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PubMed2000

Usefulness of MRI measures of entorhinal cortex versus hippocampus in AD.

OBJECTIVE: MRI-based measurements of hippocampal atrophy are a sensitive indicator of the early pathologic degeneration of the medial temporal lobe in AD. However, AD pathology appears first in the transentorhinal/entorhinal cortex, not the hippocampus. The authors tested the hypothesis that MRI-based measurements of the entorhinal cortex are more sensitive than measurements of hippocampal volume in discriminating among three clinical groups; controls, patients with a mild cognitive impairment (MCI), and patients with mild probable AD. METHODS: The authors studied 30 controls, 30 patients with MCI, and 30 patients with AD who were matched among clinical groups on age, gender, and education. All underwent a standardized MRI protocol from which the authors made measurements of hippocampal volume, entorhinal cortex volume, and the cumulative length of the medial border of the entorhinal cortex. RESULTS: Pairwise intergroup differences (p < 0.01) were found for all MRI measurements with the exception of the cumulative length of the entorhinal cortex, which did not differentiate controls from MCI patients. Whereas the hippocampal and entorhinal cortex volume measurements provided slightly better intergroup discrimination than the entorhinal distance measurement, overall differences in discriminating ability among the three MRI measurements were minor. CONCLUSIONS: Despite the theoretical rationale for the superiority of entorhinal measurements in early AD, the authors found MRI measurements of the hippocampus and entorhinal cortex were approximately equivalent at intergroup discrimination. Measurements of the hippocampus may be preferable because MRI depiction of the boundaries of the entorhinal cortex can be obscured by anatomic ambiguity, image artifact, or both.

Aged↗
PubMed2000

Olfactory inputs activate the medial entorhinal cortex via the hippocampus.

The lateral and medial regions of the entorhinal cortex differ substantially in terms of connectivity and pattern of activation. With regard to olfactory input, a detailed and extensive physiological map of the olfactory projection to the entorhinal cortex is missing, even if anatomic studies suggest that the olfactory afferents are confined to the lateral and rostral entorhinal region. We studied the contribution of the medial and lateral entorhinal areas to olfactory processing by analyzing the responses induced by lateral olfactory tract stimulation in different entorhinal subfields of the in vitro isolated guinea pig brain. The pattern of synaptic activation of the medial and lateral entorhinal regions was reconstructed either by performing simultaneous multisite recordings or by applying current source density analysis on field potential laminar profiles obtained with 16-channel silicon probes. Current source density analysis demonstrated the existence of a direct monosynaptic olfactory input into the superficial 300 microm of the most rostral part of the lateral entorhinal cortex exclusively, whereas disynaptic sinks mediated by associative fibers arising from the piriform cortex were observed at 100-350 microm depth in the entire lateral aspect of the cortex. No local field responses were recorded in the medial entorhinal region unless a large population spike was generated in the hippocampus (dentate gyrus and CA1 region) by a stimulus 3-5x the intensity necessary to obtain a maximal monosynaptic response in the piriform cortex. In these conditions, a late sink was recorded at a depth of 600-1000 microm in the medial entorhinal area (layers III-V) 10.6 +/- 0.9 (SD) msec after a population spike was simultaneously recorded in CA1. Diffuse activation of the medial entorhinal region was also obtained by repetitive low-intensity stimulation of the lateral olfactory tract at 2-8 Hz. Higher or lower stimulation frequencies did not induce hippocampal-medial entorhinal cortex activation. These results suggest that the medial and the lateral entorhinal regions have substantially different roles in processing olfactory sensory inputs.

Action Potentials↗
PubMed1999

Carbachol induces fast oscillations in the medial but not in the lateral entorhinal cortex of the isolated guinea pig brain.

