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PubMed1997

Entorhinal cortex lesioning protects hippocampal CA3 neurons from stress-induced damage.

The role of the entorhinal cortex (EC) in stress-induced damage in terms of dendritic branching points and intersections of hippocampal CA3 neurons has been investigated. Following bilateral electrolytic lesions of the EC, the rats were subjected to restraint stress, 6 h per day for 21 days. Chronic restraint stress resulted in the atrophy of hippocampal CA3 neurons and the lesioning of the EC prior to stress significantly (P < 0.001) reduced this dendritic atrophy. These results show that the neuronal vulnerability to chronic stress can be attenuated by entorhinal glutamatergic denervation.

Animals↗
PubMed1993

BDNF and trkB mRNA expression in the rat hippocampus following entorhinal cortex lesions.

Quantitative in situ hybridization was used to determine whether the prevalence or topographical distribution of brain-derived neurotrophic factor (BDNF) or tyrosine receptor kinase (trk) B mRNA is altered in the hippocampal formation following lesions of excitatory afferents from the entorhinal cortex which provides an external source of innervation for the hippocampal formation. BDNF mRNA levels were not altered in the hippocampal formation up to 10 days following entorhinal cortex lesions (ECLs). The levels of mRNA coding for all known forms of trkB receptors also remained unchanged. The prevalence of the synaptic plasticity marker SNAP-25 mRNA was increased in the CA2 and CA3 pyramidal cell layers and the dentate gyrus by 6 days following ECLs and remained elevated at 10 days following ECLs. Our findings indicate that hippocampal neuron sprouting which occurs in response to ECLs is not the result of changes in the expression of the BDNF or trkB mRNA.

Animals↗
PubMed1987

Removal of the entorhinal cortex protects hippocampal CA-1 neurons from ischemic damage.

The excitatory (glutamatergic) innervation seems to determine a nerve cells vulnerability to complete, transient ischemia. Interruption of the excitatory afferents to the hippocampus by removal of the entorhinal cortex prior to ischemia allows examination of this hypothesis. Groups of adult male Wistar rats were subjected to 20 min of ischemia (four-vessel occlusion) 4 days following a sham procedure, unilateral or bilateral entorhinotomy. CA-1 pyramidal cell survival following ischemia was assessed by light microscopic examination (cell counts) 4 days after ischemia. Compared to control animals unilateral entorhinotomy protected 50% of the CA-1 pyramidal neurons ipsilateral to the lesion, whereas bilateral entorhinotomy resulted in 84% protection. The pathophysiology of ischemic brain damage is discussed, and it is suggested that the protection of CA-1 pyramidal neurons after entorhinotomy is due to interruption of the input to the dentate granule cells, which forms a link in the trisynaptic pathway from the entorhinal cortex to the CA-1.

Animals↗
PubMed1992

Short-term ethanol intoxication in rat. Effect on the entorhinal cortex.

The effect of short-term ethanol intoxication in systems implicated in memory and other cognitive functions in rats has been assessed by studying the variation in the karyometry of the neurons in the different layers of the lateral entorhinal cortex. The analysis showed that short-term ethanol consumption produced a reduction in the nuclear area of neurons in layers V and VI, and to a lesser extent, in layers II and III. These results suggest that the deep layers of the entorhinal cortex are more sensitive to ethanol intoxication, thus more likely affecting cortical and subcortical projections than the hippocampal output.

Acute Disease↗
PubMedDate not supplied

6-OHDA lesion to the entorhinal cortex does not abolish angiotensin II improvement of recall in rats.

Our recent studies have shown that facilitating effect of angiotensin II (AII) on recall is mediated by dopaminergic systems. In this study the influence of bilateral destruction of dopaminergic endings in the entorhinal cortex on improving recall intracerebroventricular injection of AII was tested. Since this lesion did not abolish the facilitating influence of AII, it may be suggested that the dopaminergic projection to the entorhinal cortex is not responsible for the facilitating effect of AII on recall in a passive avoidance situation.

Angiotensin II↗
PubMed2001

Lesions of the entorhinal cortex impair acquisition of hippocampal-dependent trace conditioning.

