Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Entorhinal Cortex”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 937 records · Page 52Linked to original sources
PubMed1990

Neurochemical correlates of major depression in primary dementia.

Biogenic amine neurotransmitters and metabolites as well as choline acetyltransferase activity were quantified in eight brain regions from 37 demented patients, with or without major depression, and 10 controls with no history of dementia or depression. The middle frontal and temporal cortex, prosubiculum and entorhinal cortex of the hippocampus, substantia nigra, thalamus, amygdala, and caudate were examined. Demented patients with major depression exhibited a 10-fold to 20-fold reduction in the level of norepinephrine in the cortex, along with relative preservation of choline acetyltransferase activity in subcortical regions, compared with demented patients who were not depressed. Serotonin levels were reduced in all eight brain regions, but the reduction did not reach statistical significance in any region examined. A para-doxical increase in dopamine levels was observed in the entorhinal cortex of depressed, demented patients, although no consistent pattern of change in the level of this neurotransmitter emerged across brain regions. Our results indicate that the development of major depression in primary dementia is associated with a profile of concurrent neurochemical changes that is largely consistent with existing neurochemical hypotheses of idiopathic affective disorders, and qualitatively distinct from that associated with primary dementia.

Brain↗
PubMed1998

Postnatal development of dopamine D4-like receptors in rat forebrain regions: comparison with D2-like receptors.

Development of dopamine D4-like receptors in rat caudate-putamen (CPu), nucleus accumbens (NAc), frontal cortex, hippocampus, and entorhinal cortex was assessed at seven points between postnatal days 7 and 60 by computed in vitro receptor autoradiography, and compared with dopamine (DA) D2-like receptors. Density of radioligand binding to both receptor types increased from day 7 to a peak at day 28 in caudate-putamen (D4, 3.3-fold; D2, 4.3-fold) and nucleus accumbens (2.9- and 3.6-fold), then declined by 28%-33% over days 35-60 to adult levels in both brain regions. In hippocampus, frontal and entorhinal cortex, both receptor types increased by 3.8- to 5.8-fold from day 7 to maximal levels at day 35 that remained unchanged to day 60. These findings suggest: (1) D4- and D2-like receptors follow a similar course of development in several cortical, extrapyramidal, and limbic regions of rat forebrain; (2) elimination of excessive receptors of both types occurred in caudate-putamen and nucleus accumbens but not in the other brain regions.

Aging↗
PubMed1989

The temporal-hippocampal region and retention: the role of temporo-entorhinal connections in rats.

Results from previous studies suggest that the entorhinal cortex may be involved in mnemonic processes. The present study was carried out to investigate whether disruption of fibre connections between the temporal cortex and lateral entorhinal area may impair retention of a pre-operatively acquired simultaneous brightness discrimination task. The lesion resulted in a severe impairment in retaining the discrimination task (Experiment 1). The retention deficit could not be traced into the hippocampal formation by making perforant path lesions or hippocampal lesions (Experiment 2). The results indicate that the lateral entorhinal cortex is more crucial for reference memory than the hippocampal formation.

Animals↗
PubMed1997

Optical imaging of low Mg(2+)-induced spontaneous epileptiform activity in combined rat entorhinal cortex-hippocampal slices.

A reproducible increase in transmission of infrared light was observed during spontaneous seizure-like events (SLEs) induced by low Mg2+ solutions in combined rat entorhinal cortex-hippocampal slices. Comparison of half maxima of transmission change in different regions indicated propagation of SLEs from the medial entorhinal cortex towards the temporal cortex suggesting spread along existing anatomical pathways. Thus, optical imaging of spontaneous epileptiform activity is possible and may improve the assessment of spread patterns. The optical signal outlasted both SLEs and associated K+ signals. In contrast, the tetraethylammonium signal, indicating changes of the extracellular space (ECS) volume, had a longer time course than the transmission changes. ECS volume changes are widely held to be responsible for transmission change. Our data suggest that other mechanisms may also contribute to increased light transmission during epileptiform activity.

Animals↗
PubMed2005

Prenatal stress elicits regionally selective changes in basal FGF-2 gene expression in adulthood and alters the adult response to acute or chronic stress.