Fast oscillations at 25-80 Hz (gamma activity) have been proposed to play a role in attention-related mechanisms and synaptic plasticity in cortical structures. Recently, it has been demonstrated that the preservation of the entorhinal cortex is necessary to maintain gamma oscillations in the hippocampus. Because gamma activity can be reproduced in vitro by cholinergic activation, this study examined the characteristics of gamma oscillations induced by arterial perfusion or local intracortical injections of carbachol in the entorhinal cortex of the in vitro isolated guinea pig brain preparation. Shortly after carbachol administration, fast oscillatory activity at 25.2-28.2 Hz was observed in the medial but not in the lateral entorhinal cortex. Such activity was transiently associated with oscillations in the theta range that showed a variable pattern of distribution in the entorhinal cortex. No oscillatory activity was observed when carbachol was injected in the lateral entorhinal cortex. Gamma activity in the medial entorhinal cortex showed a phase reversal at 200-400 microm, had maximal amplitude at 400-500 microm depth, and was abolished by arterial perfusion of atropine (5 microM). Local carbachol application in the medial entorhinal cortex induced gamma oscillations in the hippocampus, whereas no oscillations were observed in the amygdala and in the piriform, periamygdaloid, and perirhinal cortices ipsilateral and contralateral to the carbachol injection. Hippocampal oscillations had higher frequency than the gamma activity recorded in the entorhinal cortex, suggesting the presence of independent generators in the two structures. The selective ability of the medial but not the lateral entorhinal cortex to generate gamma activity in response to cholinergic activation suggests a differential mode of signal processing in entorhinal cortex subregions.

Animals↗
PubMed1999

Hippocampal and entorhinal cortex atrophy in frontotemporal dementia and Alzheimer's disease.

OBJECTIVE: To describe atrophic changes of the hippocampus and entorhinal cortex in frontotemporal dementia (FTD) and compare them with those of AD. BACKGROUND: The medial temporal lobe shows atrophic changes early in the course of AD, but whether these changes are specific to AD or occur in other degenerative dementias, and to what extent, is unclear. METHODS: The authors measured the volumes of the left and right hippocampus and entorhinal cortex from MR images (1.5 T, 2-mm-thick slices) in 12 patients with FTD, 30 with AD, and 30 elderly control subjects. RESULTS: In FTD patients, the left and right hippocampus (16% and 21% tissue loss) and the entorhinal cortex (28% and 27% loss) were more atrophic than the control subjects. Atrophy of the hippocampus in FTD was less severe than in AD, but atrophy of the entorhinal cortex was equally severe. Greater hippocampal and entorhinal cortex atrophy was present in the most severe patients in both groups (as high as a 49% tissue loss). The sensitivity of the hippocampus and the entorhinal cortex to discriminate FTD patients from control subjects was low (49% and 52%, respectively; specificity set at 90%), whereas hippocampal volumes could better differentiate AD patients from control subjects (80% sensitivity). CONCLUSIONS: At variance with AD, detectable in vivo atrophy of the hippocampus might not be an early event in FTD. Differential patterns of atrophy might help in the diagnostic process of the degenerative dementias.

Age Factors↗
PubMed2000

Responses of rat subicular neurons to convergent stimulation of lateral entorhinal cortex and CA1 in vivo.

There has been little electrophysiological examination of the afferent projection from lateral entorhinal cortex to dorsal subiculum. Here we provide evidence that synaptic inputs from lateral entorhinal cortex and CA1 converge onto single dorsal subicular neurons in vivo. Subicular responses to CA1 stimulation consisted of excitation and/or long-duration inhibition. Neurons excited by CA1 activation usually showed inhibition to entorhinal stimulation. The latter inhibition was usually of short duration, however, long duration inhibition was seen in a significant proportion of responses. Entorhinal stimulation produced excitatory responses in four bursting cells and it was these cells that also tended to show the longest inhibition. Only bursting cells could be driven antidromically by entorhinal stimulation. Biocytin-filled multipolar and pyramidal cells displayed excitation-inhibition sequences to CA1 and inhibition to entorhinal stimulation. These data strongly suggest that subicular inhibitory neurons receive excitatory input from CA1 and display mutual inhibition. The source of entorhinal-evoked inhibition is less clear. The relative sparseness of observed entorhinal-evoked responses suggests that the input to dorsal subiculum from any one part of lateral entorhinal cortex is spatially restricted. These data show that excitation-inhibition sequences can be seen in subicular pyramidal and multipolar cells and that single subicular neurons receive convergent inputs from CA1 and entorhinal cortex. We show for the first time that bursting cells can be driven both orthodromically and antidromically by direct entorhinal stimulation. These data support the existence of a reciprocal excitatory connection between lateral entorhinal cortex and dorsal subiculum and suggest further that this connection may involve only bursting subicular neurons.

