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PubMed2006

Feedforward inhibition regulates perirhinal transmission of neocortical inputs to the entorhinal cortex: ultrastructural study in guinea pigs.

The rhinal cortices constitute the main route for impulse traffic to and from the hippocampus. Tracing studies have revealed that the perirhinal cortex forms strong reciprocal connections with the neo- and entorhinal cortex (EC). However, physiological investigations indicate that perirhinal transmission of neocortical and EC inputs occurs with a low probability. In search of an explanation for these contradictory findings, we have analyzed synaptic connections in this network by combining injections of the anterograde tracer Phaseolus vulgaris-leucoagglutinin (PHAL) into the neocortex, area 36, or area 35 with gamma-aminobutyric acid (GABA) immunocytochemistry and electron microscopic observations. Within area 36, neocortical axon terminals formed only asymmetric synapses, usually with GABA-negative spines (87%), and less frequently with GABA-immunopositive (GABA+) dendrites (13%). A similar synaptic distribution was observed within area 35 except that asymmetric synapses onto GABA+ dendrites were more frequent (23% of synapses). Examination of the projections from area 36 to area 35 and from both regions to the EC revealed an even higher incidence of asymmetric synapses onto GABA+ dendrites (35 and 32%, respectively) than what was observed in the neocortical projection to areas 36 and 35. Furthermore, some of the neocortical and perirhinal terminals containing PHAL and GABA immunolabeling formed symmetric synapses onto GABA-negative dendrites in their projection sites (neocortex to area 35, 16%; area 36 to 35, 7%; areas 36-35 to EC, 12%). Taken together, these findings suggest that impulse transmission through the rhinal circuit is subjected to strong inhibitory influences, reconciling anatomical and physiological data about this network.

Animals↗
PubMed1989

Ictal epileptiform events induced by removal of extracellular magnesium in slices of entorhinal cortex are blocked by baclofen.

Most manipulations employed to elicit epileptiform activity in brain slices result in brief, interictal-like events. In slices of the rat entorhinal cortex perfusion with a magnesium-depleted medium elicits prolonged seizure events which are more reminiscent of ictal activity. The interictal events in brain slice models are blocked by baclofen, but there is an indication from one study (H. S. Swartzwelder, D. V. Lewis, W. W. Anderson, and W. A. Wilson, 1987, Brain Res. 410: 362-366) that ictal events may not be affected by this drug. The present study examined the effects of baclofen on ictal events recorded in entorhinal cortex slices in magnesium-free medium. Simultaneous studies of effects of baclofen on interictal responses in the hippocampal region of the same slices were made on many occasions. The results show that both types of epileptiform activity are suppressed with a similar facility by baclofen.

Animals↗
PubMed1998

Hippocampal damage after injection of kainic acid into the rat entorhinal cortex.

Several experimental models of epilepsy have used kainic acid in animals to induce seizures and neuropathological changes which mimic those observed in human temporal lobe epilepsy. These models differ in the location and manner in which kainic acid is applied. In the present study, we characterized the seizure activity and neuropathological changes that occur in awake rats after kainic acid (25 ng/250 nl) is injected into the entorhinal cortex of freely moving rats. In 91% of the animals, this induced generalized motor seizures. Moreover, all of the animals survived status epilepticus. Animals were perfused two weeks after the injection for neuropathological examination. Silver-impregnation revealed that kainic acid caused pyramidal cell damage which was most severe in the CA1 subfield and to a lesser degree in the CA3c area. A loss of NADPH diaphorase-containing neurons in the hilus and the CA1 area was also consistently seen and, in most cases, a population of somatostatin-immunoreactive neurons was diminished. Our findings show that a minute amount of kainic acid delivered directly to the entorhinal cortex on unanesthetized animals reliably produces generalized seizures as well as a consistent pattern of cell damage in the hippocampus. Therefore, this model may be suitable for investigating the mechanisms underlying temporal lobe epilepsy, and may prove useful in assessing different treatment strategies for preventing seizure-induced structural damage.

