Disease relevance of Entorhinal Cortex

• Thirty minutes after the initiation of limbic motor seizures evoked by bicuculline in AT, a marked increase in c-fos mRNA was detected in the hippocampal formation, amygdala, olfactory bulb, piriform cortex, and entorhinal cortex [1].
• The release of both peptides under depolarizing conditions was significantly reduced by 15% on average from slices of the entorhinal cortex two days after kainic acid-induced status epilepticus [2].
• Focal brain injury in mice induced c-fos mRNA and protein in neurons throughout the damaged neocortex, including the piriform and the entorhinal cortices, as well as in nonneural brain cells (e.g., glia, pia, ependyma) [3].
• The neurotoxin N-methyl-D-aspartate was used to induce selective bilateral neuronal loss in the entorhinal cortex, in order to model one aspect of the neurodegeneration observed in Alzheimer's disease, Down's syndrome and aging [4].
• Transient upregulation of NCAM mRNA in astrocytes in response to entorhinal cortex lesions and ischemia [5].

Psychiatry related information on Entorhinal Cortex

• Extended temporal gradient for the retrograde and anterograde amnesia produced by ibotenate entorhinal cortex lesions in mice [6].
• These neurons with viability potential constitute 73% of the total numbers of profiles in layer II of the entorhinal cortex and 77% in the CA1 field in cases with a Clinical Dementia Rating score of 3 [7].
• Neurotensin receptor binding abnormalities in the entorhinal cortex in schizophrenia and affective disorders [8].
• Cognitive impact of neuronal pathology in the entorhinal cortex and CA1 field in Alzheimer's disease [9].
• Rat hippocampal lactate efflux during electroconvulsive shock or stress is differently dependent on entorhinal cortex and adrenal integrity [10].

High impact information on Entorhinal Cortex

• Homozygous mutant mice are viable at birth, indicating that tailless is not required for prenatal survival; however, adult mutant mice show a reduction in the size of rhinencephalic and limbic structures, including the olfactory, infrarhinal and entorhinal cortex, amygdala and dentate gyrus [11].
• Here we report direct evidence for the existence of 5-HT3 receptors in rat brain tissue and their distribution, based on high affinity binding of the potent 5-HT3 receptor antagonist 3H-GR65630 to homogenates of rat entorhinal cortex [12].
• Reverberation of neural activity was detected in the entorhinal cortex and was more prominent when the inhibition due to gamma-aminobutyric acid was slightly suppressed [13].
• In rats that had received lesions of the entorhinal cortex, axon sprouting of commissural and associational fibers into the denervated molecular layer of the dentate gyrus was paralleled by a spread in the distribution of tritiated kainic acid-binding sites [14].
• CaMKII Activation in the Entorhinal Cortex Disrupts Previously Encoded Spatial Memory [15].

Chemical compound and disease context of Entorhinal Cortex

• We chose to use a low Mg(2+) model of epilepsy in an in vitro slice preparation where, in the entorhinal cortex, SLEs progress into a type of epileptiform activity called late recurrent discharges (LRDs) that bear resemblance to status epilepticus [16].
• Loss of stimulatory effect of guanosine triphosphate on [(35)S]GTPgammaS binding correlates with Alzheimer's disease neurofibrillary pathology in entorhinal cortex and CA1 hippocampal subfield [17].
• In contrast to ionotropic glutamate receptors, GABA(A) Ralpha1 immunoreactivity was moderately increased in the frontal cortex, entorhinal cortex and molecular layer of the cerebellum in CJD [18].
• In the present study, neuronal statin was examined following lethal or sublethal neuronal injuries in the hippocampus of Alzheimer's disease patients, in rats receiving kainate lesions to the dorsal hippocampus and in entorhinal cortex lesioned rats [19].
• Quinolinic acid lesion of the rat entorhinal cortex pars medialis produces selective amnesia in allocentric working memory (WM), but not in egocentric WM [20].

Biological context of Entorhinal Cortex

• Binding sites for 125I-PYY are most concentrated in the lateral septum, stratum oriens, and radiatum of the hippocampus, amygdala, piriform cortex, entorhinal cortex, several thalamic nuclei, including the reuniens and lateral posterior nuclei, and substantia nigra, pars compacta, and pars lateralis [21].
• 6. We conclude that serotonin potently suppresses excitatory synaptic transmission via 5-HT1A receptors in layers II and III of the medial entorhinal cortex by a presynaptic mechanism [22].
• In addition to effects in the DG, BDNF-LTP was accompanied by robust phosphorylation of the calcium/cAMP-responsive element binding protein (CREB) in tissue prepared from entorhinal cortex of both young and aged rats [23].
• We have characterized excitatory effects of non-competitive NMDA receptor antagonists MK-801, PCP, and ketamine in the rat entorhinal cortex and in cultured primary entorhinal cortical neurons using expression of immediate early gene c-fos as an indicator [24].
• Basal expression, subcellular distribution, and up-regulation of the proto-oncogene c-JUN in the rat dentate gyrus after unilateral entorhinal cortex lesion [25].