Action Potentials↗
PubMed1990

Effects of MK-801 upon local cerebral glucose utilisation in conscious rats following unilateral lesion of caudal entorhinal cortex.

Local cerebral glucose utilisation was examined in 62 discrete regions of conscious rats following unilateral ibotenic acid lesion of the caudal entorhinal cortex, and subsequent pharmacological challenge with (+)-5-methyl-10,11-dihydro-5H-dibenzo[a,d]cyclohepten-5,10-imine maleate (MK-801), a non-competitive N-methyl-D-aspartate (NMDA) receptor antagonist. Fourteen days after unilateral lesion of the entorhinal cortex, there were no significant alterations in local cerebral glucose use except within the lesioned entorhinal cortex (reduced by 31% compared to sham-operated control animals). In sham-operated animals, systemic administration of MK-801 (0.5 mg/kg, i.v.) induced anatomically organised alterations in glucose use with increases in olfactory areas, subicular complex and some limbic areas (posterior cingulate cortex, mammillary body and anteroventral thalamic nucleus), and decreases in the inferior colliculus and neocortex (auditory, sensory-motor, somatosensory and frontal cortices). In animals with unilateral entorhinal cortex lesions, the metabolic response to MK-801 differed significantly from the response to the drug in sham-lesioned animals in a number of regions, viz. hippocampus, molecular layer (ipsilateral to lesion), entorhinal cortex (ipsilateral), dentate gyrus (ipsilateral), presubiculum (bilateral), parasubiculum (bilateral) and nucleus accumbens (bilateral). The ability of MK-801 to reduce glucose use in the neocortex was not altered by entorhinal cortex lesion. These data suggest that the functional consequences of non-competitive NMDA receptor blockade are dependent in some areas upon the integrity of the perforant pathway from the entorhinal cortex to the hippocampus.

Animals↗
PubMed1994

Regulation of 1,4,5-IP3, 1,3,4,5-IP4 and IP6 binding sites following entorhinal cortex lesions in rat brain.

A lesion of the entorhinal cortex produces a loss of more than 80% of the synapses in the outer molecular layer of the hippocampus in the rat. However, this synaptic loss is transient. Beginning a few days after denervation, new synapses are formed, virtually replacing the lost inputs within two months. Synaptic remodelling induced by entorhinal cortex lesion is associated with specific modifications of various neurotransmitters, hormones and growth factors. Many of these substances act at membrane bound-receptors to induce the hydrolysis of phosphatidylinositols generating various inositol phosphates. Some of the key members of this family include inositol 1,4,5-trisphosphate, inositol 1,3,4,5-tetrakisphosphate and inositol hexakisphosphate which are all associated with the maintenance Ca2+ homeostasis. To investigate the potential roles and/or alterations of inositol phosphates in entorhinal cortex lesions-induced neuronal plasticity, we quantified specific receptor sites for inositol 1,4,5-trisphosphate, inositol 1,3,4,5-tetrakisphosphate and inositol hexakisphosphate using their respective tritiated ligands, at different periods post-lesion corresponding to the degenerative and subsequent reinnervation phases. [3H]inositol 1,4,5-trisphosphate binding sites are maximally increased (30%) between two and eight days post-lesion in the hippocampal formation on both sides of the lesion. In the cortex, [3H]inositol 1,4,5-trisphosphate binding increased also bilaterally following the lesion. Changes in [3H]inositol 1,3,4,5-tetrakisphosphate binding are delayed and reduced (20% increase) in magnitude compared to these seen for [3H]inositol 1,4,5-trisphosphate binding. The maximal peak in [3H]inositol 1,3,4,5-tetrakisphosphate binding is observed between eight and 14 days after the lesion in the hippocampal formation and the cortex.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2005

Independent accumulations of tau and amyloid beta-protein in the human entorhinal cortex.

