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PubMed1998

Entorhinal cortex and fimbria-fornix role in rat's passive avoidance response memorization.

The stereotaxic administration of tetrodotoxin (TTX) was employed to induce the fully reversible inactivation of the fimbria-fornix complex (FF) and of the entorhinal cortex (EC), in order to ascertain the role of these structures in the memorization of a passive avoidance response (PAR). On permanently cannulated rats TTX (5 ng in 0.5 microliter saline) or saline (0.5 microliter) was injected uni- or bilaterally, respectively, in the FF and in the EC, 60 min before PAR acquisition, immediately after PAR acquisition and 60 min before PAR retrieval, always performed 48 h after the acquisition trial. It was shown that EC unilateral or bilateral pre-acquisition inactivation was followed by amnesia, while TTX inactivation in post-acquisition and pre-retrieval had no effects. Identical results were obtained by TTX administration in FF. The experimental evidence indicates that both EC and FF play a role during acquisition of PAR engram. The results are discussed in comparison with previous ones concerning dorsal and ventral hippocampus TTX inactivation effects on rat's PAR, and in relation to hippocampal and medial septal area connectivity.

Animals↗
PubMedDate not supplied

Comparisons between global and focal brain atrophy rates in normal aging and Alzheimer disease: Boundary Shift Integral versus tracing of the entorhinal cortex and hippocampus.

The objectives of this study were to (1) compare atrophy rates associated with normal aging and Alzheimer disease (AD) using the semi-automated Boundary Shift Integral (BSI) method and manual tracing of the entorhinal cortex (ERC) and hippocampus and (2) calculate power of BSI vs. ERC and hippocampal volume changes for clinical trials in AD. We quantified whole brain and ventricular BSI atrophy rates and ERC and hippocampal atrophy rates from longitudinal MRI data in 20 AD patients and 22 age-matched healthy controls. All methods revealed significant brain atrophy in controls and AD patients. AD patients had approximately 2.5 times greater whole brain BSI atrophy rates and more than 5 times greater ERC and hippocampal atrophy rates than controls. ERC and hippocampal atrophy rates were higher in both groups than whole brain BSI atrophy rates, but lower than ventricular BSI atrophy rates. Effect size and power calculations suggest that ERC and hippocampal measurements may be more sensitive than ventricular or whole brain BSI for detecting AD progression and the potential effects of disease modifying agents. Logistic regression analysis revealed that combined rates of ERC and ventricular BSI were the best explanatory variables for classifying AD from controls.

Aged↗
PubMed2005

Effect of apolipoprotein E deficiency on reactive sprouting in the dentate gyrus of the hippocampus following entorhinal cortex lesion: role of the astroglial response.

This study investigated the effect of apolipoporotein E (apoE) deficiency on hippocampal reactive sprouting responses of the septohippocampal cholinergic (SHC) and commissural/associational fibers (C/A) following an electrolytic lesion of the entorhinal cortex (ECL), using apoE knockout (apoEKO) and age-matched control wild-type mice. Based on recent evidence suggesting that apoE plays a role in the modulation of glial inflammation, we also tested the hypothesis that the pattern of the astroglial response to ECL might be related to the defective reinnervation previously reported in apoEKO mice. Consistent with our hypothesis, we report a differential pattern of astroglial response that concurred with impairments in the sprouting of the SHC and corresponding synaptic replacement in apoEKO mice at 14 and 30 days post-lesion (DPL), a time range covering the onset of axonal/terminal sprouting to synaptogenesis. We also report a limited sprouting of the C/A fiber system in apoEKO relative to control mice at 30 DPL, a period of active dendritic remodeling. The results of the present study confirm and extend previous findings that apoEKO mice display impaired regenerative capacity in response to ECL and argue that in addition to the effect of apoE on lipid trafficking, apoE may also influence the astroglial response to damage, and that both of these effects account for the defective reinnervation observed in apoEKO mice.

Animals↗
PubMed2004

Hippocampus and entorhinal cortex in mild cognitive impairment and early AD.