Exposure to stress during pregnancy influences the trajectory of brain development resulting in permanent alterations that may contribute to increased susceptibility to subsequent cognitive or neuropsychiatric disorders. In this manuscript, we examined the effects of prenatal stress on the expression of basic fibroblast growth factor (FGF-2), an important molecular regulator of development and plasticity, in adult male rats under basal conditions as well as in response to acute or chronic stress. Baseline FGF-2 mRNA levels were differentially influenced by gestational stress in a variety of brain regions, with significant decreases in prefrontal cortex and increases in entorhinal cortex and striatum. By itself, postnatal stress similarly decreased trophic factor expression in prefrontal cortex while evoking stimulation elsewhere. Gestational stress altered the pattern of FGF-2 expression in response to adult stress, completely reversing the pattern in the prefrontal cortex (stimulatory instead of inhibitory), blunting the response in the entorhinal cortex and desensitizing the response in the striatum. These effects point to a unique interference of chronic prenatal stress with both ongoing FGF-2 expression and its responses to subsequent stressors, lasting into adulthood. Given the multifaceted role of FGF-2 in synaptic development, maintenance and plasticity, these data provide detailed mechanistic evidence as to how prenatal stress elicits lifelong effects on synaptic function. The abnormal modulation of FGF-2 gene expression in specific brain regions in response to subsequent stress in adulthood may impair the normal adaptive responses of the cell to challenging situations.

Acute Disease↗
PubMed1989

Topographical organization of the entorhinal projection to the dentate gyrus of the monkey.

The topographic organization of the projections from the entorhinal cortex to the dentate gyrus in the macaque monkey was studied with anterograde and retrograde tracing methods. Injections of WGA-HRP or the fluorescent retrograde tracers, Fast blue and Diamidino yellow, were placed at various levels along the rostrocaudal axis of the dentate gyrus and hippocampus. In 5 experiments the fluorescent dyes were injected at 2 rostrocaudal levels of the same dentate gyrus. Labeled neurons were observed mainly in layers II and III of the entorhinal cortex, though some were also seen in layers V and VI. The labeled layer II cells resulting from each of the tracer injections were located throughout much of the rostrocaudal extent of the entorhinal cortex, though they tended to have a more limited distribution in the transverse or mediolateral axis. Injections of retrograde tracers located caudally in the dentate gyrus resulted in a rostrocaudally oriented zone of labeled cells that was situated laterally in the entorhinal cortex adjacent to the rhinal sulcus. The zone of labeled cells was not oriented strictly parallel to the rhinal sulcus since at caudal levels it extended medially to encompass the full transverse extent of the most caudal portion of the entorhinal cortex. When injections were placed more rostrally in the dentate gyrus and hippocampus, the rostrocaudally oriented zone of labeled cells was situated more medially in the entorhinal cortex. Anterograde tracing experiments using 3H-amino acid injections into different rostrocaudal and mediolateral positions of the entorhinal cortex confirmed the organization demonstrated by the retrograde tracers and further indicated that the entorhinal fibers terminate in the outer two-thirds of the molecular layer of the dentate gyrus. Unlike in the rat, where the entorhinal termination zone in the molecular layer is clearly bilaminate, projections from all portions of the entorhinal cortex appeared to terminate more diffusely throughout the outer two-thirds of the molecular layer. The results of the present study indicate that rostrocaudally oriented zones of cells that cut across several cytoarchitectonic subdivisions of the entorhinal cortex give rise to topographically organized projections to the dentate gyrus. Cells located laterally in the entorhinal cortex project to caudal levels of the dentate gyrus, whereas progressively more medially situated cells project to progressively more rostral parts of the dentate gyrus.

Animals↗
PubMed2001

Do interictal discharges promote or control seizures? Experimental evidence from an in vitro model of epileptiform discharge.