BACKGROUND: Previous studies have repeatedly described that neurofibrillary tangles arise earlier than senile plaques (SPs) in the entorhinal cortex, but one study suggested that SPs, if present, enhance the former lesions. All of these studies were performed at the histologic or immunocytochemical level, which may not accurately reflect the actual levels of amyloid beta-protein (Abeta) and tau. OBJECTIVE: To determine whether there is significant interaction between Abeta and tau in the human entorhinal cortex with regard to the Braak stage. METHODS: Biochemical studies were conducted on 50 brains from elderly people, who were mainly at Braak stages I to III. All the cases were examined neuropathologically and staged according to Braak and Braak. A small piece of brain tissue for each case was dissected from the anterior portion of the right entorhinal cortex. The amounts of tau and Abeta in the insoluble fraction of the tissue were quantified using western blotting. RESULTS: The levels of tau and possibly Abeta42 in the entorhinal cortex appeared to rise steeply at approximately age 75. The levels of insoluble tau increased as the Braak stage increased from I to II; however, it had a tendency to remain between stages II and III. The levels of Abeta42 showed a small increase, whereas those of Abeta40 increased continuously as the Braak stage advanced. In contrast, the extent of Abeta42 accumulation increased with increasing Braak stage for SPs. There was no significant correlation between the levels of insoluble tau and Abeta42 in the entorhinal cortex. Even if Abeta did not accumulate to significant extents, substantial accumulation of insoluble tau occurred. CONCLUSION: Accumulations of tau and amyloid beta-protein occur independently in the human entorhinal cortex.

Aged↗
PubMed1997

Projections of the lateral entorhinal cortex to the amygdala: a Phaseolus vulgaris leucoagglutinin study in the rat.

In addition to providing a gateway to the hippocampus, the entorhinal cortex has significant projections to the amygdala. In the present investigation, the organization of the projections of the lateral entorhinal cortex to the amygdala was studied in the rat using the sensitive anterograde tracer Phaseolus vulgaris leucoagglutinin. Each of the three main subdivisions of the lateral entorhinal cortex provided a characteristic projection to the amygdala that mainly arose from the deep cortical layers. The projections from the dorsolateral and ventrolateral entorhinal areas were much stronger than those arising from the ventromedial entorhinal area. The primary targets of the dorsolateral and ventrolateral entorhinal areas were the basolateral amygdala, lateral capsular subdivision of the central nucleus and caudal portions of the cortical nuclear complex. The dorsolateral entorhinal area projects mainly to the lateral part of the basal nucleus, while the ventrolateral entorhinal area projects mainly to its medial part. A transitional region at the rostral pole of the ventrolateral entorhinal cortex has additional strong projections to the lateral subdivision of the central nucleus, medial amygdaloid nucleus and the intra-amygdaloid portion of the bed nucleus of the stria terminalis. The results of the present study indicate that the amygdala is one of the principal targets of the entorhinal cortex. The correspondence between the topography of entorhino-hippocampal connections and entorhino-amygdaloid connections suggests that the amygdaloid projection arising in each of the three main subdivisions of the entorhinal cortex conveys information processed in different septotemporal portions of the hippocampal formation. These entorhinal projections, which probably convey complex relational (including contextual) information to the amygdala, are in a position to produce different behavioral responses by activating different portions of the amygdaloid nuclear complex.

Amygdala↗
PubMed1977

Synaptic replacement in the dentate gyrus after unilateral entorhinal lesion: electron microscopic analysis of the extent of replacement of synapses by the remaining entorhinal cortex.