Magnetic resonance imaging (MRI) has been suggested as a useful tool in early diagnosis of Alzheimer's disease (AD). Based on MRI-derived volumes, we studied the hippocampus and entorhinal cortex (ERC) in 59 controls, 65 individuals with mild cognitive impairment (MCI) and 48 patients with AD. The controls and individuals with MCI were derived from population-based cohorts. Volumes of the hippocampus and ERC were significantly reduced in the following order: control > MCI > AD. Stepwise discriminant function analysis showed that the most efficient overall classification between controls and individuals with MCI subjects was achieved with ERC measurements (65.9%). However, the best overall classification between controls and AD patients (90.7%), and between individuals with MCI and AD patients (82.3%) was achieved with hippocampal volumes. Our results suggest that the ERC atrophy precedes hippocampal atrophy in AD. The ERC volume loss is dominant over the hippocampal volume loss in MCI, whereas more pronounced hippocampal volume loss appears in mild AD.

Aged↗
PubMed2005

Microstructure of a spatial map in the entorhinal cortex.

The ability to find one's way depends on neural algorithms that integrate information about place, distance and direction, but the implementation of these operations in cortical microcircuits is poorly understood. Here we show that the dorsocaudal medial entorhinal cortex (dMEC) contains a directionally oriented, topographically organized neural map of the spatial environment. Its key unit is the 'grid cell', which is activated whenever the animal's position coincides with any vertex of a regular grid of equilateral triangles spanning the surface of the environment. Grids of neighbouring cells share a common orientation and spacing, but their vertex locations (their phases) differ. The spacing and size of individual fields increase from dorsal to ventral dMEC. The map is anchored to external landmarks, but persists in their absence, suggesting that grid cells may be part of a generalized, path-integration-based map of the spatial environment.

Action Potentials↗
PubMed2007

Evidence for a critical role of entorhinal cortex at pre-exposure for latent inhibition disruption in rats.

Latent inhibition (LI), that is the decrease in conditioned response induced by the repeated nonreinforced pre-exposures to the to-be-conditioned stimulus, is disrupted by entorhinal cortex (EC) lesions. The mechanism involved in this disruption is unknown, and in particular the experimental stage (pre-exposure or conditioning) at which the integrity of EC is necessary has to be determined. The purpose of this study was to address this issue by using reversible inactivation of the EC by local micro-infusion of tetrodotoxin (TTX). TTX was infused either before the pre-exposure phase, before the conditioning phase, or before both phases. LI was unaffected in rats that received TTX before conditioning or before both pre-exposure and conditioning. In contrast, LI was disrupted in rats that received TTX before pre-exposure only. These results are discussed in the framework of LI models.

Animals↗
PubMed2001

Differential synaptic localization of GluR2 and EAAC1 in the macaque monkey entorhinal cortex: a postembedding immunogold study.

The synaptic distribution of alpha-amino-3-hydroxy-5-methyl-4-isoxazole-propionic acid receptor subunit GluR2 and neuronal glutamate transporter subunit EAAC1 were studied using immunogold in layer II of the macaque monkey entorhinal cortex. Immunoreactivity for EAAC1 and GluR2 was frequent at asymmetric synapses and their associated membrane. The synaptic localization of EAAC1 differed considerably from that of GluR2, in that GluR2 immunolabelling was most commonly located within the postsynaptic density, but EAAC1 localization was more heterogeneous and was predominant at the edge of postsynaptic densities and perisynaptic zones. Since EAAC1 may play an important role in clearing glutamate from the synaptic cleft and intercellular spaces, the high perisynaptic expression of EAAC1 in these neurons could presumably offer a powerful mechanism through which high concentrations of glutamate could be efficiently removed from the synapses following release and interaction with glutamate receptors. The distribution of EAAC1 may also offer protection for these neurons against excessive glutamatergic stimuli that may occur under certain pathological conditions.

Amino Acid Transport System X-AG↗
PubMed2006

Low-dimensional maps encoding dynamics in entorhinal cortex and hippocampus.

