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PubMed1992

Presence of abnormally phosphorylated Tau proteins in the entorhinal cortex of aged non-demented subjects.

An immunoblot study was performed in several cortical samples from non-demented aged controls and compared with those from Alzheimer patients, using antibodies against Tau 55, 64 and 69, which are specific and reliable markers of the neurofibrillary degeneration of the Alzheimer type. The immunodetection of Tau 55, 64 and 69 was positive in all cortical areas from Alzheimer patients, in the entorhinal cortex from each control aged more than 65 but not in cortical samples from younger controls. We demonstrate that the entorhinal cortex is the most vulnerable neuronal population in aging and that the biochemical dysfunctions observed in this area are typically of the 'Alzheimer-type'.

Aged↗
PubMed1993

Ionic mechanisms for the subthreshold oscillations and differential electroresponsiveness of medial entorhinal cortex layer II neurons.

1. Layer II of the medial entorhinal cortex is composed of two electrophysiologically and morphologically distinct types of projection neurons: stellate cells (SCs), which are distinguished by rhythmic subthreshold oscillatory activity, and non-SCs. The ionic mechanisms underlying their differential electroresponsiveness, particularly in the subthreshold range of membrane potentials, were investigated in an "in vitro" slice preparation. 2. In both SCs and non-SCs, the apparent membrane input resistance was markedly voltage dependent, respectively decreasing or increasing at hyperpolarized or subthreshold depolarized potential levels. Thus the neurons displayed inward rectification in the hyperpolarizing and depolarizing range. 3. In the depolarizing range, inward rectification was blocked by tetrodotoxin (TTX, 1 microM) in both types of neurons and thus shown to depend on the presence of a persistent low-threshold Na+ conductance (gNap). However, in the presence of TTX, pronounced outward rectification became manifest in the subthreshold depolarizing range of membrane potentials (positive to -60 mV) in the SCs but not in the non-SCs. 4. The rhythmic subthreshold membrane potential oscillations that were present only in the SCs were abolished by TTX and not by Ca2+ conductance block with Cd2+ or Co2+. Subthreshold oscillations thus rely on the activation of voltage-gated Na+, and not Ca2+, conductances. The Ca2+ conductance block also had no effect on the subthreshold outward rectification. 5. Prominent time-dependent inward rectification in the hyperpolarizing range in the SCs persisted after Na(+)- and Ca2+ conductance block. This rectification was not affected by Ba2+ (1 mM), but was blocked by Cs+ (1-4 mM). Therefore, it is most probably generated by a hyperpolarization-activated cationic current (Q-like current). However, the Q-like current appears to play no major role in the generation of subthreshold rhythmic membrane potential oscillations, because these persisted in the presence of Cs+. 6. On the other hand, in the SCs, the fast, sustained, outward rectification that strongly developed (after Na+ conductance block) at the oscillatory voltage level was not affected by Cs+ but was blocked by Ba2+ (1 mM). Barium was also effective in blocking the subthreshold membrane potential oscillations. 7. In the non-SCs, which do not generate subthreshold rhythmic membrane potential oscillations or manifest subthreshold outward rectification in TTX, Ca2+ conductance block abolished spike repolarization and caused the development of long-lasting Na(+)-dependent plateau potentials at a high suprathreshold voltage level. At this level, where prominent delayed rectification is present, the Na+ plateaus sustained rhythmic membrane potential oscillations.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1992

Ageing of the human entorhinal cortex and subicular complex.

Age-dependent changes in the entorhinal cortex (EC) and subicular complex (SC) were studied in 30 brains of patients who died between 14 and 86 years of age, without CNS impairment, as determined by macro- and microscopic examination. The brains were fixed in 10% formalin and embedded in paraffin. Three series of coronal EC and SC sections (7 microns) were stained by Nissl, PAS or hematoxylin-eosin. Using neuronal count and Kariometry, age-dependent modifications were studied in layers II, III and V of the lateral area of the EC; in the pyramidal layer of the subiculum (S), and in layer II of the presubiculum (PS). All EC layers studied presented a slight (11-20%) although significant reduction up to 35 years, but from 35 to 75 years the decrease was not significant. After 75 years the neuronal loss increased slightly. The nuclear area decreased up to the age of 40-45 years, (10-18%) and augmented from this age up to 75 years (10-14%). During the last period of life, the nuclear area did not change. From 30-60 years, pyramidal layer in the S showed a significant neuronal loss (30%), thereafter, neuronal reduction was less. At early years, the nuclear area decreased insignificantly (15%), and from 35 years up to the most advanced age studied, it increased significantly (13%). In the PS, layer II manifested a cell loss throughout the lifespan (32.9%) and the changes in the nuclear area did not reach statistical significance due to the dispersions of its values.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1983

[Evidence for sensory convergences in rat entorhinal cortex].

