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PubMed1994

CNQX infused into entorhinal cortex blocks memory expression, and AMPA reverses the effect.

Rats were trained in a step-down inhibitory avoidance task using a 0.8-mA foot shock and tested for retention 26 days later. Three to five days prior to the retention test they were bilaterally implanted with cannulae aimed at the entorhinal cortex. Ten minutes before testing they received an infusion, into the entorhinal cortex, of vehicle, ciano-nitro-quinoxaline-dione (CNQX; 0.5 micrograms), amino-hydroxy-methyl-isoxalone-propionate (AMPA; 1.0 or 2.5 micrograms), or AMPA (1.0 micrograms) plus CNQX (0.5 micrograms). CNQX blocked memory expression; the effect lasted less than 90 min. AMPA had no effect of its own, but at the lower dose level it counteracted the depressant influence of CNQX. It is not likely that the effect of CNQX could have been due to an influence on performance: In separate sets of experiments the bilateral intraentorhinal infusion of CNQX (0.5 micrograms) 10 min before training did not affect either acquisition or retention of the avoidance task or general activity during 3 min of free exploration in the training box. The results indicate that the integrity of AMPA receptors in the entorhinal cortex is necessary for memory expression.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed2006

Zinc release in the lateral nucleus of the amygdala by stimulation of the entorhinal cortex.

Zinc release in the lateral nucleus of the amygdala was examined using rat brain slices. The lateral and basolateral nuclei in the amygdala were evidently stained by Timm's sulfide-silver staining method. When the amygdala including both the nuclei was stimulated with 100 mM KCl by means of in vivo microdialysis, extracellular zinc concentration was increased significantly. Zinc release in the lateral nucleus of the amygdala innervated by the entorhinal cortex was next examined in brain slices double-stained with zinc and calcium indicators. Extracellular zinc signal (ZnAF-2) in the lateral nucleus was increased with intracellular calcium signal (calcium orange) during delivery of tetanic stimuli to the entorhinal cortex. Both the increases were completely inhibited by addition of 1 micro M tetrodotoxin, a sodium channel blocker. Furthermore, calcium signal in the lateral nucleus during delivery of tetanic stimuli to the entorhinal cortex was increased in the presence of 10 micro M CNQX, an AMPA/KA receptor antagonist, and this increase was facilitated by addition of 1 mM CaEDTA, a membrane-impermeable zinc chelator. The present study suggested that zinc is released in the lateral nucleus of the amygdala by depolarization of the entorhinal neurons. In the lateral nucleus, zinc released may suppress the increase in presynaptic calcium signal.

Amygdala↗
PubMed1989

Spontaneous activity mediated by NMDA receptors in immature rat entorhinal cortex in vitro.

Intracellular recordings were made from cells in layer II of entorhinal cortex slices from 9 to 13-day-old rats. The majority of these cells showed pronounced spontaneous synaptic activity which could summate into large depolarizing events and give rise to bursts of spikes. These events could be associated with an apparent decrease in membrane conductance. They were reduced in amplitude by hyperpolarization of the cell and tended to increase on depolarization. Perfusion with 2-amino-5-phosphonovalerate abolished the spontaneous activity. Thus, in layer II of the entorhinal cortex at this stage of development there seems to be a functional enhancement of ongoing synaptic activity mediated via activation of N-methyl-D-aspartate receptors.

2-Amino-5-phosphonovalerate↗
PubMed1992

Late posttraining memory processing by entorhinal cortex: involvement of NMDA and GABAergic receptors.

The NMDA receptor antagonist, D-2-amino-5-phosphonopentanoic acid (AP5) (5 micrograms) and the GABAA receptor agonist, muscimol (0.03 microgram) were infused bilaterally into the entorhinal cortex of rats 0, 90, 180, or 360 min after training in habituation to a novel environment or in step-down inhibitory avoidance. Animals were tested for retention 22 h after training in each task. AP5 and muscimol were amnestic for both tasks when given 90 or 180 min after training, but had no effect when given 0 or 360 min after training. In contrast, intraamygdala injections or AP5 or muscimol were amnestic when given 0 but not 90 min after inhibitory avoidance training. The results indicate that the entorhinal cortex plays a late but important role in posttraining memory processing; this role involves glutamatergic NMDA receptors and is inhibited by GABAA receptors. The intervention of the entorhinal cortex in posttraining memory processing is subsequent, and could be secondary, to that of the amygdala and other limbic structures.