Interictal and ictal discharges are recorded from limbic structures in temporal lobe epilepsy patients. In clinical practice, interictal spikes are used to localize the epileptogenic area, but they also are assumed to promote ictal events. Here I review data obtained from combined slices of mouse hippocampus-entorhinal cortex that indicate an inverse relation between interictal and ictal events. In this preparation, application of 4-aminopyridine or Mg2+-free medium induce (a) interictal discharges that originated from CA3 and propagate (via the Schaffer collaterals) to CA1 and entorhinal cortex, to return to the hippocampus through the dentate area; and (b) ictal discharges that initiate in the entorhinal cortex and propagate to the hippocampus via the dentate gyrus. Interictal activity occurs throughout the experiment (up to 6 h), whereas ictal discharges disappear after 1-2 h. Schaffer collateral cut abolishes interictal discharges in CA1, entorhinal cortex, and dentate and reestablishes entorhinal ictal discharges. Moreover, ictal discharge generation in the entorhinal cortex after Schaffer collateral cut is prevented by mimicking CA3 activity with rhythmic electrical stimulation of CA1 outputs. Thus hippocampal interictal activity controls the ability of the entorhinal cortex to generate seizures. It also may be proposed that Schaffer collateral cut may model the epileptic condition in which CA3 damage results in loss of hippocampal control over the entorhinal cortex. In conclusion, these experiments demonstrate that interictal activity controls rather than promotes ictal events, and functional integrity of CA3 constitutes a critical control mechanism in temporal lobe epilepsy.

4-Aminopyridine↗
PubMed2000

Odor regulates the expression of the mitogen-activated protein kinase phosphatase gene hVH-5 in bilateral entorhinal cortex-lesioned rats.

Since it is known that several immediate early genes are induced by olfactory stimuli, we determined whether an olfactory stimulus also induces the expression of the mitogen-activated protein kinase (MAPK) phosphatase gene hVH-5 (homologue of vaccinia virus H1 phosphatase gene, clone 5), a member of a novel class of immediate early genes encoding dual-specificity protein phosphatases. The expression was studied by in situ hybridization in different brain structures involved in odor processing, in control and bilateral entorhinal cortex (EC) lesioned rats. EC-lesion did not significantly affect hVH-5 gene expression in the glomerular cell layer of the olfactory bulb (OB), while odor stimulation induced it in both control and EC-lesioned groups. In contrast, odor-induced expression of hVH-5 gene in mitral/granular cell layers was only evident after lesion of the EC. Similar results were obtained in the piriform cortex (PCx), a structure intimately connected to the mitral cell layer. In the CA1 hippocampal subfield, odor stimulation induced hVH-5 gene expression in both control and EC-lesioned animals, the increase being potentiated in lesioned rats. CA3 and dentate gyrus exhibited a similar pattern of gene expression, the odor stimulating gene expression in both control and lesioned groups. The amygdala (Am) displayed no significant change. It appears that through the induction of a MAPK phosphatase, the EC controls MAPK activities differently after odor stimulation in OB, PCx and hippocampus (Hip). The results illustrate the notion that odor representation in the brain requires plastic modifications at both anatomical and functional levels.

Amygdala↗
PubMed1998

Chronic changes in synaptic responses of entorhinal and hippocampal neurons after amino-oxyacetic acid (AOAA)-induced entorhinal cortical neuron loss.