Animals↗
PubMed2004

Protective effect of ifenprodil against spreading depression in the mouse entorhinal cortex.

In the brain, spreading depression (SD) is characterized by a large extracellular DC shift, a massive failure of ion homeostasis and a transient cessation of neuronal function. Clinically, SD is believed to be involved in various neurological disorders including migraine and cerebrovascular diseases. The propagation of cortical SD requires the release of glutamate, and N-methyl-D-aspartate (NMDA) receptors play a crucial role in this process. Here, we have isolated the NMDA receptor-mediated component of extracellularly recorded field excitatory postsynaptic potentials (fEPSPs) in layers 2-3 of the entorhinal cortex of murine brain slices. In the absence of GABAA and AMPA receptor-mediated synaptic transmission, stimulation of layer 6 afferents every 15-90 s elicited spontaneous SD on average within 18.5 min after the start of the stimulation. In the presence of ifenprodil, an NR2B receptor subunit-selective NMDA receptor antagonist, the occurrence of SD was nearly abolished. Our results are consistent with an important role of NR2B subunits in triggering SD in the entorhinal cortex.

Adrenergic alpha-Antagonists↗
PubMed2000

Properties of entorhinal cortex projection cells to the hippocampal formation.

There are multiple connections from the entorhinal cortex (EC) to the hippocampus that carry the information from the EC to the hippocampus. Layer II cells of the medial EC innervating the dentate gyrus (DG)-molecular layer possess K(+)-outward currents and inward rectifier currents that are potentially modulated by changes in intracellular second messengers. Layer II cells responded to synaptic stimulation with a rather flat input-output curve, and much stronger stimuli are required to generate action potentials in these neurons than in EC layer III cells. During repetitive stimulation at frequencies of 10 Hz and more, EC layer II cells respond with increased likelihood to generate action potentials. Two different NMDA conductances can be demonstrated in these neurons. A slow, less Mg, less voltage-dependent component is responsible for the transient depolarization between the fast and slow IPSP. A second group of neurons also projects to the DG. These are either pyramidal or nonpyramidal cells in the deep layers of the EC. At least part of these neurons also possess rhythmogenic properties. In contrast to layer II cells, layer III neurons have a steep input-output curve and show during repetitive synaptic activation a tendency to repolarize and to display long-lasting inhibitions dependent on GABAB-, atropine-, and naloxone-sensitive components. As a consequence, they are readily activated during low frequency stimulation, but project only a few action potentials to area CA1 initially during higher (more than 10 Hz) frequency synaptic stimulation.

Animals↗
PubMed2004

Entorhinal cortex lesion in the mouse induces transsynaptic death of perforant path target neurons.

Entorhinal cortex lesion (ECL) is a well described model of anterograde axonal degeneration, subsequent sprouting and reactive synaptogenesis in the hippocampus. Here, we show that such lesions induce transsynaptic degeneration of the target cells of the lesions pathway in the dentate gyrus. Peaking between 24 and 36 hours post-lesion, dying neurons were labeled with DeOlmos silver-staining and antisera against activated caspase 3 (CCP32), a downstream inductor of programmed cell death. Within caspase 3-positive neurons, fragmented nuclei were co-localized using Hoechst 33342 staining. Chromatin condensation and nuclear fragmentation were also evident in semithin sections and at the ultrastructural level, where virtually all caspase 3-positive neurons showed these hallmarks of apoptosis. There is a well-described upregulation of the apoptosis-inducing CD95/L system within the CNS after trauma, yet a comparison of caspase 3-staining patterns between CD95 (Ipr)- and CD95L (gld)-deficient with non-deficient mice (C57/bl6) provided no evidence for CD95L-mediated neuronal cell death in this setting. However, inhibition of NMDA receptors with MK-801 completely suppressed caspase 3 activation, pointing to glutamate neurotoxicity as the upstream inducer of the observed cell death. Thus, these data show that axonal injury in the CNS does not only damage the axotomized neurons themselves, but can also lethally affect their target cells, apparently by activating glutamate-mediated intracellular pathways of programmed cell death.