Rabbits with the electrolytic lesions of bilateral entorhinal cortex (EC) were trained with the hippocampal-dependent trace conditioning of the nictitating membrane response. The multiple-unit activity of the hippocampal CA1 region was recorded during conditioning. The conditioned stimulus was a tone (1 kHz, 85 dB, 200-ms duration), the unconditioned stimulus was a corneal air puff (3 psi, 150-ms duration), and the interstimulus interval was 750 ms. The EC-lesioned animals showed only 30% conditioned response (CR) by the ninth session while the sham-operated animals showed above 80% CR. The lesioned animals did not show learning-related changes in the hippocampal activity. When the training was switched to the 300-ms interstimulus interval trace conditioning, both groups learned above 80% CR. The EC-lesioned animals, however, showed less learning-related activity in the hippocampus than the sham-operated animals. These results suggest that the development of the learning-related activity in the hippocampus depends on the intact EC, and that the EC may provide a possible pathway conveying learning information from the cerebellum or cerebral cortex to the hippocampus during the trace conditioning.

Animals↗
PubMed1991

Entorhinal cortex pathology in Alzheimer's disease.

The anatomical distribution of pathological changes in Alzheimer's disease, although highly selective for only certain brain areas, can be widespread at the endstage of the illness and can affect many neural systems. Propriety for onset among these is a question of importance for clues to the etiology of the disease, but one that is formidable without an experimental animal model. The entorhinal cortex (Brodmann's area 28) of the ventromedial temporal lobe is an invariant focus of pathology in all cases of Alzheimer's disease with selective changes that alter some layers more than others. The authors' findings reveal that it is the most heavily damaged cortex in Alzheimer's disease. Neuroanatomical studies in higher mammals reveal that the entorhinal cortex gives rise to axons that interconnect the hippocampal formation bidirectionally with the rest of the cortex. Their destruction in Alzheimer's disease could play a prominent role in the memory deficits that herald the onset of Alzheimer's disease and that characterize it throughout its course.

Alzheimer Disease↗
PubMed2000

From healthy aging to early Alzheimer's disease: in vivo detection of entorhinal cortex atrophy.

Using quantitative structural MRI protocols, we examined the effects of age on alterations in entorhinal cortex (EC) volume. The left EC was found to be smaller than the right in both young and healthy aged subjects. More importantly, the right EC, but not the left, was significantly smaller in elderly participants compared to young controls. In an attempt to determine the earliest sites of involvement in mild and incipient Alzheimer's disease (AD), we compared entorhinal and hippocampal volume in (1) healthy elderly controls, (2) patients with very mild AD, and (3) elderly patients who were evaluated for cognitive complaints, but did not meet criteria for dementia. Both patient groups differed from controls in EC volume, but not from each other. In contrast, the two patient groups differed in hippocampal volume from controls, as well as from each other, with the mild AD cases showing the greatest atrophy. These results suggest that degeneration of the EC and hippocampal formation occurs before the onset of overt dementia. In fact, follow-up clinical evaluations available on 23 of 28 nondemented patients indicated that 12 of 23 had converted to AD. Converters could be best differentiated from nonconverters on the basis of entorhinal volume.

Aging↗
PubMed2005

Presubiculum stimulation in vivo evokes distinct oscillations in superficial and deep entorhinal cortex layers in chronic epileptic rats.

The characteristic cell loss in layer III of the medial entorhinal area (MEA-III) in human mesial temporal lobe epilepsy is reproduced in the rat kainate model of the disease. To understand how this cell loss affects the functional properties of the MEA, we investigated whether projections from the presubiculum (prS), providing a main input to the MEA-III, are altered in this epileptic rat model. Injections of an anterograde tracer in the prS revealed bilateral projection fibers mainly to the MEA-III in both control and chronic epileptic rats. We further examined the prS-MEA circuitry using a 16-channel electrode probe covering the MEA in anesthetized control and chronic epileptic rats. With a second 16-channel probe, we recorded signals in the hippocampus. Current source density analysis indicated that, after prS double-pulse stimulation, afterdischarges in the form of oscillations (20-45 Hz) occurred that were confined to the superficial layers of the MEA in all epileptic rats displaying MEA-III neuronal loss. Slower oscillations (theta range) were occasionally observed in the deep MEA layers and the dentate gyrus. This kind of oscillation was never observed in control rats. We conclude that dynamical changes occur in an extensive network within the temporal lobe in epileptic rats, manifested as different kinds of oscillations, the characteristics of which depend on local properties of particular subareas. These findings emphasize the significance of the entorhinal cortex in temporal lobe epilepsy and suggest that the superficial cell layers could play an important role in distributing oscillatory activity.

