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At least 775 records · Page 43Linked to original sources
PubMed2006

NG2 upregulation in the denervated rat fascia dentata following unilateral entorhinal cortex lesion.

The chondroitin sulfate proteoglycan NG2 is a component of the glial scar following brain injury. Because of its growth inhibiting properties, it has been suggested to impede axonal regeneration. To study whether NG2 could also regulate axonal growth in denervated brain areas, changes in NG2 were studied in the rat fascia dentata following entorhinal deafferentation and were correlated with the post-lesional sprouting response. Laser microdissection was employed to selectively harvest the denervated molecular layer and combined with quantitative RT-PCR to measure changes in NG2 mRNA (6 h, 12 h, 2 days, 4 days, 7 days post-lesion). This revealed increases of NG2 mRNA at day 2 (2.5-fold) and day 4 (2-fold) post-lesion. Immunocytochemistry was used to detect changes in NG2 protein (1 days, 4 days, 7 days, 10 days, 14 days, 30 days, 6 months post-lesion). NG2 staining was increased in the denervated outer molecular layer at day 1 post-lesion, reached a maximum 10 days post-lesion, and returned to control levels thereafter. Electron microscopy revealed NG2 immunoprecipitate on glial surfaces and in the extracellular matrix around neuronal profiles, indicating that NG2 is secreted following denervation. Double labeling of NG2-immunopositive cells with markers for astrocytes, microglia/macrophages, and mature oligodendrocytes suggested that NG2 cells are a distinct glial subpopulation before and after entorhinal deafferentation. BrdU labeling revealed that some of the NG2-positive cells are generated post-lesion. Taken together, our data revealed a layer-specific upregulation of NG2 in the denervated fascia dentata that coincides with the sprouting response. This suggests that NG2 could regulate lesion-induced axonal growth in denervated areas of the brain.

Acetylcholinesterase↗
PubMed2001

Training in the step-down inhibitory avoidance task time-dependently increases cAMP-dependent protein kinase activity in the entorhinal cortex.

The cAMP/cAMP-dependent protein kinase (PKA) signaling pathway has been implicated in synaptic plasticity changes and memory consolidation. Several cortical structures are involved in the consolidation of memory for inhibitory avoidance. The aim of the present work was to observe the effects of training in the inhibitory avoidance task on the levels of PKA activity in the entorhinal, parietal and posterior cingulate cortex (EC, PARIET and PC), and the medial precentral area (Fr2) of the rat, at different post-training times (0, 1.5, 3 and 6h). PKA activity, assayed using [gamma-32P]ATP and kemptide, a selective substrate, increased in the EC 3 h after training, but no changes were observed in PARIET, PC and Fr2. These results suggest that the late phase of memory consolidation of inhibitory avoidance requires a functional PKA signaling pathway in the EC in a way that a 'peak' of PKA activity is observed.

Animals↗
PubMed2003

Hippocampal and entorhinal cortex neurofibrillary tangle formation in Guamanian Chamorros free of overt neurologic dysfunction.

Since first described, amyotrophic lateral sclerosis/parkinsonism-dementia complex (ALS/PDC) of Guam has represented an important model of age-related neurodegenerative disease. ALS/PDC is characterized neuropathologically by severe widespread involvement by neurofibrillary tangles (NFTs). Over the past 30 years there has been a dramatic decrease in the incidence of ALS and a 10-year increase in the age of onset of ALS and PDC. In 1979, Anderson et al reported evidence of significant NFT involvement in Guam natives who had been free of evidence of neurologic dysfunction. Using the slides from this study, we re-examined the extent of hippocampus and entorhinal NFT involvement and compared it to brains recently obtained from neurologically intact Guam natives and age-matched controls from New York. The tendency towards hippocampal and entorhinal NFT formation continues to be encountered among the inhabitants of Guam, particularly among those over age 50. although severe involvement was less commonly noted in relatively young individuals (< 50 years). As noted by Anderson et al, the pattern of neuropathologic lesions seen in those with extensive NFT involvement suggests that such cases represent preclinical examples of ALS/PDC in individuals who have yet to accumulate a sufficient burden of pathology to attract clinical attention and diagnostic evaluation.

Adolescent↗
PubMed1994

Increased numbers of beta APP-immunoreactive neurones in the entorhinal cortex after head injury.

In a previous publication we hypothesized that Alzheimer's disease (AD) can be induced by the age-related increase in expression of beta-amyloid precursor protein (beta APP) in the medial temporal lobe. Head injury has also been identified as a risk factor for AD and as such, similarities should exist between the pathology found after head injury and the earliest stages of pathology in AD. In this study, we have quantified the number of beta APP-immunoreactive neurones in the medial temporal cortex (pre-alpha cells, layer II) of 13 head injured and 17 control patients. Significantly more beta APP immunoreactive neurones were observed in head injury cases (mean 18.4 per cluster) compared with controls (mean 13.4 per cluster, p < 0.05). These data provide a mechanism to explain how an environmental event such as head injury can generate the same molecular pathology (increased neuronal beta APP) as is found in the earliest stages of AD.