Unit neuronal activity was investigated in the Rat lateral entorhinal cortex. Neurons were found which reacted to various sensory stimulations, auditory, visual, somesthetic, gustative and olfactory. This cortex is thus a site of convergence of sensory information which could be relayed further to the hippocampus.

Animals↗
PubMed2000

Selective enhancement of non-NMDA receptor-mediated responses following induction of long-term potentiation in entorhinal cortex.

The contribution of NMDA receptors to the expression of long-term potentiation (LTP) is controversial. In entorhinal cortex (EC) previous studies reported either that LTP was exclusively expressed through NMDA receptors or that both NMDA and non-NMDA receptors were involved in LTP expression. To reexamine this issue, horizontal entorhinal cortical slices were prepared from adult rats and electrical stimulation was delivered in layer II/III, while field potential recordings were made in layer III. In the standard condition (2.5 mM Mg(++)), LTP was reliably induced by theta burst stimulation, but was blocked by 100 microM D-AP5, an NMDA receptor antagonist. This corroborates previous reports that NMDA receptor activation is required for induction of EC LTP. The field potential response was not affected by D-AP5, but completely blocked by 10 microM CNQX, a non-NMDA receptor antagonist. This indicates that the expression of LTP is mediated by non-NMDA receptors in the standard condition. LTP of NMDA receptor-mediated responses was tested by comparing NMDA responses before and after applying theta burst stimulation in medium containing low magnesium (0.4-1 mM). Theta burst stimulation induced 43.2+/-9.7% increase of non-NMDA responses (i.e., AP5-insensitive fast component) but 5.6+/-9.0% decrease of the NMDA receptor component (AP5-sensitive slow component). These results indicate that activation of NMDA receptors is critical for induction of LTP, but LTP expression is mediated by non-NMDA receptors in EC under these experimental conditions.

2-Amino-5-phosphonovalerate↗
PubMed1999

Muscarinic control of intracortical connections to layer II in rat entorhinal cortex slice.

The cholinergic system is critically involved in oscillatory network activity and synaptic plasticity in the entorhinal cortex (EC) hippocampal formation. Here we demonstrate robust inhibition of field potentials in layer II of the medial EC evoked by stimulation in the deep EC or in the lateral layer II by carbachol (CCh, 0.1-100 microM, K(D) approximately 1 microM). This effect appears not to be mediated by suppression of presynaptic Ca(2+)-signals since paired pulse facilitation was increased by CCh. Blockade of the effect by the muscarinic antagonists atropine and pirenzepine demonstrates mediation by muscarinic receptors, most likely of the M1 subtype. The effect is characterized by absence of desensitization and should be important for laminar shaping of oscillatory activity and synaptic plasticity during acetylcholine-dependent theta-rhythmic activity.

Animals↗
PubMed2005

Localization of M2 muscarinic receptor protein in parvalbumin and calretinin containing cells of the adult rat entorhinal cortex using two complementary methods.

We investigated parvalbumin (PV) and calretinin (CR) containing interneurons in the rat entorhinal cortex. RNA amplification following single cell dissection of immunohistochemically labeled cells from layers II to VI revealed that PV cells, in contrast to CR cells, express the m2 muscarinic receptor (M2AchR) protein. Double immunostaining to confirm the results of RNA amplification indicated that the majority of PV cells contain M2AchR protein, whereas only a small proportion of CR cells do. In contrast, a large number of layer I CR cells, which are mostly Cajal-Retzius cells, were positive for M2AchR. RNA amplification following dissection of these cells also revealed that they contain the M2AchR protein. These findings emphasize that there are significant differences in the expression of different proteins, even among similar neuronal types in the same brain region. This highlights the importance of accurately collecting single cells, and knowledge of anatomical details in molecular biological studies.

Animals↗
PubMed2006

Cytoarchitectonic organization of the entorhinal cortex of the canine brain.