2-Amino-5-phosphonovalerate↗
PubMed2005

Efferent connections of the main olfactory bulb in the opossum (Monodelphis domestica): a characterization of the olfactory entorhinal cortex in a marsupial.

Olfactory projections have been investigated for decades, but few reports using modern, sensitive neural tracers are available. In marsupials, only lesion-degeneration studies exist and they are restricted to the genera Didelphis and Trichosurus. Some of the territories described as olfactory-recipient such as the upper portion of the rhinal fissure and the vomeronasal amygdala are, however, controversial. Also, the characterization of the olfactory portion of the entorhinal cortex is far from clear in acallosal mammals. The present report investigates, using biotinylated dextran-amine, the olfactory connections in the short-tailed opossum (Monodelphis domestica) and characterizes the olfactory portion of the entorhinal cortex in non-placental mammals. The data indicate that olfactory projections do not reach the upper portion of the rhinal fissure, but partially end in the vomeronasal amygdala, i.e., the medial and posteromedial cortical amygdaloid nuclei; thus, although olfactory and vomeronasal system have largely segregated outputs, areas of overlap should be restudied. The olfactory portion of the entorhinal cortex is much larger than previously described, extending up to the occipital pole of the cerebral hemisphere. Collectively, these data contribute to our understanding of the organization of the hippocampal formation in marsupials.

Animals↗
PubMed2001

Response dynamics of entorhinal cortex in awake, anesthetized, and bulbotomized rats.

The generation of oscillatory activity may be crucial to brain function. The coordination of individual neurons into rhythmic and coherently active populations is thought to result from interactions between excitatory and inhibitory cells mediated by local feedback connections. By using extracellular recording wires and silicon microprobes to measure electrically evoked damped oscillatory responses at the level of neural populations in the entorhinal cortex, and by using current-source density analysis to determine the spatial pattern of evoked responses, we show that the propagation of activity through the cortical circuit and consequent oscillations in the local field potential are dependent upon background neural activity. Pharmacological manipulations as well as surgical disconnection of the olfactory bulb serve to quell the background excitatory input incident to entorhinal cortex, resulting in evoked responses without characteristic oscillations and showing no signs of polysynaptic feedback. Electrical stimulation at 200 Hz applied to the lateral olfactory tract provides a substitute for the normal background activity emanating from the bulb and enables the generation of oscillatory responses once again. We conclude that a non-zero background level of activity is necessary and sufficient to sustain normal oscillatory responses and polysynaptic transmission through the entorhinal cortex.

Action Potentials↗
PubMed1995

Effects of unilateral entorhinal cortex lesion and ganglioside GM1 treatment on performance in a novel water maze task.

Transient deficits have been reported after unilateral entorhinal cortex (EC) lesion. To determine whether there is a more persistent deficit, adult male Sprague-Dawley rats with electrolytic or sham lesions of the left entorhinal cortex were examined on acquisition of a modified working memory task in the Morris water maze. This delayed matching-to-sample task, with a 1-h intertrial interval, reveals a significant deficit in total distance to platform in both presentation (Trial 1) and matching (Trial 2) in the rats with entorhinal lesions. We have also found that this test can be used to assess significant deficits in perseveration (repeated nonproductive movement) in rats with entorhinal lesions. The deficits can be seen up to 16 days postinjury. Administration of ganglioside GM1 resulted in a moderate improvement in performance in both water maze measures analyzed. All groups (sham operated, lesion with saline treatment, and lesion with ganglioside GM1 treatment) were given three other tests, which were used to evaluate possible contributing factors to deficient water maze performance. A one-trial test for exploration of novel objects revealed no significant, simple working memory deficit in any group. Plus maze testing, to assess possible differences in levels of anxiety or increased activity as a component of water maze performance, also revealed no differences in the three groups. All groups were also similar in motor activity, shown by monitoring of activity levels. The worsened water maze performance observed in rats with EC lesion may be related to deficits in working memory ability within the framework of acquisition of a more complex spatial learning task.