Cells that produce intrinsic theta oscillations often contain the hyperpolarization-activated current I(h). In this article, we use models and dynamic clamp experiments to investigate the synchronization properties of two such cells (stellate cells of the entorhinal cortex and O-LM cells of the hippocampus) in networks with fast-spiking (FS) interneurons. The model we use for stellate cells and O-LM cells is the same, but the stellate cells are excitatory and the O-LM cells are inhibitory, with inhibitory postsynaptic potential considerably longer than those from FS interneurons. We use spike time response curve methods (STRC), expanding that technique to three-cell networks and giving two different ways in which the analysis of the three-cell network reduces to that of a two-cell network. We show that adding FS cells to a network of stellate cells can desynchronize the stellate cells, while adding them to a network of O-LM cells can synchronize the O-LM cells. These synchronization and desynchronization properties critically depend on I(h). The analysis of the deterministic system allows us to understand some effects of noise on the phase relationships in the stellate networks. The dynamic clamp experiments use biophysical stellate cells and in silico FS cells, with connections that mimic excitation or inhibition, the latter with decay times associated with FS cells or O-LM cells. The results obtained in the dynamic clamp experiments are in a good agreement with the analytical framework.

Action Potentials↗
PubMed2000

Entorhinal cortex lesion studied with the novel dye fluoro-jade.

We used the fluorescent dye Fluoro-Jade, capable of selectively staining degenerating neurons and their processes, in order to analyze degenerative effects of transecting the hippocampus from its main input, the entorhinal cortex in vivo and in organotypical hippocampal slice culture. Degenerating fibers stained with Fluoro-Jade were present as early as 1 day postlesion in the outer molecular layer of the dentate gyrus and could be detected up to 30 days postlesion. However, the intensity of the Fluoro-Jade staining in the outer molecular layer faded from postlesional day 20 onward. Punctate staining, various cells and neural processes became visible in this area suggesting that degenerating processes were phagocytosed by microglial cells or astrocytes. We conclude that Fluoro-Jade is an early and sensitive marker for studying degenerating neurites in the hippocampal system.

Animals↗
PubMed2000

Properties and role of I(h) in the pacing of subthreshold oscillations in entorhinal cortex layer II neurons.

Various subsets of brain neurons express a hyperpolarization-activated inward current (I(h)) that has been shown to be instrumental in pacing oscillatory activity at both a single-cell and a network level. A characteristic feature of the stellate cells (SCs) of entorhinal cortex (EC) layer II, those neurons giving rise to the main component of the perforant path input to the hippocampal formation, is their ability to generate persistent, Na(+)-dependent rhythmic subthreshold membrane potential oscillations, which are thought to be instrumental in implementing theta rhythmicity in the entorhinal-hippocampal network. The SCs also display a robust time-dependent inward rectification in the hyperpolarizing direction that may contribute to the generation of these oscillations. We performed whole cell recordings of SCs in in vitro slices to investigate the specific biophysical and pharmacological properties of the current underlying this inward rectification and to clarify its potential role in the genesis of the subthreshold oscillations. In voltage-clamp conditions, hyperpolarizing voltage steps evoked a slow, noninactivating inward current, which also deactivated slowly on depolarization. This current was identified as I(h) because it was resistant to extracellular Ba(2+), sensitive to Cs(+), completely and selectively abolished by ZD7288, and carried by both Na(+) and K(+) ions. I(h) in the SCs had an activation threshold and reversal potential at approximately -45 and -20 mV, respectively. Its half-activation voltage was -77 mV. Importantly, bath perfusion with ZD7288, but not Ba(2+), gradually and completely abolished the subthreshold oscillations, thus directly implicating I(h) in their generation. Using experimentally derived biophysical parameters for I(h) and the low-threshold persistent Na(+) current (I(NaP)) present in the SCs, a simplified model of these neurons was constructed and their subthreshold electroresponsiveness simulated. This indicated that the interplay between I(NaP) and I(h) can sustain persistent subthreshold oscillations in SCs. I(NaP) and I(h) operate in a "push-pull" fashion where the delay in the activation/deactivation of I(h) gives rise to the oscillatory process.