Animals↗
PubMed2003

Atrophy rates of entorhinal cortex in AD and normal aging.

OBJECTIVES: To explore the atrophy rate of entorhinal cortex (ERC) in AD and normal aging and assess the value of rate measurement of ERC atrophy for classifying subjects with AD from cognitively normal (CN) control subjects. METHODS: Twenty-one AD patients and 23 CN subjects had MRI scans and clinical evaluations twice within 1.8 +/- 0.6 years. ERC volumes were manually measured on volumetric T1-weighted MR images. RESULTS: Patients with AD had a greater annual percentage volume change of ERC than CN subjects on both sides (left: 6.8 +/- 4.3%/year for AD vs 1.4 +/- 2.5%/year for CN [F(1,42) = 25.6, p < 0.001]; right: 6.3 +/- 3.3%/year for AD vs 1.4 +/- 2.3%/year for CN [F(1,42) = 25.6, p < 0.001]). Furthermore, increased ERC atrophy rate was correlated (r = -0.56, p = 0.01) with decreased memory performance in AD. CN subjects had on average annual ERC atrophy rates greater than zero (p < 0.01). Baseline volume of ERC predicted atrophy rate of ERC (left: r = -0.53, p < 0.01; right: r = -0.42, p < 0.05) in CN subjects but not in AD subjects. Using ERC baseline volumes alone resulted in 77% overall correct classification (p < 0.01) between AD and CN subjects, with 76% sensitivity and 78% specificity and an area under receiver operator characteristic (ROC) curve of 0.83. Adding annual atrophy rate of ERC to the model accounted for most of the variance (p < 0.01), diminishing contributions from baseline volume and yielding 82% overall classification, with 76% sensitivity and 86% specificity and an area under the ROC curve of 0.93. CONCLUSION: ERC volume loss over time may be a better indicator for AD than cross-sectional measurements.

Aged↗
PubMed2000

Amyloid beta-protein (Abeta)-containing astrocytes are located preferentially near N-terminal-truncated Abeta deposits in the human entorhinal cortex.

The deposition of the amyloid beta-protein (Abeta) is a pathological hallmark of Alzheimer's disease (AD). Abeta is a peptide consisting of 39-43 amino acids and is derived by beta- and gamma-secretase cleavage from the Abeta protein precursor (AbetaPP). An N-terminal-truncated form of Abeta can occur following alpha- and gamma-secretase cleavage of AbetaPP. Fleecy amyloid is a recently identified distinct type of Abeta deposits occurring in the internal layers (pri-alpha, pri-beta and pri-gamma) of the human entorhinal cortex. Fleecy amyloid consists exclusively of N-terminal-truncated Abeta and is a transient form of Abeta deposits, which disappears in late-stage beta-amyloidosis. In this study, the entorhinal cortex of 15 cases with AD-related pathology was used to examine astrocytes in the vicinity of N-terminal-truncated Abeta in fleecy amyloid of the layers pri-alpha, pri-beta, and pri-gamma in comparison to astrocytes in the vicinity of full-length Abeta in layers pre-beta and pre-gamma. Immunohistochemistry was performed with antibodies directed against AbetaPP, Abeta40, Abeta42, APbeta17-24, Abeta1-17 and Abeta8-17 as well as by double-labeling with antibodies directed against Abeta17-24, Abeta42, and glial fibrillary acid protein (GFAP). A large number of GFAP-positive astrocytes containing N-terminal-truncated Abeta fragments appeared in the vicinity of N-terminal-truncated Abeta, whereas Abeta-containing astrocytes were rarely seen in the vicinity of full-length Abeta. These results suggest that N-terminal-truncated Abeta peptide may be cleared preferentially from the extracellular space by astrocytic uptake and processing. Such an astroglial uptake of N-terminal-truncated Abeta may account for the transient nature of fleecy amyloid and point to the use of N-terminal truncation of Abeta in potential therapeutic strategies aimed at preventing the brain from amassing full-length Abeta deposits.