Chronic changes in synaptic responses of entorhinal and hippocampal neurons after amino-oxyacetic acid (AOAA)-induced entorhinal neuron loss. J. Neurophysiol. 80: 3031-3046, 1998. Synaptic responses of entorhinal cortical and hippocampal neurons were examined in vivo and in vitro, 1 mo to 1.5 yr after a unilateral entorhinal lesion caused by a focal injection of amino-oxyacetic acid (AOAA). It has been shown previously that injection of AOAA into the medial entorhinal cortex produces cell loss in layer III preferentially. Although behavioral seizures stopped approximately 2 h after AOAA treatment, abnormal evoked responses were recorded as long as 1.5 yr later in the entorhinal cortex and hippocampus. In the majority of slices from AOAA-treated rats, responses recorded in the superficial layers of the medial entorhinal cortex to white matter, presubiculum, or parasubiculum stimulation were abnormal. Extracellularly recorded responses to white matter stimulation were prolonged and repetitive in the superficial layers. Intracellular recordings showed that residual principal cells in superficial layers produced prolonged, repetitive excitatory postsynaptic potentials (EPSPs) and discharges in response to white matter stimulation compared with brief EPSPs and a single discharge in controls. Responses of deep layer neurons of AOAA-treated rats did not differ from controls in their initial synaptic response. However, in a some of these neurons, additional periods of excitatory activity occurred after a delay. Abnormal responses were recorded from slices ipsilateral as well as contralateral to the lesioned hemisphere. Recordings from the entorhinal cortex in vivo were abnormal also, as demonstrated by prolonged and repetitive responses to stimulation of the area CA1/subiculum border. Evoked responses of hippocampal neurons, recorded in vitro or in vivo, demonstrated abnormalities in selected pathways, such as responses of CA3 neurons to hilar stimulation in vitro. There was a deficit in the duration of potentiation of CA1 population spikes in response to repetitive CA3 stimulation in AOAA-treated rats. Theta activity was reduced in amplitude in area CA1 and the dentate gyrus of AOAA-treated rats, although evoked responses to angular bundle stimulation could not be distinguished from controls. The results demonstrate that a preferential lesion of layer III of the entorhinal cortex produces a long-lasting change in evoked and spontaneous activity in parts of the entorhinal cortex and hippocampus. Given the similarity of the lesion produced by AOAA and entorhinal lesions in temporal lobe epileptics, these data support the hypothesis that preferential damage to the entorhinal cortex contributes to long-lasting changes in excitability, which could be relevant to the etiology of temporal lobe epilepsy.

Aminooxyacetic Acid↗
PubMed1994

Transfer kindling between sites in the entorhinal cortex-perforant path-dentate gyrus system.

Repeated electrical stimulation of forebrain sites can lead to an enhanced epileptogenic response (the kindling phenomenon). When stimulation is subsequently applied to related sites, these developments occur more rapidly (the transfer effect). Axonal pathways do not support epileptiform discharge, so it is generally assumed that the kindling develops, when these pathways are stimulated, in the target structures of those pathways. Consequently, transfer kindling should be immediate, or at least very rapid. Primary and 'transfer' kindling effects were examined in the excitatory, monosynaptically coupled, entorhinal cortex-dentate gyrus system. Transfer kindling was begun following either a 24 h delay or a 4 week delay between the last primary site convulsion and the start of transfer kindling in the secondary site. A 4 week delay between kindling sites was chosen to minimize the effects of a previously reported transient suppression of transfer kindling and the increased inhibition that has been shown to develop in the dentate gyrus as a result of kindling the perforant path. Although there was a significant transfer to the dentate gyrus following perforant path stimulation, the dentate gyrus still required a mean of 18.5 (24 h delay) and 20.3 (4 week delay) stimulations to reach criterion. In the entorhinal cortex, there was a significant positive transfer following primary kindling of the perforant path only in the group in which transfer kindling was begun after a 4 week delay. When the perforant path itself was the transfer site, there was a significant savings in number of afterdischarges needed to reach criterion following dentate gyrus kindling but no savings following entorhinal cortex kindling.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1997

192 IgG-saporin-induced loss of cholinergic neurons in the septum abolishes cholinergic sprouting after unilateral entorhinal lesion in the rat.

After unilateral lesion of the entorhinal cortex, cholinergic septohippocampal fibres are believed to sprout in the denervated outer molecular layer of the rat dentate gyrus. This cholinergic sprouting has been demonstrated by acetylcholinesterase (AChE) histochemistry, a method said selectively to label cholinergic septohippocampal fibres in the hippocampus. However, a recent report has questioned this concept, suggesting that AChE may not be an adequate marker to monitor cholinergic sprouting and that other, non-cholinergic axons sprouting after entorhinal cortex lesion cause the dense AChE-positive band in the denervated outer molecular layer. In order to determine the contribution of cholinergic septohippocampal fibres to the dense AChE band appearing after entorhinal cortex lesion, the neurotoxin 192 IgG-saporin, known to destroy cholinergic neurons in the basal forebrain selectively, was used. Rats received bilateral injections of 192 IgG-saporin into the lateral ventricles 3 weeks before entorhinal cortex lesion, simultaneously with entorhinal cortex lesion, or 8 weeks after entorhinal cortex lesion. Immunocytochemistry for choline acetyltransferase (ChAT) and in situ hybridization for ChAT mRNA demonstrated the loss of cholinergic neurons in the medial septum and diagonal band after 192 IgG-saporin treatment. The cholinergic sprouting response in the molecular layer, as visualized with AChE histochemistry, was abolished in all animals treated with immunotoxin. These data indicate that the dense AChE band forming after entorhinal cortex lesion represents the sprouting of cholinergic septohippocampal fibres.