The present study describes the cytoarchitectonic and chemoarchitectonic organization of the canine entorhinal cortex (EC). We distinguished medial, laterodorsal, and latero-intermediate subdivisions based on the organization of cortical layers using Nissl and Timm staining and AChE histochemistry. The medial subdivision is located at the border of the parasubiculum and is characterized by a narrow cortex, wide layer II, and densely packed cells in layer V. At its caudal extent, distinct spherical groups of small cells are situated at the border of layer I/II. The laterodorsal subdivision is located along the rhinal sulcus and borders area 35 of the perirhinal cortex. Its cortex is wide and layers tend to merge. Layer II of the laterodorsal subdivision contains scattered "stellate" cells, which are not organized into islands. The latero-intermediate subdivision displays a complex layer organization. The most easily distinguished is layer II, which is comprised of two main cell populations; "stellate" neurons arranged into "islands" and small, round cells distributed within and below the stellate cells. Layer III contains sparse cells that are arranged into vertical clusters, whereas layer IV (lamina dissecans) is especially wide. Nine fields, named according to their rostral to caudal position, were distinguished based on further analyses of layer differentiation. The main features of the rostrocaudal differentiation are a gradual disappearance of "island" organization in layer II, increasing cortical thickness, and wider layers containing small and more densely packed cells. Cytoarchitectonic differentiation was determined by observation of specific histochemical patterns of AChE- and Timm-stained sections.

Amygdala↗
PubMed1998

Comparison of the electrophysiology and morphology of layers III and II neurons of the rat medial entorhinal cortex in vitro.

The basic membrane characteristics of neurons in layers II and III of the medial entorhinal cortex (MEA) were recorded using the intracellular current clamp technique in in vitro slices of the rat brain. Two types of cells were distinguished according to the presence of a time-dependent inward rectification (SAG current) with hyperpolarizing current pulses. The cells in which this inward rectification was not observed (No-SAG cells) had a larger input resistance, a more negative resting membrane potential and a more depolarized firing threshold. They more often displayed a strongly adapting firing pattern, and their action potentials had a slower decay rate and lacked a depolarizing afterpotential, compared with the SAG cells. SAG cells typically had a prominent rebound depolarization at the end of a hyperpolarizing current and membrane potential oscillations (7 Hz) upon subthreshold depolarizations. Cs+ blocked the time-dependent inward rectification. The rebound depolarization persisted, even in the presence of tetrodotoxin. Biocytin labelling showed that layer III consisted mainly of pyramidal-shaped cells. Most layer III cells were of the No-SAG type. All cells in layer II, stellate and pyramidal cells, were classified as SAG cells. We conclude that the cells in MEA layers II and III display different electroresponsiveness, but that this appears to be more related to the layer where they are located than to a specific morphology. As layer III consisted mainly of cells of the No-SAG type, we suggest that layer III cells are less excitable than the SAG type layer II cells.

Animals↗
PubMed2007

Effects of serotonin on the intrinsic membrane properties of layer II medial entorhinal cortex neurons.

Although serotonin (5-HT) is an important neuromodulator in the superficial layers of the medial entorhinal cortex (mEC), there is some disagreement concerning its influences upon the membrane properties of neurons within this region. We performed whole cell recordings of mEC Layer II projection neurons in rat brain slices in order to characterize the intrinsic influences of 5-HT. In current clamp, 5-HT evoked a biphasic response consisting of a moderately short latency and large amplitude hyperpolarization followed by a slowly developing, long lasting, and small amplitude depolarization. Correspondingly, in voltage clamp, 5-HT evoked a robust outward followed by a smaller inward shift of holding current. The outward current evoked by 5-HT showed a consistent current/voltage (I/V) relationship across cells with inward rectification, and demonstrating a reversal potential that was systematically dependent upon the extracellular concentration of K(+), suggesting that it was predominantly carried by potassium ions. However, the inward current showed a less consistent I/V relationship across different cells, suggesting multiple independent ionic mechanisms. The outward current was mediated through activation of 5-HT(1A) receptors via a G-protein dependent mechanism while inward currents were evoked in a 5-HT(1A)-independent fashion. A significant proportion of the inward current was blocked by the I(h) inhibitor ZD7288 and appeared to be due to 5-HT modulation of I(h) as 5-HT shifted the activation curve of I(h) in a depolarizing fashion. Serotonin is thus likely to influence, in a composite fashion, the information processing of Layer II neurons in the mEC and thus, the passage of neocortical information via the perforant pathway to the hippocampus.