Animals↗
PubMed1978

Polysynaptic activation of the dentate gyrus of the hippocampal formation: an olfactory input via the lateral entorhinal cortex.

The possibility that olfactory input is transmitted to specific subregions of the hippocampal formation via the entorhinal cortex was investigated electrophysiologically by analyzing the laminar profiles of potentials evoked in the hippocampal formation by stimulation of the lateral olfactory tract (LOT). LOT stimulation resulted in long latency (14--20 ms) evoked responses in the dentate gyrus of the hippocampal formation ipsilateral to the stimulation. The variable long latency of these responses and their inability to follow stimulus rates of 40/s suggested that these potentials reflected polysynaptic activation. Analysis of the laminar profiles of the evoked potentials indicated that the responses originated from a synaptic field localized in the outer portion of the stratum moleculare of the dentate gyrus, a terminal distribution which overlaps that of the lateral entorhinal cortical (LEC) projection to the dentate gyrus. Lesions of the LEC eliminated the long latency responses in the dentate gyrus evoked by LOT stimulation. In addition, a conditioning pulse delivered either to the LOT or to the LEC produced paired pulse potentiation of the response elicited by subsequent stimulation of the other structure. No evidence was found to indicate that responses were generated in regio superior of the hippocampus proper following LOT stimulation. Taken together, these results suggest that stimulation of the LOT activates the dentate gyrus of the hippocampal formation by multisynaptic pathways which relay through the lateral portion of the entorhinal area. This finding is discussed with regard to entorhinal cortical organization and the known olfactory projections to the LEC.

Animals↗
PubMed1997

Electrolytic lesions of the fimbria/fornix, dorsal hippocampus, or entorhinal cortex produce anterograde deficits in contextual fear conditioning in rats.

Recent data indicate that dorsal hippocampal (DH) lesions disrupt Pavlovian fear conditioning to contextual cues in rats. In the present study, we examined the effects of electrolytic lesions of the fimbria/fornix (FX) or entorhinal cortex (EC), the primary afferent projection systems to the DH, on contextual fear conditioning in rats. Conditioning consisted of the delivery of unsignaled footshocks in a novel observation chamber, and freezing served as the measure of conditional fear. Electrolytic lesions of the FX, DH, or EC made 1 week before training produced anterograde impairments in both immediate postshock freezing on the conditioning day and freezing during the context extinction test 24 h following training. The deficits in conditional freezing produced by FX, DH, and EC lesions were not statistically different, although the deficits in rats with FX or EC lesions tended to be more severe than those in rats with DH lesions. In addition to producing deficits in conditional freezing, FX, DH, or EC lesions produced a pronounced locomotor hyperactivity. Within the lesion and sham groups, however, locomotor activity was not significantly correlated with conditional freezing. These results indicate that contextual fear deficits in rats with hippocampal formation damage are equivalent following either FX, DH, or EC lesions. The relationship of freezing deficits and locomotor hyperactivity in rats with hippocampal formation lesions is discussed.

Animals↗
PubMed1997

Parallel involvement of perirhinal and lateral entorhinal cortex in the polysynaptic activation of hippocampus by olfactory inputs.

It has previously been shown that olfactory input to the hippocampus (HPC) is mediated polysynaptically via the lateral entorhinal cortex (LEC), the site of origin of the lateral perforant pathway (LPP). Because previous anatomical studies have shown that olfactory projections also terminate in perirhinal cortex and that this latter region projects directly to the hippocampus, we investigated the role of perirhinal cortex (PRC) in the mediation of the olfactory-hippocampal potential in the rat. Single-pulse stimulation of the lateral olfactory tract (LOT) resulted in a long onset latency (12-20 ms) evoked response in the dentate gyrus of the ipsilateral hippocampal formation. LOT-HPC potentials were rapidly and completely abolished following the microinfusion of procaine into the LPP, suggesting that they are ultimately mediated via this pathway. In support of this finding, current source density analysis indicated that the LOT-HPC response was generated by a current sink at the outer molecular layer of both dorsal and ventral blades of the dentate gurus. Electrolytic and ibotenic acid lesions of PRC produced a significant decrease in the amplitude of LOT-HPC potentials when testing was conducted 4-7 days postlesion. Lesions of LEC produced similar effects and combined lesions of LEC and PRC resulted in an almost complete eradication of the potential, suggesting that parallel entorhinal-hippocampal and perirhinal-hippocampal pathways are involved. These data suggest, therefore, that a portion of the olfactory input to the hippocampus is mediated via polysynaptic connections routed through perirhinal cortex. Because recent research has suggested that PRC plays an important role within the temporal lobe memory system, this connectivity may be important for olfactory memory processes.