In response to a unilateral entorhinal lesion the input from the contralateral entorhinal cortex to the dentate gyrus appears to increase. We have studied this crossed projection by electron microscopy in normal animals and in animals one year or more after a unilateral entorhinal lesion. In normal animals few degenerating boutons are found after a contralateral entorhinal lesion. However, when the contralateral lesion was made one year after an ipsilateral entorhinal lesion, degenerating boutons were readily identified. The boutons were relatively few in number, but formed an abnormally large number of synaptic contacts. These results support the previous conclusion that fibres from the contralateral entorhinal cortex form additional synapses when their ipsilateral homologues are removed. However, these new cortical synapses probably account for only a small portion of those formed in response to the lesion. Thus an anatomically homologous input does not, in this case, selectively capture most of the newly available synaptic sites.

Animals↗
PubMed1993

Gender-specific impairment on Morris water maze task after entorhinal cortex lesion.

After unilateral entorhinal cortex lesion, deficits on a working spatial memory Morris water maze task were examined in male and female rats to determine if gender differences exist in response to hippocampal deafferentation. Brain-damaged males showed a persistent water maze deficit that persisted throughout the 10 days of testing. Brain-damaged females did not. The performance of the injured females was only slightly impaired relative to sham males and females, and was significantly better than males with EC damage. This lack of a water maze deficit in lesion females is hypothesized to be due either to gender differences in sprouting responses or to a more flexible use of multiple cues by females relative to males.

Animals↗
PubMed1995

Morphology and kainate-receptor immunoreactivity of identified neurons within the entorhinal cortex projecting to superior temporal sulcus in the cynomolgus monkey.

Projections of the entorhinal cortex to the hippocampus are well known from the classical studies of Cajal (Ramon y Cajal, 1904) and Lorente de Nó (1933). Projections from the entorhinal cortex to neocortical areas are less well understood. Such connectivity is likely to underlie the consolidation of long-term declarative memory in neocortical sites. In the present study, a projection arising in layer V of the entorhinal cortex and terminating in a polymodal association area of the superior temporal gyrus has been identified with the use of retrograde tracing. The dendritic arbors of neurons giving rise to this projection were further investigated by cell filling and confocal microscopy with computer reconstruction. This analysis demonstrated that the dendritic arbor of identified projection neurons was largely confined to layer V, with the exception of a solitary, simple apical dendrite occasionally ascending to superficial laminae but often confined to the lamina dissecans (layer IV). Finally, immunoreactivity for glutamate-receptor subunit proteins GluR 5/6/7 of the dendritic arbor of identified entorhinal projection neurons was examined. The solitary apical dendrite of identified entorhinal projection neurons was prominently immunolabeled for GluR 5/6/7, as was the dendritic arbor of basilar dendrites of these neurons. The restriction of the large bulk of the dendritic arbor of identified entorhinal projection neurons to layer V implies that these neurons are likely to be heavily influenced by hippocampal output arriving in the deep layers of the entorhinal cortex. Immunoreactivity for GluR 5/6/7 throughout the dendritic arbor of such neurons indicates that this class of glutamate receptor is in a position to play a prominent role in mediating excitatory neurotransmission within hippocampal-entorhinal circuits.

Amidines↗
PubMed2003

Stereologic evidence for persistence of viable neurons in layer II of the entorhinal cortex and the CA1 field in Alzheimer disease.