8-Hydroxy-2-(di-n-propylamino)tetralin↗
PubMed2003

Kinetic diversity of single-channel burst openings underlying persistent Na(+) current in entorhinal cortex neurons.

The kinetic diversity of burst openings responsible for the persistent Na(+) current (I(NaP)) in entorhinal cortex neurons was examined by separately analyzing single bursts. Although remarkable kinetic variability was observed among bursts in terms of intraburst opening probability and mean open and closed times, the values of time constants describing intraburst open times (tau(o(b))s) and closed times (tau(c(b))s) were distributed around well-defined peaks. At -40 mV, tau(o(b)) peaks were found at approximately 0.34 (tau(o(b))1) and 0.77 (tau(o(b))2) ms, and major tau(c(b)) peaks were found at approximately 0.24 (tau(c(b))1) and 0.54 (tau(c(b))2) ms. In approximately 80% of the bursts two preferential gating modes were found that consisted of a combination of either tau(o(b))1 and tau(c(b))2 ("intraburst mode 1"), or tau(o(b))2 and tau(c(b))1 ("intraburst mode 2"). Individual channels could switch between different gating modalities, but normally tended to maintain a specific gating mode for long periods. Mean burst duration also displayed considerable variability. At least three time constants were found to describe burst duration, and the frequencies at which each of the corresponding "bursting states" occurred varied in different channels. Short-lasting bursting states were preferentially associated with intraburst mode 1, whereas very-long-lasting bursts tended to gate according to mode 2 only or other modes that included considerably longer mean open times. These results show that I(NaP) channels can generate multiple intraburst open and closed states and bursting states, but these different kinetic states tend to combine in definite ways to produce a limited number of prevalent, well-defined gating modalities. Modulation of distinct gating modalities in individual Na(+) channels may be a powerful form of plasticity to influence neuronal excitability and function.

Action Potentials↗
PubMed1991

Senile dementia of the Alzheimer type: is there a correlation between entorhinal cortex and dentate gyrus lesions?

Senile plaques (SP) are one of the neuropathological hallmarks of senile dementia of the Alzheimer type (SDAT). In 14 patients affected with SDAT (over 74 years of age), thioflavine S, Tau and acetylcholinesterase (AChE) stainings demonstrated an increased density of SP in the outer two thirds of the dentate gyrus molecular layer. However, a wide range of SP density was observed among the cases. The molecular layer of the dentate gyrus is one of the termination site of the perforant pathway that originates in layers II and III of the entorhinal cortex. We have found that the number of AChE-, thioflavine S- and Tau-positive SP that accumulate in the dentate gyrus is positively correlated with the density of thioflavine S-stained neurofibrillary tangles in layers II and III of the entorhinal cortex. In contrast, a similar correlation is not found when using Tau immunolabeling of the entorhinal tangles. These observations show an association between the accumulation of AChE-positive SP in the dentate molecular layer and the lesions of the perforant pathway. Furthermore, they suggest that the density of SP in the dentate gyrus correlates with the late stages of neurofibrillary tangles formation (thioflavine S positive), but not with the early stages (Tau positive).

Acetylcholinesterase↗
PubMed2000

Intrinsic and commissural connections within the entorhinal cortex. An anterograde and retrograde tract-tracing study in the cat.

Intrinsic and commissural connections within the entorhinal cortex (EC) were examined in the cat by the anterograde and retrograde tract-tracing methods with Phaseolus vulgaris leucoagglutinin and cholera toxin B subunit. Intrinsic axons to the superficial layers (layers I-III) arose mainly from layers II, III, Vd (deep part of layer V), and VI, were distributed more widely in the superficial layers than in the deep layers, and terminated progressively more densely in more superficial layers; most densely in layer I. In the medial entorhinal area (MEA) and the ventromedial and the ventrolateral divisions of the lateral entorhinal area (VMEA and VLEA), the longitudinal connections through the intrinsic fibers to the superficial layers is often more restricted in rostral direction than in caudal direction. In the dorsolateral division of the lateral EC (DLEA), the longitudinal connections through the intrinsic fibers to the superficial layers extended distantly in both rostral and caudal directions. Intrinsic fibers to the deep layers (layers IV-VI) originated mainly from layers IV and Vs (superficial part of layer V) and were distributed rather sparsely and diffusely; they were distributed more widely in the deep layers than in the superficial layers. Commissural axons to the homotopic EC regions originated from layers II and III of the MEA and DLEA and terminated in all EC layers, most densely in layer I.