Animals↗
PubMed2000

Neurons in layer III of the entorhinal cortex. A role in epileptogenesis and epilepsy?

A preferential lesion of neurons in layer III of the entorhinal cortex (EC) is often observed in patients suffering from temporal lobe epilepsy and in several animal models of the disease. This lesion is duplicated in rats by a focal, intra-entorhinal injection of the "indirect" excitotoxin aminooxyacetic acid (AOAA), providing a model that can be used to study the mechanisms underlying seizure-induced cell death and epilepsy. Doomed neurons in the EC and in several associated limbic structures show pathological changes within hours after the AOAA injection, but GABAergic neurons in layer III of the EC are quite resistant. This pattern of neuron loss eventually results in hippocampal and entorhinal hyperexcitability. Notably, the seizure-induced death of layer III neurons in the EC can be attenuated by eliminating the prominent excitatory input from the presubiculum. Taken together, these results suggest opportunities to target parahippocampal structures for the treatment of temporal lobe epilepsy.

Aminooxyacetic Acid↗
PubMed1983

Enhanced acetylcholinesterase staining in the hippocampal perforant pathway zone after combined lesions of the septum and entorhinal cortex.

A lesion of the septum or a transection of the fimbria-fornix diminishes most, but not all, acetylcholinesterase (AChE) staining in the hippocampal formation. The residual AChE is located in the outer part of the molecular layer of the hippocampal CA1 zone and adjacent subicular field (zone 31). We report that following combined lesions of the septum and entorhinal cortex, the residual hippocampal AChE staining pattern expands and occupies the zone innervated normally by perforant pathway terminals from the entorhinal cortex.

Acetylcholinesterase↗
PubMed2005

Entorhinal cortex entrains epileptiform activity in CA1 in pilocarpine-treated rats.

Layer III neurons of the medial entorhinal cortex (mEC) project to CA1 via the temporoammonic pathway and exert a powerful feed-forward inhibition of CA1 pyramidal neurons. The present study evaluates the hypothesis that disrupted inhibition of CA1 pyramidal neurons causes an eased propagation of entorhinal seizures to the hippocampus via the temporoammonic pathway. Using a method to induce a confined epileptic focus in brain slices, we investigated the spread of epileptiform activity from the disinhibited mEC to CA1 in control and pilocarpine-treated rats that had displayed status epilepticus and spontaneous recurrent seizures. In pilocarpine-treated rats, the mEC showed a moderate layer III cell loss and an enhanced susceptibility to epileptiform discharges compared to control animals. Entorhinal discharges propagated to CA1 in pilocarpine-treated rats but not in controls. Disconnecting CA3 from CA1 did not affect the spread of epileptiform activity to CA1 excluding its propagation via the trisynaptic hippocampal loop. Mimicking the invasion of epileptiform discharges by repetitive stimulation of the temporoammonic pathway caused a facilitation of field potentials in CA1 that were contaminated by population spikes and afterdischarges in pilocarpine-treated but not control rats. Single cell recordings of CA1 pyramidal neurons revealed a dramatic loss of feed-forward inhibition and the occurrence of strong postsynaptic excitatory potentials in pilocarpine-treated rats. Excitatory responses in CA1 were characterized by multiple NMDA receptor-mediated afterdischarges and a strong paired-pulse facilitation in response to activation of the temporoammonic pathway. Our results suggest that, irrespective of the enhanced seizure-susceptibility of the mEC in epileptic rats, the loss of feed-forward inhibition and the enhanced NMDA receptor-mediated excitability CA1 pyramidal cells ease the spread of epileptiform activity from the mEC to CA1 via the temporoammonic pathway bypassing the classical trisynaptic hippocampal loop.

Animals↗
PubMedDate not supplied

MRI of human entorhinal cortex: a reliable protocol for volumetric measurement.

A new protocol for measuring the volume of the entorhinal cortex (EC) from magnetic resonance images (MRI) was developed specifically to measure the EC from oblique coronal sections used in hippocampal volumetric studies. The relative positions of the anatomic landmarks demarcating EC boundaries were transposed from standard coronal sections to oblique ones. The lateral EC border, which is the most controversial among anatomists, was defined in a standard and conservative manner at the medial edge of the collateral sulcus. Two raters measured the EC twice for 78 subjects (healthy aged individuals, very mild AD patients, and elderly patients who did not meet criteria for dementia) to study intra- and inter-rater reproducibility and reliability of measurements. The level of accuracy achieved (coefficients of reproducibility of 1.40-3.86%) and reliability of measurements (intraclass correlation coefficients of 0.959-0.997) indicated that this method provides a feasible tool for measuring the volume of the EC in vivo.