Aged↗
PubMed2006

MRI of hippocampus and entorhinal cortex in mild cognitive impairment: a follow-up study.

The concept of mild cognitive impairment (MCI) has been proposed to represent a transitional stage between normal aging and dementia. We studied the predictive value of the MRI-derived volumes of medial temporal lobe (MTL) structures, white matter lesions (WML), neuropsychological tests, and Apolipoprotein E (APOE) genotype on conversion of MCI to dementia and AD. The study included 60 subjects with MCI identified from population cohorts. During the mean follow-up period of 34 months, 13 patients had progressed to dementia (9 to Alzheimer's disease (AD)). In Cox regression analysis the baseline volumes of the right hippocampus, the right entorhinal cortex and CDR sum of boxes predicted the progression of MCI to dementia during the follow-up. In a bivariate analysis, only the baseline volumes of entorhinal cortex predicted conversion of MCI to AD. The Mini-Mental State Examination (MMSE) score at baseline, WML load, or APOE genotype were not significant predictors of progression. The MTL volumetry helps in identifying among the MCI subjects a group, which is at high risk for developing AD.

Aged↗
PubMed1996

Tonic facilitation of glutamate release by presynaptic N-methyl-D-aspartate autoreceptors in the entorhinal cortex.

N-Methyl-D-aspartate receptors are fundamental for neuronal plasticity and development in the CNS. Most studies have examined postsynaptic roles of this receptor, but there are also indications for a presynaptic location and function. Here, we provide electrophysiological evidence for the existence of presynaptic N-methyl-D-aspartate receptors which can tonically facilitate glutamate release in the CNS. The N-methyl-D-aspartate receptor antagonist 2-amino-5-phosphonopentanoate reduced the frequency, but not amplitude, of glutamate-mediated spontaneous excitatory postsynaptic currents in layer II neurons of the rat entorhinal cortex. This effect was also observed in the presence of tetrodotoxin and when postsynaptic N-methyl-D-aspartate receptors were blocked by dialysis with dizocilpine maleate. When extracellular calcium was replaced with strontium, 2-amino-5-phosphonopentanoate reduced the "tail" of spontaneous excitatory postsynaptic currents that followed an evoked excitatory postsynaptic current. Finally, there was a tendency for paired-pulse facilitation of excitatory postsynaptic currents evoked at short (50 ms) intervals with postsynaptic N-methyl-D-aspartate receptors blocked) to be reduced by 2-amino-5-phosphonopentanoate, although this did not reach significance. These data strongly support the presence of presynaptic N-methyl-D-aspartate autoreceptors which may facilitate glutamate release in layer II of the entorhinal cortex.

2-Amino-5-phosphonovalerate↗
PubMed2003

Morphological and numerical analysis of synaptic interactions between neurons in deep and superficial layers of the entorhinal cortex of the rat.

Neurons providing connections between the deep and superficial layers of the entorhinal cortex (EC) constitute a pivotal link in the network underlying reverberation and gating of neuronal activity in the entorhinal-hippocampal system. To learn more of these deep-to-superficial neurons and their targets, we applied the tracer Neurobiotin pericellularly in layer V of the medial EC of 12 rats. Labeled axons in the superficial layers were studied with light and electron microscopy, and their synaptic organization recorded. Neurobiotin-labeled layer V neurons displayed "Golgi-like" staining. Two major cell types were distinguished among these neurons: (1) pyramidal neurons with apical spiny dendrites traversing all layers and ramifying in layer I, and (2) horizontal neurons with dendrites confined to the deep layers. Labeled axons ramified profusely in layer III, superficially in layer II and deep in layer I. Analysis of labeled axon terminals in layers I-II and III showed that most synapses (95%) were asymmetrical. Of these synapses, 56% occurred with spines (presumably belonging to principal neurons) and 44% with dendritic shafts (presumably interneurons). A small fraction of the synapses (5%) was of the symmetrical type. Such synapses were mainly seen on dendritic shafts. We found in two sections a symmetrical synapse on a spine. These findings suggest that the deep to superficial projection is mainly excitatory in nature, and that these fibers subserve both excitation and feed-forward inhibition. There is an additional, much weaker, inhibitory component in this projection, which may have a disinhibitory effect on the entorhinal network in the superficial layers.