Adolescent↗
PubMed2003

Selective neurodegeneration of hippocampus and entorhinal cortex correlates with spatial learning impairments in rats with bilateral ibotenate lesions of ventral subiculum.

Rats with bilateral ibotenic acid lesions of ventral subiculum were tested in an eight-arm radial maze task for spatial learning and memory functions. The performance of the lesioned rats was severely impaired relative to control rats in both acquisition and retention of the spatial task. Following subicular lesions, profound neurodegeneration of the CA1 and CA3 sub sectors of hippocampus and entorhinocortical layers I, II, III, V and VI was observed. These results support the concept that neurons in the ventral subiculum are a part of the neural network along with the above neurons, which could be involved in the processing of spatial information.

Animals↗
PubMed2002

Consistent immunohistochemical detection of intracellular beta-amyloid42 in pyramidal neurons of Alzheimer's disease entorhinal cortex.

We compared the effects of three pretreatment immunohistochemical techniques (no pretreatment, pepsin predigestion and heat pretreatment (HEAT)) for detecting intracellular beta-amyloid42 (Abeta42) in pyramidal neurons of formalin-fixed Alzheimer's disease (AD) cortices (n = 25). Although all three protocols immunostained Abeta42 in amyloid plaques using four commercially-obtained Abeta42 specific antibodies, only the HEAT protocol consistently detected prominent intracellular Abeta42 in pyramidal neurons. This suggests that the Abeta42 present in amyloid plaques may be structurally distinct from that located within the neurons perhaps due to differential binding proteins coupling or a consequence of formalin fixation. Detection of an abundant intracellular Abeta42 in neurons may provide alternate explanations for the origin of dense-core amyloid plaques in AD cortices other than the conventional chronic extracellular Abeta42 deposition hypothesis.

Aged↗
PubMed1995

Quantification of beta APP immunoreactive pre-alpha cells in the entorhinal cortex using image analysis.

The neuropathological diagnosis of Alzheimer's disease requires an assessment of the quantity of pathology present. Advances in molecular biology have highlighted the role of beta-amyloid precursor protein (beta APP) in the pathogenesis of the disease. This protein is found in neurons and other cells and many neuropathological studies would benefit from a method which generates reliable data on the numbers of cells containing significant amounts of the protein. Classically, generation of such data would have involved laborious manual counting. This particular approach carries low levels of inter- and intra-rater reliability and is much dependent on the skill and experience of the operator. We have used immunocytochemistry to specifically define a single cell population, pre-alpha cells, containing beta APP, and have developed a computerized cell counting programme that can reliably quantify these cells in human post-mortem brain samples. We have obtained a high level of accuracy (> 95%) and efficiency in identifying and quantifying target cells and have demonstrated that our protocol can be used effectively by both novice and expert. This method could be easily configured to provide quantitative data for a wide range of immunocytochemically defined cell populations.

Adolescent↗
PubMed2002

Sleep states differentiate single neuron activity recorded from human epileptic hippocampus, entorhinal cortex, and subiculum.

Animal models of epilepsy have shown that synchronous burst firing is associated with epileptogenesis, yet the evidence from human studies linking neuronal synchrony and burst firing to epileptogenesis remains equivocal. Sleep-wake states have been shown to differentially modulate the generation of epileptiform EEG spikes between brain regions of greater and lesser seizure-generating potential, providing information that helps to identify the primary epileptogenic region. Using these state-dependent mechanisms to assist us in identifying neuronal correlates of human epilepsy, we recorded interictal neuronal activity from mesial temporal lobe (MTL) areas in epileptic patients implanted with depth electrodes required for medical diagnosis during polysomnographically defined sleep-wake states. Results show that single neurons recorded ipsilateral to seizure-initiating MTL ("epileptic") areas had significantly higher firing rates (p = 0.01) and burst propensity (p = 0.01) and greater synchrony of discharges (p = 0.003) compared with neurons recorded from contralateral non-seizure-generating MTL ("non-epileptic") areas. In particular, during episodes of slow wave sleep (SWS) and rapid eye movement (REM) sleep, epileptic hippocampal neurons had significantly higher burst rates compared with non-epileptic hippocampal neurons (both p = 0.01). In contrast, during episodes of wakefulness (Aw), no difference in burst firing between epileptic and non-epileptic hippocampal neurons was observed. Furthermore, synchronous firing was significantly higher between epileptic MTL neurons compared with non-epileptic MTL neurons during SWS (p = 0.04) and REM sleep (p = 0.02), but no difference in neuronal synchrony was found between epileptic and non-epileptic neurons during Aw. These results provide evidence that sleep states differentially modulate abnormal epileptogenic neuronal discharge properties within human MTL and confirm that neuronal burst firing and enhanced neuronal synchrony observed in experimental animal models of epilepsy characterizes human epilepsy as well.