Animals↗
PubMed1994

AMPA-selective glutamate receptor subtype immunoreactivity in the entorhinal cortex of non-demented elderly and patients with Alzheimer's disease.

The present work employed immunocytochemical techniques and examined the distribution and cytological features of the AMPA receptor subunits, GluR2/3 and GluR1 within the entorhinal cortex of non-demented elderly (NC), patients with neuropathological and clinical verification of Alzheimer's disease (AD) and patients without a clinical history of dementia yet exhibiting sufficient quantities of senile plaques to meet neuropathological criteria of Alzheimer's disease (HPND). In NC cases, GluR2/3-immunolabeled neurons were abundantly distributed throughout layers II, III, V and VI of the entorhinal cortex. In contrast, GluR1-positive cells were comparatively sparse in number and largely restricted to layers V and VI. In AD, GluR2/3- and GluR1-labeled neurons were markedly reduced. Similarly, adjacent Nissl-stained tissue sections revealed substantial cell loss in the entorhinal cortex thus providing a reasonable explanation for the loss of these receptor subunits. Importantly, a dramatic loss of GluR2/3- and GluR1-immunolabeled neurons is also observed in the HPND cases, although examination of Nissl-stained tissue sections reveals little if any evidence of cell loss. The latter data suggest that a 'down-regulation' of these receptor subunits occurs prior to the actual loss of these cells. Furthermore, we hypothesize that the decrease of specific AMPA receptor subunits may influence neuronal vulnerability via a mechanism involving increased intracellular calcium and the destabilization of intracellular calcium homeostasis.

Aged↗
PubMed2005

Cytoarchitectonic mapping of the human amygdala, hippocampal region and entorhinal cortex: intersubject variability and probability maps.

Probabilistic maps of neocortical areas and subcortical fiber tracts, warped to a common reference brain, have been published using microscopic architectonic parcellations in ten human postmortem brains. The maps have been successfully applied as topographical references for the anatomical localization of activations observed in functional imaging studies. Here, for the first time, we present stereotaxic, probabilistic maps of the hippocampus, the amygdala and the entorhinal cortex and some of their subdivisions. Cytoarchitectonic mapping was performed in serial, cell-body stained histological sections. The positions and the extent of cytoarchitectonically defined structures were traced in digitized histological sections, 3-D reconstructed and warped to the reference space of the MNI single subject brain using both linear and non-linear elastic tools of alignment. The probability maps and volumes of all structures were calculated. The precise localization of the borders of the mapped regions cannot be predicted consistently by macroanatomical landmarks. Many borders, e.g. between the subiculum and entorhinal cortex, subiculum and Cornu ammonis, and amygdala and hippocampus, do not match sulcal landmarks such as the bottom of a sulcus. Only microscopic observation enables the precise localization of the borders of these brain regions. The superposition of the cytoarchitectonic maps in the common spatial reference system shows a considerably lower degree of intersubject variability in size and position of the allocortical structures and nuclei than the previously delineated neocortical areas. For the first time, the present observations provide cytoarchitectonically verified maps of the human amygdala, hippocampus and entorhinal cortex, which take into account the stereotaxic position of the brain structures as well as intersubject variability. We believe that these maps are efficient tools for the precise microstructural localization of fMRI, PET and anatomical MR data, both in healthy and pathologically altered brains.

Aged↗
PubMed1995

Quantitative morphological analysis of subicular terminals in the rat entorhinal cortex.