The entorhinal cortex and hippocampus are the first cortical regions to be affected by the degenerative cellular process that leads to Alzheimer disease (AD) and display a limited degree of neuronal alterations in normal aging. Several quantitative studies have reported a substantial loss of neurons in these regions and a parallel increase in the number of neurofibrillary tangles (NFTs). However, accurate quantitative data on the dynamics of NFT formation are lacking. Here, we performed a stereologic assessment of the proportions of intracellular and extracellular (ghost) NFTs (iNFTs and eNFTs, respectively) and unaffected neurons in layer II of the entorhinal cortex and in the pyramidal cell layer of the CA1 field of the hippocampus in elderly control cases compared to cases with varying degrees of cognitive dysfunction. The data revealed differential rates of formation of iNFTs and eNFTs between the 2 regions and confirmed the presence of a severe disease-associated, but not age-related, neuronal loss. They also revealed that large numbers of neurons may persist either unaffected or in a transitional stage of NFT formation until the late stages of AD progression. 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. Whereas it is not possible in the present study to assess how functional such neurons with altered physiology might be, it is nonetheless likely that these transitional neurons open new options for potential therapeutic interventions aimed at protecting neurons vulnerable to neurofibrillary degeneration.

Aged↗
PubMedDate not supplied

Species differences in the projections from the entorhinal cortex to the hippocampus.

Both differences and similarities exist between mammalian species in the projections from entorhinal cortex to the hippocampal formation. In most species, layer II cells of the entorhinal cortex project to the dentate gyrus, and they terminate in the outer two-thirds of the molecular layer of the dentate gyrus. The axons from layer III cells project bilaterally to areas CA(1) and CA(3) of the hippocampus, terminating in the stratum lacunosum moleculare. We have analyzed these projections in mice, and in general, the entorhinal cortex-to-hippocampus projections are similar to those in rats. Axons from layer II neurons terminate in the outer and middle thirds of the molecular layer of the dentate gyrus, and axons from layer III neurons terminate bilaterally in the stratum lacunosum moleculare of areas CA(1) and CA(3), and in the molecular layer of the subiculum. However, in contrast to rat, mouse entorhinal cortex neurons do not appreciably project to the contralateral dentate gyrus. Most species, including mice, show a similar topographical organization of the entorhinal-hippocampal projections, with neurons in the lateral part of both the lateral and medial entorhinal cortex projecting to the dorsal part or septal pole of the hippocampus, whereas the projection to the ventral hippocampus originates primarily from neurons in medial parts of the entorhinal cortex.

Animals↗
PubMed2004

Input from the presubiculum to dendrites of layer-V neurons of the medial entorhinal cortex of the rat.

The entorhinal cortex (EC) and the hippocampus are reciprocally connected. Neurons in the superficial layers of EC project to the hippocampus, whereas deep entorhinal layers receive return connections. In the deep layers of EC, pyramidal neurons in layer V possess apical dendrites that ascend towards the cortical surface through layers IIII and II. These dendrites ramify in layer I. By way of their apical dendrites, such layer-V pyramidal cells may be exposed to input destined for the superficial entorhinal neurons. A specific and dense fiber projection that typically ends in superficial entorhinal layers of the medial EC originates in the presubiculum. To investigate whether apical dendrites of deep entorhinal pyramidal neurons indeed receive input from this projection, we injected the anterograde tracer PHA-L in the presubiculum or we lesioned the presubiculum, and we applied in the same experiments the tracer Neurobiotin trade mark pericellularly in layer V of the medial EC of 17 rats. PHA-L labeled presubiculum axons in the superficial layers apposing apical segments of Neurobiotin labeled layer-V cell dendrites were studied with a confocal fluorescence laserscanning microscope. Axons and dendrites were 3D reconstructed from series of confocal images. In cases in which the presubiculum had been lesioned, material was investigated in the electron microscope. At the confocal fluorescence microscope level we found numerous close contacts, i.e. appositions of boutons on labeled presubiculum fibers with identified dendrites of layer-V neurons. In the electron microscope we observed synapses between degenerating axon terminals and spines on dendrites belonging to layer-V neurons. Hence we conclude that layer-V neurons receive synaptic contacts from presubiculum neurons. These findings indicate that entorhinal layer-V neurons have access to information destined for the superficial layers and eventually the hippocampal formation. At the same time, they have access to the hippocampally processed version of that information.

Animals↗
PubMed2002

Morphological and electrophysiological characteristics of layer V neurons of the rat lateral entorhinal cortex.