Action Potentials↗
PubMed2001

Monitoring NAD(P)H autofluorescence to assess mitochondrial metabolic functions in rat hippocampal-entorhinal cortex slices.

Changes in neuronal energy metabolism, mitochondrial functions and homeostasis of reactive oxygen species are often supposed to induce alterations in neuronal activity in hippocampal slice models. In order to investigate the NAD(P)H autofluorescence signal in brain slice models, methods to monitor NAD(P)H signal in isolated mitochondria as described by Chance et al. [J. Biol. Chem. 254 (1979) 4764] and dissociated neurons as described by Duchen [Biochem. J. 283 (1992) 41] were adapted to recording conditions required for brain slices. Considering different experimental questions, we established an approach to monitor NAD(P)H autofluorescence signals from hippocampal slices of 400 microm thickness under either submerged or interface conditions. Therefore the procedure described here allows the measurement of NAD(P)H autofluorescence under conditions typically required in electrophysiological experiments. Depolarization of plasma membrane caused by electrical stimulation or application of glutamate (100 microM) resulted in a characteristic initial decrease followed by a long-lasting increase in the NAD(P)H autofluorescence signal. H(2)O(2) (100 microM) evoked a strong NAD(P)H signal decrease indicating direct oxidation to the nonfluorescencend NAD(P)(+). In contrast, the increase in NAD(P)H signal that followed a brief inhibition of mitochondrial respiratory chain complex I using rotenone (1 microM) indicated an accumulation of NAD(P)H. However, in presence of rotenone (1 microM) electrically evoked long-lasting NAD(P)H signal overshoot decreased progressively, due to a negative feedback of accumulated NAD(P)H to the citrate cycle. A comparable reduction in NAD(P)H signal increase were observed during low-Mg(2+) induced epileptiform activity, indicating a relative energy failure. In conclusion, the method presented here allows to monitor NAD(P)H autofluorescence signals to gain insight into the coupling of neuronal activity, energy metabolism and mitochondrial function in brain slice models.

Animals↗
PubMed1982

Entorhinal cortex lesions induce a decreased calcium transport in hippocampal mitochondria.

Lesions to the entorhinal afferent of the hippocampus in rats caused marked changes in calcium transport into mitochondria. Pyruvate-supported calcium transport into mitochondria from the denervated hippocampus was decreased to a larger extent than succinate-supported transport, and adenosine triphosphate-supported transport was not significantly modified. Although cytochrome oxidase and succinate dehydrogenase activities were not significantly changed by entorhinal lesions, pyruvate flux through pyruvate dehydrogenase was significantly decreased, and this effect was correlated with changes in pyruvate-supported calcium transport. The active portion of pyruvate dehydrogenase decreased, whereas total pyruvate dehydrogenase was not modified. These data suggest that denervation might initiate dendritic atrophy and subsequent growth responses by modifying calcium regulation through a change in the phosphorylation of pyruvate dehydrogenase.

Adenosine Triphosphate↗
PubMed1975

The topographical and laminar organization of the presubiculum's projection to the ipsi- and contralateral entorhinal cortex in the guinea pig.

This is a detailed report of a previously described projection from the presubiculum to the entorhinal area (Shipley, '74). The terminal degeneration in the entorhinal area is specifically confined to the outer three layers of this cortex. The projection is topogtaphically organized and confined to dorsal and medial parts of the entorhinal area. A similarly organized projection courses via the dorsal psalterium (dorsal hippocampal commissure) to the contralateral entorhinal area. Thus each presubiculum has an organized terminal pathway to the entorhinal cortices of both hemispheres.

Animals↗
PubMedDate not supplied

The squirrel monkey entorhinal cortex: architecture and medial frontal afferents.

The cytoarchitecture of the periallocortex was studied in cresyl-violet-stained frontal and sagittal sections in six adult squirrel monkeys (Saimiri sciureus). The entorhinal area, located between the sulcus semiannularis and sulcus rhinalis in the rostral parahippocampal gyrus, has been divided into a caudal-medial Area 28a and rostral-lateral Area 28b. Of the six paleocortical laminae, Layer II is the most distinctive, for in 28a it consists of a deeply-stained, dense, continuous lamina and in 28b is interrupted into cell islands. Layer IV, lamina dissecans, is thick and irregular in 28b, thin and of uniform thickness in rostral 28a, and disappears in caudal 28a intransition to the isocortex of the more caudal parahippocampal gyrus. Further observations in Fink-Heimser silver material of fiber degeneration resulting from medial prefrontal ablations in these monkeys suggest that Areas 9 and 10 project to syperficial layers (Layer II) of 28a whereas the orbital probably projects to the deeper layers (Layer V) of 28b. The topography and laminar specificity of prefrontal-entorhinal connections may have important functional consequences in terms of hippocampal input.