Amygdala↗
PubMed1993

Differential electroresponsiveness of stellate and pyramidal-like cells of medial entorhinal cortex layer II.

1. The electroresponsive properties of neurons from layer II of the rat medial entorhinal cortex (MEC) were studied by intracellular recording under current clamp in an in vitro brain slice preparation. From a total of 184 cells that fulfilled our criteria for recording stability, two groups of projection neurons were distinguished on the basis of their intrinsic biophysical properties and morphological characteristics (demonstrated by intracellular biocytin injection; n = 34). 2. Stellate cells (SCs) were the most abundant (69%). They were highly electroresponsive, and minimal changes (1-3 mV) of membrane potential generated an active response. Subthreshold depolarizing or hyperpolarizing current pulse injection always caused the membrane potential to attain an early peak and then sag to a lower level. Depolarization-induced "sags" were larger and determined early firing in all cells. The voltage-current relationship of SCs was markedly non-linear, demonstrating robust inward rectification in the hyperpolarizing and depolarizing range. 3. SCs generated persistent rhythmic subthreshold voltage oscillations on DC depolarization positive to -60 mV. The mean frequency of the oscillations was 8.6 Hz (theta range) at a membrane potential of approximately -55 mV, at which level occasional single spiking also occurred. At slightly more positive potentials, a striking 1- to 3-Hz repetitive bursting pattern emerged. This consisted of nonadapting trains of spikes ("clusters") interspersed with subthreshold oscillations that had a mean frequency of 21.7 Hz (beta range). 4. Nonstellate cells (39%; mostly pyramidal-like) displayed time-dependent inward rectification that was less pronounced than that of SCs, and minimal depolarization-induced sags. On threshold depolarization, firing was always preceded by a slowly rising ramp depolarization and thus occurred with a long delay. Inward rectification in the depolarizing range was very pronounced. However, non-SCs did not generate persistent rhythmic subthreshold oscillatory activity or spike clusters. 5. Of the electrophysiological parameters quantified, spike threshold, spike duration, depolarizing afterpotential amplitude and apparent membrane time constant demonstrated statistically significant differences between SCs and non-SCs. 6. The repetitive hiring properties in response to square current pulses of short duration (< 500 ms) were also different between SCs and non-SCs. First, most SCs displayed a bilinear frequency-current (f-I) relationship for only the first interspike interval, whereas most non-SCs displayed a bilinear relationship for all intervals. Second, SCs had a much steeper primary f-I slope for early intervals than non-SCs. Finally, SCs displayed more pronounced and faster spike frequency adaptation than non-SCs.(ABSTRACT TRUNCATED AT 400 WORDS)

Afferent Pathways↗
PubMed1987

Ganglioside-induced enhancement of behavioral recovery after bilateral lesions of the entorhinal cortex.

Previous research has shown that exogenous gangliosides improve recovery of learned alternation after unilateral lesions of the entorhinal cortex. Since this recovery is thought to depend upon axonal sprouting, it has been hypothesized that ganglioside-induced improvement may be due to enhanced sprouting. The present study examined the effects of ganglioside treatments on learned alternation after bilateral entorhinal lesions. Whereas control rats exhibited a severe impairment postoperatively, ganglioside-treated (50 mg/kg total brain gangliosides; i.m.) rats committed significantly fewer errors and perseverative errors, and reached criterion sooner. The two groups exhibited comparable rates of daily improvement in performance. Since bilateral entorhinal lesions preclude the sprouting which is important for recovery of alternation, the ganglioside-induced improvement observed in the present study appears to be independent of sprouting.