In the present report, we describe a morphological and quantitative analysis of subicular synapses in layer V of the lateral entorhinal cortex (LEA) of the rat. Projections from the dorsal subiculum were labeled anterogradely, and areas in LEA showing high terminal density were randomly selected for ultrathin sectioning. More than 400 terminals in LEA were photographed in the electron microscope, and synapse types and postsynaptic targets were identified and, subsequently, quantified with the unbiased disector method. Most subicular terminals appeared to form asymmetrical synapses. A majority of asymmetrical synapses terminated on spines (67.5%), whereas a smaller fraction of asymmetrical synapses (23.5%) terminated on dendritic shafts. A small fraction of the terminals (7%) had symmetrical features. These symmetrical synapses had an almost equal percentage of spines and dendritic shafts as postsynaptic elements. Labeled synapses on somata or axons were never observed. The findings of this study in conjunction with relevant electrophysiological observations (Jones [1987] Neurosci Left 81:209-214) leads to the conclusion that the subiculo-entorhinal pathway comprises a large excitatory and a smaller inhibitory projection, both making synaptic contacts with presumed principal neurons and interneurons in the entorhinal cortex.

Animals↗
PubMed1994

Multiple cholinergic markers are unexpectedly not altered in the rat dentate gyrus following entorhinal cortex lesions.

Since major cholinergic deficits are observed in Alzheimer's disease, the development of models to study possible cholinergic plasticity has generated great interest. In this regard, it has been shown that lesions of the entorhinal cortex, which sends glutamatergic projections to the hippocampus, promote the sprouting and plasticity of presumptive cholinergic septohippocampal fibers in the dentate gyrus, as revealed by AChE histochemistry. This sprouting was reported to be evident at 8 d and up to 30 d postlesion (DPL) and is now widely used as a model of cholinergic neuronal plasticity. In the present study, unilateral lesions of the entorhinal cortex were made in adult rats, and the status of various putative pre- and postsynaptic cholinergic markers was assessed after 2, 4, 8, 14, and 30 DPL. As expected, AChE was increased in the outer molecular layer of the ipsilateral dentate gyrus from 8 to 30 DPL. In contrast, the activity of ChAT, the enzyme responsible for the synthesis of ACh, and the densities of specific binding sites for 3H-AH5 183/vesamicol (blocker of the ACh vesicular transport sites), 3H-hemicholinium-3 (blocker of the high-affinity choline uptake sites), muscarinic-M2 (3H-AF-DX 384 and 3H-ACh), muscarinic-M1 (3H-pirenzepine), and nicotinic (3H-N-methylcarbamylcholine) cholinergic receptors were not increased on the ipsilateral molecular layer of the dentate gyrus, as compared to their contralateral controls. We conclude that the increase in AChE staining in the molecular layer of the dentate gyrus following entorhinal cortex lesions may be due to changes in noncholinergic neurons.

Acetylcholine↗
PubMed1996

Involvement of GABA systems in acetylcholine release induced by 5-HT3 receptor blockade in slices from rat entorhinal cortex.

The aim of the present study was to examine the role of 5-HT3 receptors in spontaneous and K(+)-evoked acetylcholine (ACh) release from rat entorhinal cortex and striatal slices. The 5-HT3 receptor antagonists ondansetron and granisetron (0.01-10 microM) produced a concentration-dependent increase in both spontaneous and K(+)-evoked [3H]ACh release in the two brain regions studied. The release of ACh was Ca(2+)-dependent and tetrodotoxin-sensitive. 5-HT3 receptor agonists, such as 2-methyl-5-HT and 1-phenylbiguanide, at concentrations up to 1 microM, did not show any intrinsic effect on [3H]ACh release in both rat brain regions. However, 2-methyl-5-HT, 1 microM, fully blocked the ondansetron-induced enhancement in both basal and K(+)-evoked ACh release, suggesting that 5-HT, through 5-HT3 receptor activation, tonically inhibits ACh release. The possible implication of interposed inhibitory systems in ACh release after 5-HT3 receptor blockade was subsequently analyzed. While the effect of ondansetron was not modified by haloperidol or naloxone, the GABAA receptor antagonist bicuculline produced a marked potentiation of ACh release in the entorhinal cortex but not in the striatum. The results suggest that in this cortical area 5-HT activates 5-HT3 receptors located on GABAergic neurons which in turn inhibit cholinergic function.

