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PubMed1996

Modulation of A-currents by [K+]o in acutely isolated pyramidal neurones of juvenile rat entorhinal cortex and hippocampus.

Pyramidal neurones of the entorhinal cortex and of hippocampal areas CA1 and CA3 were acutely isolated from juvenile rats. The effect of lowering the concentration of extracellular potassium ions ([K+]o) on fast transient A-currents (IA) was studied using the whole-cell configuration of the patch-clamp technique. Upon lowering [K+]o from 5.4 to 0 mM amplitudes of IA in all pyramidal neurones were reduced only at test potentials positive to -20 mV, but were increased at potentials below -20 mV. Omission of magnesium ions from the intracellular perfusate resulted in an increase of IA in external K+-free solution at any potential tested. Moreover, when [K+]o was reduced steady-state activation and inactivation curves of IA were shifted in the hyperpolarizing direction.

Animals↗
PubMed2000

Reorganization of the rat fascia dentata after a unilateral entorhinal cortex lesion. Role of the extracellular matrix.

Entorhinal cortex lesion (ECL) partially denervates the fascia dentata of the hippocampus. This is said to induce the sprouting of intact fibers from neighboring layers that invade the zone of the degenerating axons. However, recent studies using anterograde tracing failed to demonstrate sprouting across laminar boundaries. Sprouting does occur, but it mainly involves unlesioned fiber systems terminating within the layer of fiber degeneration. It is now of interest to identify the cues that could underlie this layer-specific sprouting response. Since extracellular matrix (ECM) molecules delineate boundaries of axonal growth during development, it was tested whether these molecules play a similar role during the sprouting process following ECL. After ECL, reactive astrocytes rapidly synthesize and secrete growth-inhibiting ECM molecules, such as tenascin-C and the chondroitin sulfate proteoglycan neurocan, into the ECM of the outer molecular layer. These molecules form a sharp border against the nondenervated inner molecular layer. This pattern of ECM molecule expression may contribute to the layer-specific sprouting response of surviving afferents after ECL: axons trying to grow into the denervated outer molecular layer, for example, from the inner molecular layer, would be deflected by a growth-inhibiting ECM barrier.

Animals↗
PubMed1994

Synaptic and intrinsic properties of neurons of origin of the perforant path in layer II of the rat entorhinal cortex in vitro.

Layer II of the entorhinal cortex (EC) provides the first step in the hippocampal trisynaptic loop via the perforant path projection to the dentate gyrus. While a great deal is known about this projection and the properties of the dentate granule cells, much less information is available concerning the properties of and synaptic inputs to the cells of origin of the pathway in layer II. The present experiments have employed a slice preparation of the rat EC to study the intrinsic membrane properties and synaptic organization of layer II neurons. Two types of neurons could be identified electrophysiologically. The majority were designated type I and displayed a pronounced time-dependent inward rectification in the hyperpolarizing direction. Type II displayed little evidence of this characteristic. However, morphological examination suggested that both types were spiny stellate neurons projecting via the perforant path. Synaptic responses of both types displayed evidence of excitatory inputs mediated by both N-methyl-D-aspartate (NMDA) and non-NMDA glutamate receptors. In general, however, at low frequencies the responses were dominated by inhibitory inputs mediated by both GABAA and GABAB receptors. At higher frequencies the bias was shifted much more toward excitation. The contribution of synaptic and intrinsic properties of layer II neurons to the processing capabilities of the EC is discussed.

Animals↗
PubMed2003

Ca2+-independent muscarinic excitation of rat medial entorhinal cortex layer V neurons.

Cholinergic activation of entorhinal cortex (EC) layer V neurons plays a crucial role in the medial temporal lobe memory system and in the pathophysiology of temporal lobe epilepsy. Here, we demonstrate that muscarinic activation by focal application of carbachol depolarizes EC layer V neurons and induces epileptiform activity in rat brain slices. These seizure-like bursts are associated with a somatic [Ca2+]i increase of 293 +/- 82 nm and are blocked by the glutamate receptor antagonists CNQX and APV. Muscarinic activation did not directly evoke a [Ca2+]i increase, but subthreshold and suprathreshold depolarization did. Functional axon mapping revealed local axon branching as well as axon collaterals ascending to layers II and III. During blockade of ionotropic glutamatergic AMPA and NMDA receptors, carbachol depolarized layer V neurons by +7.5 +/- 3.4 mV. This direct muscarinic depolarization was associated with a conductance increase of 35 +/- 10.3% (+4.3 +/- 1.25 nS). Intracellular buffering of [Ca2+]i changes did not block this depolarization, but prolonged action potential duration and reduced adaptation of action potential firing. The muscarinic depolarization was neither blocked by combining intracellular Ca2+-buffering (EGTA or BAPTA) with non-specific Ca2+-channel inhibition by Ni+ (1 mm), nor by Ba2+ (1 mm) nor during inhibition of the h-current by 2 mm Cs+. In whole-cell patch-clamp recording, reversal of the muscarinic current occurred at about -45 mV and -5 mV with complete substitution of intrapipette K+ with Cs+. Thus, muscarinic depolarization of EC layer V neurons appears to be primarily mediated by Ca2+-independent activation of non-specific cation channels that conduct K+ about three times as well as Na+.