Acetylcholinesterase↗
PubMed1977

Histochemical evidence of altered development of cholinergic fibers in the rat dentate gyrus following lesions. II. Effects of partial entorhinal and simultaneous multiple lesions.

It has been concluded previously that the septohippocampal fibers which project to the rat dentate gyrus extend or branch in the denervated area of the molecular layer following a complete ipsilateral entorhinal lesion. The septohippocampal fibers thus appear to replace some of the perforant fibers which degenerate as a result of the lesion. The reactive fibers eventually become localized to a much smaller and more superficial area after lesions of immature rats than after lesions made in adulthood. To determine whether this difference in the response results from a selective reaction to loss of the lateral perforant path in the immature rat, various portions of the entorhinal cortex were removed at the age of 11 days, and the cholinergic septohippocampal fibers were visualized by acetylcholinesterase histochemistry. An alternative possibility, that the difference between immature and adult rats is attributable to an interaction with other reactive afferents, was tested by removing other sources of input (the contralateral entorhinal cortex, contralateral hippocampal formation or both) along with the ipsilateral entorhinal cortex at the age of 11 days and then demonstrating the septohippocampal fibers histochemically. Lesions of the lateral part of the ipsilateral entorhinal cortex (source of the lateral perforant path) at 11 days of age evoked a septohippocampal reaction along the outer edge of the molecular layer, where the lateral perforant path fibers normally terminate. This result matched that produced by a complete entorhinal lesion. Lesions of the medial entorhinal cortex evoked no obvious reaction. In contrast, the septohippocampal fibers in adult rats proliferated in the denervated area of the molecular layer after lesions of either part of the entorhinal cortex. Combining lesions of other sources of innervation to the dentate gyrus with an ipsilateral entorhinal lesion at 11 days of age did not alter the response of septohippocampal fibers, as determined histochemically. Neither did the septohippocampal fibers react to removal of commissural afferents alone. The response at any age was unaffected by prior or subsequent removal of the contralateral entorhinal cortex. These results indicate that in immature rats the septohippocampal fibers respond only to loss of the lateral perforant path, but these same fibers can later react to loss of any part of the perforant path. They are regarded as support for the hypothesis that the reactive septohippocampal fibers preferentially interact with dendritic growth cones. Our results do not support explanations based on a hypothetical attraction between septohippocampal and crossed perforant path fibers (which react in the same area) or on competition with commissural fibers (which reinnervate an adjacent area). We suggest further that proximity to the degenerating elements does not in itself determine the pattern of reinnervation after lesions of the central nervous system.

Acetylcholinesterase↗
PubMed2004

Two reentrant pathways in the hippocampal-entorhinal system.

The entorhinal cortex has long been recognized as an important interface between the hippocampal formation and the neocortex. The notion of bidirectional connections between the entorhinal cortex and the hippocampal formation have led to the suggestion that hippocampal output originating in CA1 and subiculum may reenter hippocampal subfields via the entorhinal cortex. To investigate this, we used simultaneous multi-site field potential recordings and current source density analysis in the entorhinal cortex and hippocampal formation of the rat in vivo. Under ketamine/xylazine anesthesia, we found that repetitive stimulation of subiculum or Schaffer collaterals facilitated entorhinal responses, such that a population spike appeared in layer III. In addition, a current sink in stratum lacunosum-moleculare of area CA1 was found, that followed responses in the entorhinal cortex, indicating reentrance into this area. Responses indicating reentrance in the dentate gyrus were not found under ketamine/xylazine anesthesia, but were readily evoked under urethane anesthesia. Reentrance into CA1 was also encountered under urethane anesthesia. These results suggest that parallel, but possibly functionally distinct, connections are present between the output of the hippocampal formation and cells in layers III and II of the entorhinal cortex that project to area CA1 and the dentate gyrus, respectively.