Animals↗
PubMed2000

Topical correlation of increased hippocampal glutamine synthetase immunoreactivity and glutamatergic terminal fields after entorhinal cortex lesion.

Many astrocyte functions are related to glutamatergic transmission and to other synaptic functions, such as glutamate uptake and glutamate metabolism. While many of these functions can be executed by perisynaptic astrocyte processes, it is not clear how these processes are formed. One of the factors guiding them to the synapse may be synaptically released glutamate. This would explain the topical correlation between laminated glutamatergic terminal fields and laminae most intensely labeled by a cytoplasmic astrocyte marker, anti-glutamine synthetase (GS). This hypothesis was tested by selectively increasing the glutamate content in one terminal field. The rat entorhinal cortex, the origin of the glutamatergic projection to the outer molecular layer (OML) of the hippocampal fascia dentata, was lesioned electrolytically. In line with the hypothesis, GS immunoreactivity was strongly increased in the OML at 6 and 8 days postlesion. Lesion of only the medial entorhinal cortex resulted in heavily increased GS immunoreactivity only in the central portion of the molecular layer (i.e., the corresponding terminal field). The laminae affected were always separated from neighboring fields by a straight and clear-cut line. Although many other factors are released in the terminal field after lesion, the results are consistent with a guiding role for glutamate. The lamina-specific effect suggests that the factor(s) involved have a very limited diffusion distance. The straight border line between affected and unaffected laminae, which cuts across astrocyte territories, can best be explained by ramification of only those processes of a given astrocyte that are contained within the lamina affected.

Animals↗
PubMed1990

Disynaptic olfactory input to the hippocampus mediated by stellate cells in the entorhinal cortex.

Electrophysiological and anatomical studies indicate functional relationships between the olfactory bulb and the hippocampus, mediated by the lateral olfactory tract and perforant path. Fibres from the lateral olfactory bulb terminate in the molecular layer of the lateral entorhinal cortex, which contains stellate and pyramidal cells that project to the hippocampus. Therefore this study was performed to analyze whether a trineuronal, disynaptic chain connects the olfactory bulb and the hippocampus. In adult rats, Fast Blue was unilaterally injected into the septal hippocampus to label cells of origin of the entorhinohippocampal pathway. Lesions of the ipsilateral olfactory bulb induced anterograde terminal degeneration in the entorhinal cortex of the same animals. Fast Blue labelled, and thus hippocampally projecting entorhinal neurones in fixed vibratome slices of the operated brains were injected with Lucifer Yellow. Most of these neurones were stellate layer II and pyramidal layer III cells; in addition there were some sparsely spinous multipolar cells in layers II and III and sparsely spinous horizontal cells at the layer I/II border. Injected cells were photoconverted and processed for electron microscopy. Olfactory bulb lesions resulted in electron-dense degeneration of abundant terminal boutons in the outer zone of entorhinal layer I. The relative frequency of degenerating boutons decreased towards deeper zones of the layer. In the outer zone, degenerated terminals predominantly contacted dendritic spines. These contacts could be seen on injected stellate cells but not on pyramidal cells. This study shows that the area dentata of the rat is reached by disynaptic afferent input from the olfactory bulb and thus is likely to process olfactory information. Oligosynaptic pathways might provide the hippocampus also with visual and auditory inputs; such fast transmitted polysensory information could be essential for the proposed participation of the hippocampus in attention-related mechanisms.