Acetylcholine↗
PubMed2000

Entorhinal cortex lesion does not alter reelin messenger RNA expression in the dentate gyrus of young and adult rats.

The extracellular matrix protein reelin plays an important role in neuronal pattern formation and axonal collateralization during the development of the central nervous system. With the concept that reelin might also be important for axonal growth in the injured nervous system we investigated whether reelin is re-expressed in areas of collateral sprouting after brain injury. The expression of reelin messenger RNA was studied in the denervated fascia dentata of adult rats one, four, seven and 14 days following entorhinal cortex lesion. In adult control animals, in situ hybridization histochemistry with digoxigenin-labeled reelin riboprobes revealed reelin messenger RNA expression in neurons located in the outer molecular layer and beneath the granule cell layer of the dentate gyrus. After entorhinal cortex lesion, this expression pattern did not change during the whole post-lesional time period investigated despite a strong glial activation and reactive sprouting in the outer molecular layer of the dentate gyrus as visualized by immunohistochemistry for glial fibrillary acidic protein and acetylcholinesterase histochemistry, respectively. The expression of reelin messenger RNA was also unaffected by entorhinal cortex lesion in the dentate gyrus of young animals (postnatal day seven), where an even stronger sprouting response occurs.

Age Factors↗
PubMed1998

Remodeling of neuronal circuitries in human temporal lobe epilepsy: increased expression of highly polysialylated neural cell adhesion molecule in the hippocampus and the entorhinal cortex.

Neuronal loss and axonal sprouting are the most typical histopathological findings in the hippocampus of patients with drug-refractory temporal lobe epilepsy (TLE). It is under dispute, however, whether remodeling of neuronal circuits is a continuous process or whether it occurs only during epileptogenesis. Also, little is known about the plasticity outside of the hippocampus. We investigated the immunoreactivity of the highly polysialylated neural cell adhesion molecule (PSA-NCAM) in the surgically removed hippocampus and the entorhinal cortex of patients with drug-refractory TLE (n=25) and autopsy controls (n=7). Previous studies have shown that the expression of PSA-NCAM is associated with the induction of synaptic plasticity, neurite outgrowth, neuronal migration, and events requiring remodeling or repair of tissue. In patients with TLE, the optical density (OD) of punctate PSA-NCAM immunoreactivity was increased both in the inner and outer molecular layers of the dentate gyrus, compared with controls. The intensity of PSA-NCAM immunoreactivity in the inner molecular layer correlated with the duration of epilepsy, severity of hippocampal neuronal loss, density of mossy fiber sprouting, and astrogliosis. In TLE patients with only mild neuronal loss in the hippocampus, the density of infragranular immunopositive neurons was increased twofold compared with controls, whereas in TLE patients with severe neuronal loss, the infragranular PSA-NCAM-positive cells were not present. In the hilus, the somata and tortuous dendrites of some surviving neurons were intensely stained in TLE. PSA-NCAM immunoreactivity was also increased in CA1 and in layer II of the rostral entorhinal cortex, where immunopositive neurons were surrounded by PSA-NCAM-positive fibers and puncta. Our data provide evidence that synaptic reorganization is an active process in human drug-refractory TLE. Moreover, remodeling is not limited to the dentate gyrus, but also occurs in the CA1 subfield and the entorhinal cortex.

Adult↗
PubMed1985

Replacement of damaged cortical projections by homotypic transplants of entorhinal cortex.