Action Potentials↗
PubMed1996

Regional specificity of alterations in NGF, BDNF and NT-3 levels in Alzheimer's disease.

Using two-site enzyme immunoassays (EIAs), we measured the levels of neurotrophins, nerve growth factor (NGF), brain-derived neurotrophic factor (BDNF) and neurotrophin-3 (NT-3) simultaneously in three brain regions (motor cortex, dentate gyrus and entorhinal cortex) of patients with Alzheimer's disease (AD) and control individuals. Significant differences between the neurotrophin levels of these two groups were found in the different brain regions depending on the neurotrophin. The NGF level in the dentate gyrus of AD patients was higher, whereas the BDNF level in the entorhinal cortex and the NT-3 level in the motor cortex were lower than the corresponding control levels. These results indicate that protein levels of individual neurotrophins in different brain regions are affected differently by AD, and such differential changes may contribute to the complex pathology of AD.

Aged↗
PubMed2001

Expression of amyloid precursor protein, tau and presenilin RNAs in rat hippocampus following deafferentation lesions.

In this study, entorhinal cortex lesions and/or medial septal area cholinergic lesions were used in the rat to mimic some of the principal and earliest affects in Alzheimer's disease, namely hippocampal deafferentation. We wished to test the hypothesis that deafferentation lesions cause changes in the regulation of three proteins that are known to be important in Alzheimer's disease pathology, namely amyloid precursor protein, presenilin and tau. Expression of amyloid precursor protein mRNA was increased in several subfields of hippocampus when examined 1 week after entorhinal cortex lesion, but was reduced, compared to sham operated controls, after medial septal area cholinergic lesions. Cholinergic lesions were combined with entorhinal cortex lesions and produced no change in APP mRNA levels compared to controls. No significant changes were observed in the parietal cortex after entorhinal cortex or cholinergic lesions either alone or in combination. Tau mRNA level in hippocampus was unchanged after lesions. Presenilin-1 mRNA was expressed in the hippocampus at very low levels, and appeared to be increased following entorhinal cortex lesion. Our results support the hypothesis that amyloid precursor protein expression in hippocampal neurons is differentially affected by glutamatergic and cholinergic afferent input, and that presenilin-1, but not tau, may be subject to the same type of control in vivo.

Acetylcholinesterase↗
PubMed1996

Epileptiform activity induced by pilocarpine in the rat hippocampal-entorhinal slice preparation.

An in vitro slice preparation of combined hippocampus and entorhinal cortex from adult rats was used to study the modalities of generation and propagation, as well as the pharmacological properties of the epileptiform activity induced by the muscarinic agonist pilocarpine (10 microM). Simultaneous field potentials recordings were made from the medial entorhinal cortex and from the dentate gyrus, CA3 and CA1 subfields. Pilocarpine application induced two types of interictal epileptiform discharges. The first occurred in the entorhinal cortex and consisted of bursts of population spikes lasting 408 +/- 135 ms (n = 20 slices) and repeating at a rate of 0.26 +/- 0.07 Hz (n = 20); this interictal activity propagated to the hippocampus via the perforant path. The second type was only observed in CA3 and CA1 subfields, had shorter duration (82 +/- 16 ms; n = 20) and occurred at a higher rate (1.42 +/- 0.7 Hz; n = 20) than the first type. Ictal epileptiform discharges (duration: 11.5 +/- 4.1 s; rate: 0.002 +/- 0.0009 Hz; n = 10) were also seen in the entorhinal cortex, from where they propagated to the dentate, CA3 and CA1 via the hippocampal trisynaptic loop as revealed by latency analysis and lesion experiments. Ictal and interictal discharges of entorhinal origin disappeared in the hippocampal sectors, but continued to occur in the entorhinal cortex following a cut of the perforant path (n = 5). Fast interictal discharges observed solely in the hippocampus originated in CA3, since sectioning the Schaffer collaterals made them disappear in CA1 (n = 7). All types of epileptiform activity disappeared during application of the non-N-methyl-D-aspartate receptor antagonist 6-cyano-7-nitroquinoxaline-2, 3-dione (10 microM; n = 7). By contrast, the N-methyl-D-aspartate receptor antagonist 3-3(2-carboxy-piperazine-4-yl) propyl-1-phosphonate (10 microM) abolished ictal discharges in the entorhinal cortex and reduced the duration of the interictal events recorded in this area (n = 7). Interictal discharges originating from CA3 continued to occur at a higher rate than in control during application of this N-methyl-D-aspartate receptor antagonist. Our study confirms that the combined hippocampal-entorhinal slice preparation represents a suitable model for understanding the modalities of origin and propagation of epileptiform activity within the limbic system. In this in vitro preparation, the entorhinal cortex is the site of origin for ictal discharges. Moreover, the different types of epileptiform activity induced by this muscarinic agonist have specific, structure-dependent pharmacological profiles. These results are discussed in relation to those obtained in vivo.