Amidines↗
PubMed2001

Evidence for glutamate, in addition to acetylcholine and GABA, neurotransmitter synthesis in basal forebrain neurons projecting to the entorhinal cortex.

Basal forebrain neurons play important parts in processes of cortical activation and memory that have been attributed to the cortically projecting, cholinergic neurons. Yet, non-cholinergic neurons also project to the cerebral cortex and also appear to participate in processes of cortical modulation and plasticity. GABAergic neurons compose a portion of the cortically projecting cell group, but do not fully account for the non-cholinergic cell contingent. In the present study in the rat, we investigated whether the non-cholinergic, non-GABAergic cell component might be composed of glutamatergic neurons. We examined afferents to the entorhinal cortex, which is known to be modulated by basal forebrain neurons and to be critically involved in memory. Dual immunofluorescent staining was performed for cholera toxin, as retrograde tracer, and phosphate-activated glutaminase, the synthetic enzyme for the neurotransmitter pool of glutamate. The retrogradely labeled cells were distributed across the basal forebrain through the medial septum, diagonal band, magnocellular preoptic area and substantia innominata. The major proportion (approximately 80%) of the retrogradely labeled cells was found to be immunopositive for phosphate-activated glutaminase. Equal minor proportions (approximately 40%) were immunopositive for choline acetyltransferase and glutamic acid decarboxylase. In other material dual-immunostained for neurotransmitter enzymes, approximately 95% of choline acetyltransferase- and approximately 60% of glutamic acid decarboxylase-immunopositive neurons were also immunopositive for phosphate-activated glutaminase. From these results it appears that a significant proportion of these cell groups, including their cortically projecting contingents, could synthesize glutamate together with acetylcholine or GABA as neurotransmitters and another proportion of cells could synthesize glutamate alone. Accordingly, as either co-transmitter or primary transmitter within basalocortical afferents, glutamate could have the capacity to modulate the entorhinal cortex and promote its role in memory.

Acetylcholine↗
PubMed2004

Coexistence of gamma and high-frequency oscillations in rat medial entorhinal cortex in vitro.

High frequency oscillations (> 80-90 Hz) occur in neocortex and hippocampus in vivo where they are associated with specific behavioural states and more classical EEG frequency bands. In the hippocampus in vitro these oscillations can occur in the absence of pyramidal neuronal somatodendritic compartments and are temporally correlated with on-going, persistent gamma frequency oscillations. Their occurrence in the hippocampus is dependent on gap-junctional communication and it has been suggested that these high frequency oscillations originate as collective behaviour in populations of electrically coupled principal cell axonal compartments. Here we demonstrate that the superficial layers of medial entorhinal cortex can also generate high frequency oscillations associated with gamma rhythms. During persistent gamma frequency oscillations high frequency oscillations occur with a high bispectral coherence with the field gamma activity. Bursts of high frequency oscillations are temporally correlated with both the onset of compound excitatory postsynaptic potentials in fast-spiking interneurones and spikelet potentials in both pyramidal and stellate principal neurones. Both the gamma frequency and high frequency oscillations were attenuated by the gap junction blocker carbenoxolone. These data suggest that high frequency oscillations may represent the substrate for phasic drive to interneurones during persistent gamma oscillations in the medial entorhinal cortex.

Animals↗
PubMed2002

N-methyl-D-aspartate receptor subunit NR2A and NR2B messenger RNA levels are altered in the hippocampus and entorhinal cortex in Alzheimer's disease.