Anatomical context of Entorhinal Cortex

• This alteration in the NMDA receptor-mediated input to the hippocampus from the entorhinal cortex may represent a molecular/cellular substrate for age-associated memory impairments [26].
• In advanced age and AD, numerous NGF receptor-positive neurons were located within laminae II-VI of temporal association cortices whereas only a few were seen in the subicular complex, entorhinal cortex, parahippocampal gyrus, and amygdaloid complex [27].
• GFAP mRNA levels were also increased in other areas that receive projections from the entorhinal cortex, including the septum, lateral-dorsal thalamus, and entorhinal cortex contralateral to the lesion [28].
• To examine the fate of APP in the CNS, we injected [35S]methionine into the rat entorhinal cortex and examined the trafficking and processing of de novo synthesized APP in the perforant pathway and at presynaptic sites in the hippocampal formation [29].
• In contrast, the entorhinal cortex, nucleus accumbens core, ventromedial and posterior hypothalamic nuclei, median raphe, and locus coeruleus were particularly resistant to diazepam, all failing to show statistically significant decreases in conditioned fear-induced c-fos expression even at the highest dose [30].

Associations of Entorhinal Cortex with chemical compounds

• We show how the enhancement of synaptic sprouting by estradiol (E2) in response to an entorhinal cortex (EC) lesion model of AD may operate via an apolipoprotein E (apoE)-dependent mechanism [31].
• No tyrosine hydroxylase-immunoreactive neurons were found in Ammon's horn or the subiculum of any of the control specimens, but were found in the entorhinal cortex of 6 of the 13 specimens [32].
• Leupeptin plus Abeta40 caused limited but significant neuronal phospho-tau immunostaining in the entorhinal cortex [33].
• We found argyrophilic grains, coiled bodies, abundant Alz-50-positive and thioflavine S-negative neurofibrillary tangles, and neuropil threads in the hippocampus, entorhinal cortex, locus ceruleus, substantia nigra, subthalamic nucleus, and inferior olives [34].
• [K+]o elevations were recorded in the entorhinal cortex during the ictal discharge (peak values = 13.9 +/- 0.9 mM) and the synchronous GABA-mediated potentials (peak values = 4.2 +/- 0.1 mM); the latter increases were presumably attributable to postsynaptic GABAa-receptor activation because they were abolished by DAGO or BMI [35].

Gene context of Entorhinal Cortex

• In five of the six subjects with schizophrenia, prominent and specific alterations were found in the distribution of two microtubule-associated proteins, MAP2 and MAP5, which were anatomically selective for the subiculum and entorhinal cortex [36].
• We find age-related cortical and limbic Abeta deposition that begins at 8 months and progresses to cover 20-50% of the neuropil in cingulate cortex, entorhinal cortex, and hippocampus of 18-month-old heterozygotic animals [37].
• In situ hybridization analysis in adult mouse brain revealed that PS1 and PS2 mRNAs are enriched in neurons of the hippocampal formation and entorhinal cortex [38].
• An antibody against Neuropilin-1 blocks the repulsive action of Sema III and the entorhinal cortex, but has no effect on Sema IV-induced repulsion [39].
• In order to study the deposition of N-terminal truncated forms of Abeta in the human entorhinal cortex, serial sections from 16 autopsy cases with AD-related pathology were immunostained with antibodies against Abeta1-40, Abeta1-42, Abeta17-23, and Abeta8-17, as well as with the Campbell-Switzer silver impregnation for amyloid [40].

Analytical, diagnostic and therapeutic context of Entorhinal Cortex

• MSA lesions abolished or decreased theta rhythm in dorsal hippocampus (DHPC) and MEC; acetylcholinesterase (AChE) staining was depleted or diminished in all of the hippocampus and entorhinal cortex [41].
• The integrity of hippocampal cell populations and projections to the hippocampal formation from entorhinal cortex was assessed with radioimmunoassay and immunostaining for methionine-enkephalin (ME) and dynorphin (DYN) A, as well as with Timm and Nissl staining [42].
• Moreover, prior castration had an additive effect with entorhinal cortex lesions in the increase in GFAP and SGP-2 mRNA [43].
• In order to understand the role of different guidance factors, we analyzed the effects of Sema3C and Netrin-1 on explants from the entorhinal cortex, dentate gyrus, cornu ammonis regions CA1 and CA3 and medial septum in a collagen coculture assay [44].
• Extracellular lactate was measured on-line using microdialysis and enzyme reactions (a technique named lactography); in some rats, unilateral lesions of the entorhinal cortex were made or the bilateral adrenal glands were removed [10].

References