Acetylcholine↗
PubMed1999

Columnar activity supports propagation of population bursts in slices of rat entorhinal cortex.

Population bursts including epileptiform spikes and sharp waves can be generated in and propagate through the retrohippocampal cortices. The propagation of these events within the entorhinal cortex was studied with field potential recordings in horizontal slices from rat brain. Population bursts were elicited by repetitive extracellular stimuli in normal media. Transections of particular laminae and microknife cuts parallel to the pial surface were used to interrupt propagation or to isolate potential pathways. Population spikes were not found to propagate more than 0.5 mm in either superficial (layers I-III) or deep (layers V-VI) strips of tissue formed by cuts along layer IV. Events propagated over 2 mm when 'columnar' connectivity was intact. Population spikes propagated past microknife cuts which started at the pial surface and sectioned layers I-IV. Population spikes also propagated past microknife cuts which sectioned the angular bundle and layers V-VI. When deep layer cuts included layer IV, horizontal propagation of population spikes was blocked. Cuts running approximately in layer IV diminished the amplitude and duration of population events recorded in layers II and V (above and below the cut, respectively) and eliminated a high frequency oscillation which occurred during the burst event. It is concluded that superficial and deep layer neurons interact during propagation of population events in entorhinal cortex and that this 'columnar' activity: (a) intensifies the excitatory activity of superficial and deep layer neurons; and (b) provides multiple paths for the spread of activity from column to column within the entorhinal cortex.

Action Potentials↗
PubMed1991

c-fos protooncogene expression in rat hippocampus and entorhinal cortex following tetanic stimulation of the perforant path.

The elevated expression of the c-fos protooncogene has been proposed to be a marker of cell activation leading to a long term cellular response. In this communication we compared the c-fos mRNA accumulation in the hippocampus (i.e. postsynaptic cells) and entorhinal cortex (i.e. presynaptic cells) following high (tetanic) and low frequency electrical stimulation of the perforant path. Using Northern blot analysis we have found that high frequency stimulation elevates c-fos expression in both hippocampus and entorhinal cortex, and the increase of c-fos mRNA levels in the entorhinal cortex is less pronounced, but longer lasting, than in the hippocampus. Slight increase of c-fos mRNA levels has been also observed in low frequency treated animals in the entorhinal cortex, but not in the hippocampus. These findings raise the question about differences in mechanisms involved in c-fos activation in both parts of the brain after stimulation which evokes long term potentiation (LTP) of synaptic efficacy.

Animals↗
PubMed1997

Changes in protein synthesis and synthesis of the synaptic vesicle protein, synaptophysin, in entorhinal cortex following induction of long-term potentiation in dentate gyrus: an age-related study in the rat.

We have examined protein synthesis in entorhinal cortex following induction of long-term potentiation (LTP) in perforant path-granule cell synapses. The data presented here indicate that there was an increase in [35S]methionine labelling of TCA-precipitated proteins and [35S]methionine labelling of synaptophysin in the ipsilateral entorhinal cortex 40 min after induction of LTP in dentate gyrus. Intraventricular injection of both the NMDA antagonist, D-amino-phosphonovalerate, and the protein synthesis inhibitor, anisomycin reduced protein synthesis though the decrease caused by anisomycin was much more profound. Both agents blocked induction of LTP and the increase in protein synthesis and synaptophysin synthesis which accompanied LTP. These data indicate a close coupling of increased protein synthesis in the entorhinal cortex and expression of LTP in the dentate gyrus. This coupling was further suggested by the absence of an LTP-associated increase in protein synthesis in aged animals, in which LTP was markedly attenuated. The possibility that these changes impact on morphological changes which accompany LTP is discussed.