Adult↗
PubMedDate not supplied

Extracellular signal-regulated kinase activity in the entorhinal cortex is necessary for long-term spatial memory.

Lesion studies have provided evidence that the entorhinal cortex (EC) participates in spatial memory. However, the molecular cascades that underlie memory-associated changes in the EC and its specific role in spatial memory, however, have not been clearly delineated. Recently, it has been shown that activation of extracellular signal-regulated kinase (Erk, a mitogen-activated protein kinase family member) in the dorsal hippocampus is necessary for spatial memory. To examine whether similar mechanisms are used for spatial memory storage in the EC, Erk activity was inhibited after training in the Morris water maze. Bilateral infusion of the mitogen-activated protein kinase kinase inhibitor PD098059 into the EC immediately after training resulted in a memory deficit observed during a retention test performed 48 h later. This deficit was abolished with pretraining in a different water maze in which animals were able to learn the general task requirements and the appropriate search strategies. The absence of a deficit indicates that Erk activity in the EC may be involved in storing the task requirements or the search strategies. The findings presented in this article are consistent with the idea that the EC is involved in spatial memory and indicate that Erk activity is necessary for memory consolidation in this structure.

Animals↗
PubMed2002

Variation in effective stimulus patterns for induction of long-term potentiation across different layers of rat entorhinal cortex.

Neuronal activities in superficial (II and III) and deep (V and VI) layers of the entorhinal cortex (EC) are preferentially modulated by theta and sharp wave (SPW) EEG, respectively. We investigated the possibility that distinct EEG patterns represent optimal stimulus patterns for induction of long-term potentiation (LTP) in different layers of the EC. We examined effects of three different stimulation patterns on LTP induction in layers I, II-III, and V of medial EC slices of the rat. The stimulation patterns we used were a single, long high-frequency train (1 sec at 100 Hz, repeated 3x), theta burst stimulation [TBS; 10 bursts (four pulses, 100 Hz) at 5 Hz, repeated 3x], and SPW-like burst stimulation [ SPWBS; three bursts (20 pulses, 200 Hz) at 2 Hz, repeated 6x]. Similar degrees of LTP were induced by the three stimulation patterns in layer I. In layers II--III and layer V, however, the largest degrees of LTP were induced by TBS and SPWBS, respectively. These results suggest that burst stimulation constructed to mimic naturally occurring patterns of neuronal activity in the corresponding layer is optimal for LTP induction in layers II-III and layer V of the EC. The differences may play important roles in shaping hippocampal-neocortical interactions in encoding and retrieval of memory.

Analysis of Variance↗
PubMed2004

Shrinkage of the entorhinal cortex over five years predicts memory performance in healthy adults.

Lesions in the hippocampus (HC), the entorhinal cortex (EC), and the prefrontal cortex (PFC) are associated with impairment of episodic memory; reduced HC volume is linked to memory declines in dementia; and decline in EC volume predicts progression from mild cognitive impairment to dementia. However, in healthy adults, the relationship between memory and regional volumes is unclear, and no data are available on the relationship of longitudinal regional shrinkage to memory performance in a cognitively intact population. The objective of this study was to examine whether shrinkage of the EC, HC, and PFC over a 5 year period can predict declarative memory performance in healthy adults. The volumes of three brain regions were measured on magnetic resonance images that were acquired twice, 5 years apart. Multiple measures of episodic memory were administered at follow-up. Results indicated that the volume of HC and PFC (but not EC) correlated with age at baseline and follow-up. However, after age differences in memory were taken into account, none of the regional volumes was associated with memory performance at follow-up. In contrast, greater annual rate of shrinkage in EC (but not HC or PFC) predicted poorer memory performance. Thus, in a healthy and educated population, even mild age-related shrinkage of the EC may be a sensitive predictor of memory decline.

Age Distribution↗
PubMed2005

The role of adenosine A(1) receptors in the interaction between amygdala and entorhinal cortex of kindled rats.