The N-methyl-D-aspartate (NMDA) receptor is a subtype of ionotropic glutamate receptor that is involved in synaptic mechanisms of learning and memory, and mediates excitotoxic neuronal injury. In this study, we tested the hypothesis that NMDA receptor subunit gene expression is altered in Alzheimer's disease (AD), especially in brain regions known to be important in memory. Quantitative reverse transcriptase-polymerase chain reaction (RT-PCR) was used to determine the messenger RNA (mRNA) levels of the NMDA receptor subunits NR1, NR2A, and NR2B in the hippocampus and entorhinal cortex of postmortem brain samples from nine clinically well-characterized AD patients and nine aged controls. Cerebellum, a site minimally affected by AD, was also chosen for comparison assessment. Results showed decreased levels of the NR2 mRNAs in AD brains compared to controls. Reductions of NR2A (46.2%, p<0.01) and NR2B (43.2%, p<0.0001) mRNA levels were identified in the entorhinal cortex. Reductions of NR2A (41.4%, p<0.05) and NR2B (40.6%, p=0.058) mRNA levels were found in the hippocampus. NR1 mRNA levels were similar in all three brain regions in both AD and controls. No significant changes of subunit NR2A and NR2B mRNA levels were identified in the cerebellum. Postmortem delay (PMD), tissue storage time, brain weight, or age of the subjects did not affect these changes. These data suggest that alterations in NMDA receptor subunits, especially the NR2A and NR2B, may be important in AD, particularly in neuronal populations that underlie impaired learning and memory.

Aged↗
PubMed1996

Alzheimer's disease severely affects areas of the claustrum connected with the entorhinal cortex.

Pathological changes in the claustrum and its main parts (dorsal, temporal, orbital and paramygdalar) were studied on ten brains of patients with Alzheimer's disease and five control brains. The brains after fixation in formalin were embedded in paraffin, coronal-8-micron-thick serial sections were cut and stained either with cresyl violet or with immunocytochemical methods for amyloid and tangles. Morphometrical studies were performed in all parts of the claustrum along its whole extension. The claustrum in control brains was free of neurofibrillary and amyloid pathology except for one case with few senile plaques in the paramygdalar part. In AD affected brains the most severe changes were found in the paramygdalar part connected with the entorhinal cortex (neuronal loss -46%; 698 +/- 244.6 neurofibrillary tangles per mm3, tangle/neuron ratio -6.8 +/- 2.4%). In other parts of the claustrum related mainly with the neocortex pathological changes were significantly less expressed. As pathological AD type alteration affects severely practically the whole hippocampal formation, including the entorhinal cortex, the extensive neuronal pathology of the paramygdalar part of the claustrum is probably related to this process and may deeper memory dysfunction.

Aged↗
PubMed1990

Feedforward excitation of the hippocampus by afferents from the entorhinal cortex: redefinition of the role of the trisynaptic pathway.

For the past 3 decades, functional characterizations of the hippocampus have emphasized its intrinsic trisynaptic circuitry, which consists of successive excitatory projections from the entorhinal cortex to the dentate gyrus, from granule cells of the dentate to the CA3/4 pyramidal cell region, and from CA3/4 to the CA1/2 pyramidal cell region. Despite unequivocal anatomical evidence for a monosynaptic projection from entorhinal to CA3 and CA1/2, few in vivo electrophysiological studies of the direct pathway have been reported. In the experiments presented here, we stimulated axons of entorhinal cortical neurons in vivo and recorded evoked single unit and population spike responses in the dentate, CA3, and CA1 of hippocampus, to determine if pyramidal cells are driven primarily via the monosynaptic or trisynaptic pathways. Our results show that neurons within the three subfields of the hippocampus discharge simultaneously in response to input from a given subpopulation of entorhinal cortical neurons and that the initial monosynaptic excitation of pyramidal cells then is followed by weaker excitatory volleys transmitted through the trisynaptic pathway. In addition, we found that responses of CA3 pyramidal cells often precede those of dentate granule cells and that excitation of CA3 and CA1 pyramidal cells can occur in the absence of granule cell excitation. In total, these results argue for a different conceptualization of the functional organization of the hippocampus with respect to the propagation of activity through its intrinsic pathways: input from the entorhinal cortex initiates a two-phase feedforward excitation of pyramidal cells, with the dentate gyrus providing feedforward excitation of CA3, and with both the dentate and CA3 providing feedforward excitation of CA1.

Afferent Pathways↗