The intrinsic electrophysiological and morphological properties of lateral entorhinal area (LEA) layer V neurons were investigated by sharp electrode intracellular recording and biocytin labeling in vitro. The morphological analysis revealed that layer V of the LEA contains three distinct subtypes of principal neurons, which were classified as pyramidal, horizontal, and polymorphic neurons. Pyramidal cells were the most abundant subtype (57%) and could be further subdivided into neurons with large, small, and star-like somas. Similarly to pyramidal cells, horizontal neurons (11%) had a prominent apical dendrite. However, their distinctive basal dendritic plexus extended primarily in the horizontal plane. Polymorphic neurons (32%) were characterized by a multipolar dendritic organization. Electrophysiological analysis of neurons in the three categories demonstrated a diversity of electrophysiological profiles within each category and no significant differences between groups. Neurons in the three subgroups could display instantaneous and/or time-dependent inward rectification and different degrees of spike frequency adaptation. None of the recorded cells displayed an intrinsic oscillatory bursting discharge. Many neurons in the three subgroups, however, displayed slow (3.5-14 Hz), sustained, subthreshold membrane potential oscillations. The morphological and electrophysiological diversity of principal neurons in the LEA parallels that previously reported for the medial entorhinal area and suggests that, with respect to the deep layers, similar information processing is performed across the mediolateral extent of the entorhinal cortex. Layer V of the entorhinal cortex may undertake very complex operations beyond acting as a relay station of hippocampal processed information to the neocortex.

Action Potentials↗
PubMed1994

Glial beta-amyloid precursor protein: expression in the dentate gyrus after entorhinal cortex lesion.

Stereotactic lesioning of the rat entorhinal cortex leads to an induction of beta-amyloid precursor protein (APP) immunoreactivity in non-neuronal cells of the deafferented dentate gyrus. Double immunofluorescence against APP and the microglia-binding isolectin B4 from Griffonia simplicifolia revealed that APP immunoreactivity was confined to activated microglia. The microglial APP expression became detectable 3 days after lesioning, reached its peak after 7 days and disappeared after 10 days. The early accumulation of APP in microglia supports the view that microglia play an important role in the initial stages of amyloid plaque formation. Such a glial APP accumulation occurs rapidly in distant but anatomically connected areas. This is in line with the preferential localization of amyloid plaques in the dentate gyrus, which is the projection field of the degenerating neurones of the entorhinal cortex in patients with developing dementia.

Amyloid beta-Protein Precursor↗
PubMed2007

Contributions of Ih to feature selectivity in layer II stellate cells of the entorhinal cortex.

Abstract Stellate cells (SCs) of the entorhinal cortex generate prominent subthreshold oscillations that are believed to be important contributors to the hippocampal theta rhythm. The slow inward rectifier Ih is expressed prominently in SCs and has been suggested to be a dominant factor in their integrative properties. We studied the input-output relationships in stellate cells (SCs) of the entorhinal cortex, both in control conditions and in the presence of the Ih antagonist ZD7288. Our results show that Ih is responsible for SCs' subthreshold resonance, and contributes to enhanced spiking reliability to theta-rich stimuli. However, SCs still exhibit other traits of rhythmicity, such as subthreshold oscillations, under Ih blockade. To clarify the effects of Ih on SC spiking, we used a generalized form of principal component analysis to show that SCs select particular features with relevant temporal signatures from stimuli. The spike-selected mix of those features varies with the frequency content of the stimulus, emphasizing the inherent nonlinearity of SC responses. A number of controls confirmed that this selectivity represents a stimulus-induced change in the cellular input-output relationship rather than an artifact of the analysis technique. Sensitivity to slow features remained statistically significant in ZD7288. However, with Ih blocked, slow stimulus features were less predictive of spikes and spikes conveyed less information about the stimulus over long time scales. Together, these results suggest that Ih is an important contributor to the input-output relationships expressed by SCs, but that other factors in SCs also contribute to subthreshold oscillations and nonlinear selectivity to slow features.

Action Potentials↗