Aging↗
PubMed1980

[Memory facilitation induced by delayed electric stimulation of the entorhinal cortex in mice].

A subconvulsive bilateral stimulation of the lateral entorhinal cortex has been applied in BALB/c mice at different time intervals after an appetitive operant conditioning task. 24 hrs later, compared to the control subjects, the performance was improved only in animals stimulated 30 min. after the first learning session. No change was observed in animals stimulated 30 sec. or 3 hrs. post-trial. These results suggest that entorhinal cortex is involved rather late in memory processes.

Animals↗
PubMed2000

Learning-specific decrease in synaptosomal ATP diphosphohydrolase activity from hippocampus and entorhinal cortex of adult rats.

Considering the involvement of extracellular ATP in the memory formation, we analyzed the effect of inhibitory avoidance training on ectonucleotidase activities in synaptosomes from hippocampus, entorhinal cortex and parietal cortex. ATP diphosphohydrolase activity presented a decrease (33%) in hippocampal synaptosomes of rats sacrificed 180 min after training. Our results also showed a decrease in synaptosomal ATP diphosphohydrolase (30% and 42% for ATP and ADP, respectively) in entorhinal cortex immediately after training. These findings suggest an integrated action of ATP diphosphohydrolase from hippocampus and entorhinal cortex in the formation of inhibitory avoidance memory.

Animals↗
PubMed2000

Conservation of neuron number and size in entorhinal cortex layers II, III, and V/VI of aged primates.

Past dogma asserted that extensive loss of cortical neurons accompanies normal aging. However, recent stereologic studies in humans, monkeys, and rodents have found little evidence of age-related neuronal loss in several cortical regions, including the neocortex and hippocampus. Yet to date, a complete investigation of age-related neuronal loss or size change has not been undertaken in the entorhinal cortex, a retrohippocampal structure essential for learning and memory. The aged rhesus macaque monkey (Macaca mulatta), a species that develops beta-amyloid plaques and exhibits cognitive deficits with age, is considered the best commonly available model of aging in humans. In the present study, we examined changes in total neuron number and size in layers II, III, and V/VI of the intermediate division of the entorhinal cortex in aged vs. nonaged rhesus monkeys by using unbiased stereologic methods. Total neuron number was conserved in aged primates when compared with nonaged adults in entorhinal cortex layer II (aged = 56,500 +/- 12,100, nonaged adult = 48,500 +/- 10,900; P = 0.37), layer III (aged = 205, 600 +/- 50,700, nonaged adult = 187,600 +/- 60,300; P = 0.66), and layers V/VI (aged = 246,400 +/- 76,700, nonaged adult = 236,800 +/- 69,600; P = 0.87). In each of the layers examined, neuronal area and volume were also conserved with aging. This lack of morphologically evident neurodegeneration in primate entorhinal cortex with aging further supports the concept that fundamental differences exist between the processes of normal "healthy" aging and pathologic age-related neurodegenerative disorders such as Alzheimer's disease.

Aging↗
PubMed1993

Entorhinal cortex regulation of multiple brain-derived neurotrophic factor promoters in the rat hippocampus.

Developmental or degenerative damage of the neuronal architecture in the entorhinal cortex may disintegrate a functional part of hippocampal input since the entorhinal cortex provides a major source of neocortical and subcortical input to the hippocampus. These alterations, such as seen in Alzheimer's disease, schizophrenia and temporal lobe epilepsy are likely to be associated with cognitive deficits. To understand the basis for pathological changes in the corticohippocampal loop it is important to study mechanisms involved in neuronal plasticity. Brain-derived neurotrophic factor provides a possible substrate to mediate such plasticity. We have previously provided evidence that stimulation of hippocampal afferents transynaptically increase the level of brain-derived neurotrophic factor messenger RNA within the hippocampus. In the present study we have investigated whether different brain-derived neurotrophic factor messenger RNAs are specifically regulated in the hippocampus. We provide evidence for a differential and dose-dependent regulation of the different brain-derived neurotrophic factor promoters in the hippocampus by afferents in the entorhinal cortex. Our finding of a graded regulation is in contrast to earlier evidence of an "all-or-none" type of regulation.

Animals↗
PubMed1998

Highest trkB mRNA expression in the entorhinal cortex among hippocampal subregions in the adult rat: contrasting pattern with BDNF mRNA expression.