In this study the effect of adenosine A(1) receptors of the entorhinal cortex (EC) and amygdala on kindled seizures was investigated. Animals were kindled by daily electrical stimulation of amygdala (group 1) or EC (group 2). In the fully kindled animals, N(6)-cyclohexyladenosine (CHA), a selective A(1) receptor agonist, and 1,3-dimethyl-8-cyclopenthylxanthine (CPT), a selective A(1) receptor antagonist, were microinjected bilaterally into the EC (group 1) or amygdala (group 2). The seizure parameters were measured at 5, 15, 60 and 120 min post injection. Obtained data showed that in group 1, intra-EC microinjection of CHA at concentration of 10 microM reduced amygdala- and, EC-afterdischarge duration and stage 5 seizure duration at 5, 15, 60 and 120 min post drug injection. It also increased the latency to stage 4 seizure but no alteration was observed in seizure stage. At concentrations of 0.1 and 1 microM, CHA reduced only EC-afterdischarge duration at 5 and 15 min post drug infusion. Bilateral microinjection CPT at concentrations of 5 and 10 microM into the EC did not alter seizure parameters. Intra-EC microinjection of CPT (5 microM), 5 min before CHA (10 microM), blocked the anticonvulsant effects of CHA. On the other hand, in group 2 animals, intra-amygdala CHA (10, 50 and 100 microM) or CPT (5 and 10 microM) had no significant effect on seizure parameters of EC-kindled rats. These results suggest that adenosine A(1) receptors activation of the EC may have an inhibitory effect on amygdala-kindled seizures. But, despite of reciprocal interconnections between these two regions, activation of the A(1) receptors of the amygdala has no effect on EC-kindled seizures.

Adenosine↗
PubMed1998

Responses of deep entorhinal cortex are epileptiform in an electrogenic rat model of chronic temporal lobe epilepsy.

We investigated whether entorhinal cortex (EC) layer IV neurons are hyperexcitable in the post-selfsustaining limbic status epilepticus (post-SSLSE) animal model of temporal lobe epilepsy. We studied naive rats (n = 44), epileptic rats that had experienced SSLSE resulting in spontaneous seizures (n = 45), and electrode controls (n = 7). There were no differences between electrode control and naive groups, which were pooled into a single control group. Intracellular and extracellular recordings were made from deep layers of EC, targeting layer IV, which was activated by stimulation of the superficial layers of EC or the angular bundle. There were no differences between epileptic and control neurons in basic cellular characteristics, and all neurons were quiescent under resting conditions. In control tissue, 77% of evoked intracellular responses consisted of a short-duration [8.6 +/- 1.3 (SE) ms] excitatory postsynaptic potential and a single action potential followed by gamma-aminobutyric acid-A (GABAA) and GABAB inhibitory post synaptic potentials (IPSPs). Ten percent of controls did not contain IPSPs. In chronically epileptic tissue, evoked intracellular responses demonstrated prolonged depolarizing potentials (256 +/- 39 ms), multiple action potentials (13 +/- 4), and no IPSPs. Ten percent of epileptic responses were followed by rhythmic "clonic" depolarizations. Epileptic responses exhibited an all-or-none response to progressive increases in stimulus intensity and required less stimulation to elicit action potentials. In both epileptic and control animals, intracellular responses correlated precisely in morphology and duration with extracellular field potentials. Severing the hippocampus from the EC did not alter the responses. Duration of intracellular epileptic responses was reduced 22% by the N-methyl--aspartate (NMDA) antagonist (-)-2-amino-5-phosphonovaleric acid (APV), but they did not return to normal and IPSPs were not restored. Epileptic and control responses were abolished by the non-NMDA antagonist 6, 7-dinitroquinoxaline-2-3-dione (DNQX). A monosynaptic IPSP protocol was used to test connectivity of inhibitory interneurons to primary cells by direct activation of interneurons with a stimulating electrode placed near the recording electrode in the presence of APV and DNQX. Using this protocol, IPSPs similar to control (P > 0.05) were seen in epileptic cells. The findings demonstrate that deep layer EC cells are hyperexcitable or "epileptiform" in this model. Hyperexcitability is not due to interactions with the hippocampus. It is due partially to augmented NMDA-mediated excitation. The lack of IPSPs in epileptic neurons may suggest inhibition is impaired, but we found evidence that inhibitory interneurons are connected to their target cells and are capable of inducing IPSPs.

Action Potentials↗