Animals↗
PubMed1998

Dopamine suppresses stimulus-induced field potentials in layer III of rat medial entorhinal cortex.

We studied the effect of dopamine (DA) on field potential responses in layer III of the medial entorhinal cortex (mEC) evoked by synaptic stimulation of superficial layers of the lateral EC either by single or paired-pulses. The maximum amplitude of the field response was reduced to 50.6+/-2.6% by DA (500 microM) bath-applied for 5 min. Both the D1 antagonist SCH 23390 (20 microM) and the D2 antagonist sulpiride (20-50 microM) reduced the effect of DA to the same extent, namely 18% less reduction in their presence. The D2 agonist quinelorane (500 microM) reduced the field response to 75+/-4.0%, whereas the D1 agonist SKF38393 was without significant effect. The paired-pulse ratio increased significantly during DA application. These results suggest predominant D2 receptor involvement in the decrement of synaptic transmission in layer III by dopamine. Paired-pulse experiments may be indicative of a presynaptic mechanism of action.

Action Potentials↗
PubMed2000

The effects of combined lesions of the subicular complex and the entorhinal cortex on two forms of spatial navigation in the water maze.

The role of the subicular complex and entorhinal cortex (SUB-EC) in spatial learning was examined in 2 water maze experiments. In Experiment 1, rats had to locate a hidden platform that was always a fixed distance and direction from an intramaze landmark. Each day, the landmark and platform were moved to a new location. Both control and SUB-EC-lesioned rats learned to locate the platform equally readily during training. However, the control group was impaired in locating the platform when the visual extramaze cues were concealed, whereas the lesioned group was unaffected by this manipulation. In Experiment 2, the lesioned rats were impaired in finding a hidden platform that was in a fixed place in the water maze and showed no evidence of having learned its location in a probe test. These results suggest that damage to the SUB-EC impairs the integration of geometric information but spares a more general navigational-directional strategy.

Animals↗
PubMed1994

Noradrenaline reduces synaptic responses in normal and tottering mouse entorhinal cortex via alpha 2 receptors.

The effects of noradrenaline (NA) on synaptic responses in layer II of the entorhinal cortex (EC) were studied in normal and spontaneously epileptic mutant mice tottering using intracellular recording in a slice preparation. Neither the membrane properties of neurones nor the responses to NA differed between normal and tottering mice. NA (50 microM) hyperpolarized most (29/54) of the neurones via alpha 2 adrenergic receptors. Synaptic responses of EC neurones were complex. NA (10-100 microM) reduced all the components of the synaptic response in a concentration-dependent and reversible manner. The pharmacological properties of the inhibitory effect of NA were characterised and quantified on one component of the complex synaptic response, the fast excitatory postsynaptic potential. The effect of NA was mimicked by the alpha 2 agonist UK 14,304 and blocked by the alpha 2 antagonist yohimbine. It is concluded that NA can inhibit via an alpha 2 receptor-mediated action synaptic responses in the superficial layers of the EC.

Adrenergic alpha-2 Receptor Agonists↗
PubMed2006

Lesion of the lateral entorhinal cortex amplifies odor-induced expression of c-fos, junB, and zif 268 mRNA in rat brain.

Paradoxical facilitation of olfactory learning following entorhinal cortex (EC) lesion has been described, which may result from widespread functional alterations taking place within the olfactory system. To test this hypothesis, expression of the immediate early genes c-fos, junB, and zif 268 was studied in response to an olfactory stimulation in several brain areas in control and in EC-lesioned rats. Olfactory stimulation in control rats induced the expression of the three genes in the granular/mitral and glomerular layers of the olfactory bulb, as well as c-fos and junB expression in the piriform cortex. However EC lesion was devoid of effects in nonstimulated animals; it significantly amplified the odor-induced expression of the three genes in these areas, as well as in the amygdala, hippocampus, and parietal-temporal cortices. The data suggest that EC lesion modifies the neural processing of odor by suppressing an inhibitory influence on brain areas connected to this cortex.

Amygdala↗