Brain-derived neurotrophic factor (BDNF) and its receptor, TrkB, regulate synaptic functions in the hippocampus of the adult rodent. In previous studies, in situ hybridization methods have been used to evaluate regional differences in BDNF and trkB mRNA expression levels in hippocampal subregions. However, these studies have failed to reach consensus regarding the regional differences in the mRNA expression levels. In the present study, we quantitated mRNA expression levels using two different methods, ribonuclease protection assays and a quantitative reverse-transcription polymerase chain reaction technique, in four hippocampal subregions: the entorhinal cortex, dentate gyrus (DG), CA3 and CA1. These two methods yielded the same results. We found that BDNF and trkB mRNA expression levels did not covary in the four subregions. BDNF and full length trkB (trkB FL) mRNA in the entorhinal cortex and the DG show contrasting expression patterns. The expression level of BDNF mRNA was highest in the DG among the hippocampal subregions and low in the entorhinal cortex and the CA1, whereas the trkB FL mRNA expression level was highest in the entorhinal cortex, low in the DG and lowest in the CA3. These results suggest regional differences in BDNF/TrkB signaling for maintenance and modifiability of neuronal connections in the hippocampal formation.

Animals↗
PubMed1998

Differential vulnerability of the subiculum and entorhinal cortex of the adult rat to prolonged protein deprivation.

Protein deprivation experienced in adult life leads to deficits in the number of hippocampal granule and CA3-CA1 pyramidal cells and to changes in the dendritic domain of granule cells and CA3 pyramids. To obtain a more complete insight into the effects of malnutrition on the limbic system of the adult rat we have analyzed the subiculum and the entorhinal cortex (neuronal layers II, III, and V-VI) in groups of 8-month-old rats fed with a low-protein diet (8% casein) since the age of 2 months and in age-matched control rats. Stereological methods were employed to estimate the total number of neurons in the subiculum and layers II, III, and V-VI of the entorhinal cortex and the volume of the respective cell layers. Moreover, to evaluate whether protein deprivation affects the dendritic domains of the neurons from these regions we have analyzed, in Golgi-impregnated material, the dendritic trees of the pyramidal cells of the subiculum and of the stellate neurons of the entorhinal cortex layer II applying quantitative and metric methods. The volume of the subiculum and the total number of its neurons were reduced in malnourished animals. In these animals we also found marked regressive changes in the apical and basal dendritic trees of the pyramidal subicular neurons. However, the spine density was increased in malnourished rats. No differences in the volume of the neuronal layers of the entorhinal cortex or in the total number of their neurons were found between protein-deprived and control rats, and no alterations were depicted in the dendritic trees of the stellate neurons of layer II. We can thus conclude that the effects of long-term protein deprivation are region specific and that the resulting structural alterations are confined to the three-layered components of the hippocampal region.

Analysis of Variance↗
PubMedDate not supplied

Reverberation of excitation in living "hippocampal formation-entorhinal cortex" slices from rats. Optical recording.

A vital potential-dependent dye was used to conduct optical recording of the electrical activity of the hippocampal formation in living slices of the rat brain including the hippocampal formation and the entorhinal cortex. These studies showed that single electrical stimuli applied to the entorhinal cortex, subiculum. and dentate gyrus produced responses in which waves of excitation passed across the hippocampal formation sequentially from the dentate gyrus, through CA3, to the CA1 field of the hippocampus. When GABAergic inhibition was partially blocked with picrotoxin, the first wave of excitation was immediately followed by several further waves in all zones of the hippocampal formation, with a constant shift in latency, which increased from the dentate gyrus to CA3 and CA1. Reverberation of excitation in the "hippocampal formation-entorhinal cortex" structure is regarded as the most probable cause for the appearance of these sequences of waves.

Animals↗
PubMed1993

Quantitative assessment of synaptic density in the entorhinal cortex in Alzheimer's disease.

We quantified the synaptic density in the entorhinal cortex (Brodmann area 28) in autopsy material from 10 individuals with Alzheimer's disease and compared them to 11 age-matched, postmortem-matched control subjects without dementia, using standard electron microscopy. The statistical data showed no change in synaptic density between control and Alzheimer subjects, in either lamina III or V of the cortex. There were no correlations between synaptic density and synaptic apposition length or density of senile plaques. The entorhinal cortex stands in marked contrast to other cortical areas that show a significant decline in synaptic numbers with Alzheimer's disease. This preservation of synaptic numbers may be related to a plasticity response that is greater in the entorhinal area than in other areas of the cortex.