The extent to which transplants of embryonic cortical tissue can be used to replace damaged cortical projections has been examined. Embryonic entorhinal cortex was implanted into the entorhinal region of young adult rats that had previously received a lesion through the angular bundle. Projections between transplant and host were examined by using WGA-HRP and the fluorescent dye Fast Blue. Implants selectively innervated areas of the host hippocampus and amygdala which normally receive entorhinal afferents. Implants were innervated by cells in the host diagonal band and, in one case, by cells in the contralateral entorhinal and/or presubicular cortex. In most cases, host fibers were differentially distributed within transplants, possibly reflecting an ability of host fibers to recognize and selectively innervate their appropriate targets even though the cellular organization of the implant is different from that present during normal development. These data suggest that homotypic implants of embryonic entorhinal cortex can, in some ways, replace severed cortical projections and may eventually be able to reconstitute normal cortical circuitry.

Amidines↗
PubMed1994

The human entorhinal cortex participates in associative memory.

Animal studies have shown that lesions of the parahippocampal cortex impair learning of visual stimulus-stimulus associations. We tested the hypothesis that recall of paired associates, in contrast to recall of non-associated items, activates the parahippocampal cortex in humans. Ten volunteers had their regional cerebral blood flow measured with positron emission tomography during non-associative recall, and during two conditions with associative recall of visual stimuli. Compared with non-associative recall, associative recall specifically increased the blood flow in a field located in the entorhinal cortex, extending into the presubiculum. Our results demonstrate functional differences between the human hippocampal and parahippocampal cortex, and show that the entorhinal cortex is engaged in associative memory.

Association Learning↗
PubMed1983

Activity and exploratory behavior after lesions of the medial entorhinal cortex in the woodmouse (Apodemus sylvaticus).

The effects of bilateral electrolytic lesions of the entorhinal cortex were studied in male adult woodmice. Experiments were designed to allow separate analysis of the basal activity level and exploratory behavior. Activity recording was conducted in three situations: (a) 24-hr wheel running in the home cage pre- and postoperatively; (b) 24-hr activity composition in a large enclosure over 4 days, 5 to 9 days postoperatively; and (c) sequence and duration of visits in a residential plus maze 11 to 14 days postoperatively. Medial entorhinal cortex lesion involving the para- and presubiculum increased the 24-hr amount of movements in the enclosure (b) without increasing wheel running in any situation (a or b). This lesion also enhanced the locomotor reactivity to being introduced into the plus maze and impaired exploratory behavior. This last effect was equally apparent when the whole situation was new or when part of the familiar maze was modified. Lesioned woodmice did notice the new element but did not show active focalization of their behavior on that element. Data showed that lesion induced hyperactivity and changes of exploratory behavior were not necessarily associated. Novelty detection was performed but it is not clear now on what information this discrimination was based.

Animals↗
PubMed1995

Effects of methysticin on three different models of seizure like events studied in rat hippocampal and entorhinal cortex slices.

Methysticin is one of the constituents of Piper methysticum which possesses anticonvulsant and neuroprotective properties. Its effects on different in vitro seizure models were tested using extracellular recordings in rat temporal cortex slices containing the hippocampus and the entorhinal cortex. Elevating [K+]0 induced seizure-like events with tonic and clonic electrographic phases in area CA1. Lowering [Ca2+]0 caused recurrent seizure like episodes with large negative field potential shifts. Lowering Mg2+ induced short recurrent discharges in area CA3 and CA1 while ictaform events lasting for many seconds were induced in the subiculum, entorhinal and temporal neocortex. In the hippocampus the activity stayed stable over a number of hours. In contrast, the ictaform events in the subiculum, entorhinal and temporal cortex changed their characteristics after one to two hours to late recurrent discharges. In a concentration-range from 10 to 100 microM methysticin reversibly blocked all these types of epileptiform activity. Decreases in [Ca2+]0 and associated slow field potentials evoked by repetitive stimulation of the stratum radiatum or the alveus remained almost unaffected by methysticin. A paired pulse stimulus paradigm used to test for effects of methysticin on synaptically evoked transient field potentials in normal medium revealed interference with mechanisms involved in frequency potentiation. While responses to alvear stimulation were largely unaffected, the responses to a paired pulse stimulus to stratum radiatum were depressed over the whole range of tested stimulus intervals. The findings suggest that methysticin has effects on different patterns of epileptiform activity possibly by interfering with processes responsible for frequency potentiation.

Animals↗