Animals↗
PubMed2001

Transient accumulation of Gallyas-Braak-positive and phosphorylated tau-immunopositive substances in neuronal lipofuscin granules in the amygdala, hippocampus and entorhinal cortex of rats during long-term chloroquine intoxication.

Long-term chloroquine (CQ) intoxication of normal and groggy mutant rats resulted in transient accumulation of Gallyas-Braak (G-B) -positive and phosphorylated tau (AT8) -immunopositive substances in neuronal lipofuscin granules in the amygdala, hippocampus and entorhinal cortex. In the facial nuclei of normal rats, the neuronal lipofuscin granules were only AT8-immunopositive but G-B-negative, throughout CQ intoxication, while in groggy rats, the granules were positive by both staining methods irrespective of CQ intoxication. The results indicate that there are different mechanisms in the production of G-B-positive substances in neuronal lipofuscin granules between CQ-intoxicated rats and untreated groggy mutant rats.

Alzheimer Disease↗
PubMedDate not supplied

Autoradiography of L-type and N-type calcium channels in aged rat hippocampus, entorhinal cortex, and neocortex.

The present study examined brains from 6, 17, and 32 month old male (F344x BN)F1 rats to determine whether there was any age-related change in the distribution or density of L-type and N-type Ca2+ channels in hippocampus, entorhinal cortex, and neocortex, areas commonly involved in the generation of epileptic seizures. The L-type channel antagonist PN200-110 and the N-type channel antagonist omega-conotoxin GVIA were used to determine specific binding densities and the autoradiographic distribution of ligand binding was quantified by computer-assisted densitometry. One-way ANOVA noted a significant variance in the mean value of binding density between different age groups only in neocortex laminae IV-VI for [(3)H]PN200-110 binding (P < 0.05). Post-hoc testing indicated that the mean value of the 17 month old group was significantly less than those of the 6 and 32 month old groups (P < 0.05). These results indicate no overall age-related change in the number of L-type and N-type Ca2+ channels in brain areas frequently involved in seizure activity and suggest that age-related changes in brain Ca2+ physiology may be associated with changes in voltage-gated Ca2+ channel function rather than channel number.

Age Factors↗
PubMed1994

Rapid expression and transport of embryonic N-CAM in dentate gyrus following entorhinal cortex lesion: ultrastructural analysis.

Neural cell adhesion molecules are known to be important in axon guidance and synapse formation in the developing brain. The embryonic form of neural cell adhesion molecule (eN-CAM) is reexpressed in the outer molecular layer (OML) of the dentate gyrus following entorhinal cortex (ERC) lesion. Ultrastructural analysis revealed localization of eN-CAM to the membrane of granule-cell dendritic membranes and occasionally axons within the denervated zone. Because eN-CAM is expressed rapidly (within 2 days) after ERC lesion, we were interested in the temporal sequence of expression. Denervated hippocampi (12, 15, 24, and 48 hours post-ERC lesion) were stained with anti-eN-CAM and processed for immunoelectron microscopy. At 12 hours, there was no evidence of staining for eN-CAM. By 15 hours after lesion, membranes of both dendrites and axons throughout the molecular layer exhibited moderate eN-CAM staining, and dendritic cytoplasm was heavily labeled. Twenty-four hours following lesion, plasma membrane staining of eN-CAM on both axons and dendrites had increased in intensity within the OML, whereas membrane eN-CAM staining was diminished in the inner molecular layer (IML), and the intradendritic cytoplasmic staining disappeared. By 48 hours after lesion, eN-CAM staining had disappeared from the IML but remained intense and widely distributed in the OML. These findings suggest a rapid transport of de novo synthesized protein. A generalized reaction appears to occur immediately following denervation, and eN-CAM is up-regulated in the complete expanse of the dendritic membrane, despite the fact that only the OML is denervated.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