Animals↗
PubMed1993

Entorhinal axons project to dentate gyrus in organotypic slice co-culture.

We have demonstrated the formation of entorhinodentate projections by axons arising from explants of embryonic mouse entorhinal cortex or slices of postnatal rat entorhinal area co-cultured in contact with slices of postnatal rat hippocampus in roller tube and static culture. Species-specific markers (Thy-1 alleles and M6) showed that the most dense part of the projection was to the outer part of the molecular layer of the dentate gyrus (i.e. excluding the commissural-association zone). Retrograde axonal transport of fluorescent tracers placed in the dentate gyrus labelled a densely packed superficial layer of stellate cells in the entorhinal cortex. Anterograde axonal transport of biocytin placed in the entorhinal cortex showed that the entorhinodentate fibres formed typical parallel bundles oriented at right angles to the dentate granule cell dendrites and had short-stalked boutons. The formation of entorhinodentate synapses was confirmed in the electron microscope by electron-dense degeneration after cutting the previously formed connection between the co-cultures. Synaptic transmission was demonstrated by extracellular recording of postsynaptic field potentials after entorhinal stimulation. The entorhinal fibres also projected to the hippocampal stratum lacunosum-moleculare of fields CA1 and CA3, and were present in the outer part of the stratum oriens of the subiculum; in some cases they perforated the pyramidal cell layer of the subiculum. We conclude that the necessary molecular and tissue organizational signals for the formation of an entorhinodentate projection are present in tissues maintained in organotypic slice co-culture, and remain effective in the cross-species mouse-to-rat situation.

Animals↗
PubMed2000

The parahippocampal region: corticocortical connectivity.

The parahippocampal region, as defined in this review, comprises the cortical regions that surround the rodent hippocampus including the perirhinal, postrhinal, and entorhinal cortices. The comparable regions in the primate brain are the perirhinal, parahippocampal, and entorhinal cortices. The perirhinal and postrhinal/parahippocampal cortices provide the major polysensory input to the hippocampus through their entorhinal connections and are the recipients of differing combinations of sensory information. The differences in the perirhinal and postrhinal cortical afferentation have important functional implications, in part, because these two regions project with different terminal patterns to the entorhinal cortex. The perirhinal cortex projects preferentially to the lateral entorhinal area (LEA), and the postrhinal cortex projects preferentially to the medial entorhinal area (MEA) and the caudal portion of LEA. Although the perirhinal and postrhinal cortices provide the major cortical input to the entorhinal cortex, the entorhinal cortex itself receives some direct cortical input. An examination of the cortical afferentation of the entorhinal cortex reveals an interesting principle of connectivity among these regions; the composition of the direct neocortical input to the LEA is more similar to that of the perirhinal cortex, and the composition of the direct neocortical input to the MEA is more similar to that of the postrhinal cortex. Thus, polymodal associational input to the LEA and the MEA exhibits some segregation and is organized in parallel. The organization of intrinsic connections for each of the parahippocampal regions also contributes to the segregation of information into parallel pathways.

Animals↗