Aged↗
PubMed1999

Basal and stimulated hippocampal adenylate cyclase activity in the experimentally lesioned rat entorhinal cortex.

Early stage development of Alzheimer-related neurofibrillary tangles occurs primarily in neurons of entorhinal cortex layers pre-alpha and pre-beta. These excitatory neurons project into the hippocampus. At this stage ('entorhinal' case), while neurofibrillary tangles are still absent from the hippocampus, a significant reduction in hippocampal adenylate cyclase activity has been detected. To test whether this reduction is a consequence of a deafferentation (and thus not a specifically disease-related alteration), we performed unilateral electrolytic lesions and sham-operations of the rat entorhinal cortex. The animals were killed 2, 12 and 55 days post lesion (dpl) and hippocampal adenylate cyclase activity was assayed. The major results were as follows: (1) both lesioned and unlesioned sides showed higher activity than a sham-operated control; (2) the adenylate cyclase activity of the lesioned side increased to a significantly lesser degree than that of the unlesioned side at 12 dpl; (3) this 'decrease' was attributed to changes in G protein-mediated activation of adenylate cyclase; (4) at no time point post lesion did the pattern of rat adenylate cyclase activity resemble that observed in Alzheimer's disease. Our data suggests that the loss of entorhinal afferents alone cannot explain the reduction in cyclase-activity seen in 'entorhinal' cases.

Adenylyl Cyclases↗
PubMed2005

Hemispheric asymmetry, modular variability and age-related changes in the human entorhinal cortex.

The verrucae areae entorhinalis (VAE) are a characteristic feature of the human brain that occupy the anterior and posterolateral parts of the parahippocampal gyri and correspond to the islands of layer II neurons. We analyzed VAE in 60 neurologically normal subjects ranging from 23 to 85 years of age using a casting method. In 10 of these subjects the total number of neurons in the entorhinal islands was estimated stereologically using the optical fractionator. The number and surface area of VAE were higher in the left hemisphere compared with the right, and this leftward asymmetry was highly significant. Regression analysis showed a negative correlation between average VAE area and age in both hemispheres, representing a rate loss of about 800 microm2 per year. The estimated number of neurons obtained with the optical fractionator showed no significant difference between the left and the right hemisphere (468,000+/-144,000 vs. 405,000+/-117,000). There was a highly significant negative correlation between neuron numbers and age in both sides. In addition, clusters of small, undifferentiated layer II neurons ('heterotopias') were frequently observed in the rostral part of the entorhinal cortex in young and elderly adults. Layer II entorhinal neurons are among the first to show neurofibrillary changes during normal aging. The present data confirm the occurrence of age-related neuron loss in the entorhinal cortex. Considering the consistent projections from ipsilateral auditory association areas that, together with Broca's motor-speech area (Brodmann areas 44 and 45), show leftward asymmetry from early infancy (such as Brodmann area 22, planum temporale, and area 52 in the long insular gyrus), we speculate that functional lateralization of the human entorhinal cortex may be associated with specialization for memory processing related to language. Due to the dependence of hippocampal formation on entorhinal projections, this finding is also consistent with the greater capacity of the left hippocampus for verbal episodic memory.

Adult↗
PubMed2000

Molecular effects of the psychotropic NMDA receptor antagonist MK-801 in the rat entorhinal cortex: increases in AP-1 DNA binding activity and expression of Fos and Jun family members.

Noncompetitive NMDA receptor antagonists such as phencyclidine and MK-801 produce psychotropic symptoms that closely resemble schizophrenic psychosis and induce the expression of immediate early genes in limbic cortical areas. We are concentrating on analyzing molecular and physiological effects that these drugs produce in the entorhinal cortex and on the potential connection between these effects and the psychotic symptoms. We show here that MK-801 increases the DNA binding activity of the activator protein-1 (AP-1) complex in the entorhinal cortex. We also observed increased expression of mRNAs for Fos and Jun transcription factor family members c-Fos, FosB, Fra-2, and JunB, as well as Fos family proteins in the entorhinal cortex after MK-801 administration. This suggests that the activated AP-1 complex consists of these transcription factors. Genes regulated by the AP-1 complex in the entorhinal cortex might be involved in the pathophysiology of psychotic behavior and are potential targets for new antipsychotic drugs.

Animals↗