This study tested the hypothesis that the flow of contextual information along the disynaptic "ESA" (entorhinal cortex-ventral subiculum-nucleus accumbens) pathway is responsible for context-related modulation of CRs.
The convergence of inputs from entorhinal cortex and hippocampal region CA3 onto CA1 pyramidal cells make them potentially important for integrating information about place and temporal context on the network level.
In addition, they provide evidence in support of a cholinergically mediated mechanism for novelty detection, have important implications for our understanding of oscillatory coding within memory and for the interpretation of event-related potentials, and provide indirect support for the oscillatory interference model of grid cell firing in medial entorhinal cortex..
Density of neuritic plaques (NPs) and neurofibrillary tangles (NFTs) in the hippocampus, entorhinal cortex, amygdala and multiple regions of the cerebral cortex, as well as composites of these indices reflecting overall neuropathology, were analyzed.
DiI-crystals were injected into the entorhinal cortex.
Cortical information is mostly funneled to the hippocampus through the entorhinal cortex (EC) in a bi-directional way that ultimately ends in the cortex.
With the mouse pilocarpine model of temporal lobe epilepsy (TLE), we showed a progressive loss of both principal cells and calbindin (CB)-, calretinin (CR)-, and parvalbumin (PV)-immunopositive interneurons in layers II-III of lateral entorhinal cortex (LEnt) from 2 months to 1 year after pilocarpine-induced status epilepticus (PISE).
Six months after the infusion, tau pathology was induced in the injected hippocampus but also in brain regions well beyond the injection sites such as the entorhinal cortex and amygdala, areas with neuronal projection to the injection site.
We have examined the effects of the gap junction blocker carbenoxolone (CBX) on the generation and propagation of epileptiform activity induced by 4-aminopyridine (4-AP) in the rat entorhinal cortex and hippocampus. We analyzed the epileptiform pattern generated on awaked rats by administering 10 nmol of 4-AP and we studied the effect of administering CBX (50 nmol) 30 min later by injection into the entorhinal cortex. The application of CBX to rats that had received 4-AP decreased the amplitude and frequency of the epileptiform discharges, as well as the number and duration of the epileptiform trains in the entorhinal cortex and hippocampus.
The entorhinal cortex of the rat (EC) contains a dense fiber plexus that expresses the calcium-binding protein calretinin (CR). We also examined the colocalization of VGluT2 and CR in the entorhinal cortex by using in situ hybridization and CR immunofluorescence.
Taken together, the accumulation of hyperphosphorylated tau and synapse loss in aged mice, leading to inhibition of neural activity in parahippocampal areas, including the entorhinal cortex, may underlie place learning impairment. Thus, the accumulation of hyperphosphorylated tau that occurs before NFT formation in entorhinal cortex may contribute to the memory problems seen in Alzheimer's disease (AD)..
The recall process generates the phase precession in dentate, CA3, and entorhinal cortex..
These seemingly disparate results are effectively simulated by the same model, based on mechanisms similar to a model of grid cell firing in entorhinal cortex.
Although bound to spatial coordinates, the CA3 network can rapidly alter its firing rate in response to novel sensory inputs and is thus not as strictly tied to spatial mapping as grid cells in the medial entorhinal cortex.
Whereas recent studies have elucidated principles for representation of information within the entorhinal cortex, less is known about the molecular basis for information processing by entorhinal neurons. We asked whether hyperpolarization-activated, cation nonselective 1 (HCN1) channels control processing of information by stellate cells found within layer II of the entorhinal cortex. These data suggest that HCN1 channels expressed by stellate neurons in layer II of the entorhinal cortex are key molecular components in the processing of inputs to the hippocampal dentate gyrus, with distinct integrative roles during resting and active states..
Furthermore, we evaluated evoked excitatory post-synaptic potentials (EPSPs) in the hippocampal CA1 to RE stimulation, as well as entorhinal cortex (EC) stimulation.
The entorhinal cortex (EC) conveys information to hippocampal field CA1 either directly by way of projections from principal neurons in layer III, or indirectly by axons from layer II via the dentate gyrus, CA3, and Schaffer collaterals.
NE iontophoresis inhibited spontaneous firing and decreased the responsiveness of BLA neurons to electrical stimulation of entorhinal cortex and sensory association cortex (Te3).
Several studies have pointed to the hippocampus as a key brain structure in novelty detection, a claim substantiated by its wide access to sensory information through the entorhinal cortex and also distinct aspects of its intrinsic circuitry.
We have shown that a number of anticonvulsant drugs can reduce glutamate release at synapses in the rat entorhinal cortex (EC) in vitro.
We studied the distribution and coexpression of vesicular glutamate transporters (VGluT1, VGluT2), glutamic acid decarboxylase (GAD) and calretinin (CR, calcium-binding protein) in rat entorhinal cortex, using immunofluorescence staining and multichannel confocal laser scanning microscopy. An intense, punctate VGluT1-staining occurred everywhere in the entorhinal cortex. We conclude that the CR-containing axon terminals in the entorhinal cortex belong to at least two subpopulations of CR-neurons: a glutamatergic excitatory and a GABAergic inhibitory..
In region CA1 of the rat (Sprague Dawley) hippocampus, the cholinergic agonist carbachol (CCh) suppresses transmission in stratum radiatum (SR), at synapses of the Schaffer collateral projection from CA3, while having lesser effects in stratum lacunosum-moleculare (SLM), the perforant path projection from entorhinal cortex (Hasselmo and Schnell, 1994).
The cortical regions with retrogradely labelled cells, as well as the entorhinal cortex, also contained anterogradely labelled axons and their terminations, which means that they are also target areas of direct projections from AI.
4-Aminopyridine (10 nmol) was administered into the entorhinal cortex to induce seizures.
Dentate granule cells receive inputs from the entorhinal cortex as the "perforant path".
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