Afferent Pathways↗
PubMed2000

MRI volumetry of the hippocampus, amygdala, entorhinal cortex, and perirhinal cortex after status epilepticus.

Neuronal damage has been observed in the medial temporal lobe of both humans and animals following status epilepticus. The aim of the present study was to investigate the occurrence of medial temporal lobe damage in status epilepticus patients treated in hospital with a predetermined protocol and to assess whether the changes progress in a long-term follow-up. The volumes of the hippocampus, amygdala, entorhinal and perirhinal cortices were measured using magnetic resonance imaging (MRI) in nine adult patients with status epilepticus 3 weeks, 6 and 12 months after the insult. The control group included 20 healthy subjects. The etiology of status epilepticus was an acute process in one patient and a chronic process in eight cases. The mean duration of secondarily generalized tonic-clonic status epilepticus episodes was 1 h and 44 min. Volumetric MRI indicated that none of the patients developed marked volume reduction in the hippocampus, amygdala, or the entorhinal and perirhinal cortices during the 1-year follow-up period. Status epilepticus does not invariably lead to a progressive volume reduction in the medial temporal lobe structures of adult patients treated promptly in hospital with a predetermined protocol for rapid cessation of seizure activity.

Adolescent↗
PubMed1998

Beta-frequency (15-35 Hz) electroencephalogram activities elicited by toluene and electrical stimulation in the behaving rat.

Bursts of beta-frequency (15-35 Hz) electroencephalogram activity occur in the olfactory system during odour sampling, but their mode of propagation within the olfactory system and potential contribution to the mechanisms of learning and memory are unclear. We have elicited large-amplitude beta activity in the rat olfactory system by applying noxious olfactory stimuli (toluene), and have monitored the bursts via chronically-implanted electrodes. Following exposure to toluene, coherent bursts with a peak frequency of 19.8 +/- 0.9 Hz were observed in the olfactory bulb, piriform cortex, entorhinal cortex and dentate gyrus. The timing of the bursts and the phases of electroencephalogram cross-spectra indicate that beta bursts propagate in a caudal direction from the olfactory bulb to the entorhinal cortex. The time delays between peaks of bursts in these structures were similar to latency differences for field potentials evoked by olfactory bulb or piriform cortex test-pulses. Peaks of burst cycles in the dentate region, however, were observed just prior to those in the entorhinal cortex. Surprisingly, power in toluene-induced beta-frequency oscillations was not increased following long-term potentiation induced by tetanic stimulation of the olfactory bulb, piriform cortex and entorhinal cortex. The activity of local inhibitory mechanisms may therefore counteract the effects of synaptic enhancements in afferent pathways during beta bursts. Low-frequency electrical stimulation of the piriform cortex was most effective in inducing coherent oscillatory responses in the entorhinal cortex and dentate gyrus at stimulation frequencies between 12 and 16 Hz. The results show that repetitive polysynaptic volleys at frequencies in the beta band induced by either toluene or electrical stimulation are transmitted readily within the olfactory system. The propagation of neural activity within this frequency range may therefore contribute to the transmission of olfactory signals to the hippocampal formation, particularly for those odours which induce high-amplitude bursts of beta activity.

Algorithms↗
PubMed1977

Projections from the amygdaloid complex and adjacent olfactory structures to the entorhinal cortex and to the subiculum in the rat and cat.

Axonal projections are described from the lateral and basolateral nuclei of the amygdaloid complex, and from the overlying periamygdaloid and prepiriform cortices and the endopiriform nucleus, to the lateral entohinal area, the ventral part of the subiculum, and the parasubiculum in the cat and rat. All of these projections have well-defined laminar patterns of termination, which are complementary to those of other projections to the same structure. Based on these results, and on cytoarchitectonic distinctions, the lateral entohinal area has been divided into dorsal, ventral, and ventromedial subdivisions. The olfactory bulb and prepiriform cortex project to layers IA and IB, respectively, of all three subdivisions, but the lateral amygdaloid nucleus has a restricted projection to layer III of the ventral subdivision only. The periamygdaloid cortex projects to layer II of the ventromedial and adjoining parts of the ventral subdivisions. The ventral part of the subiculum receives fibers from the posterior division of the basolateral nucleus, which terminate in the cellular layer and the deep half to one-third of the plexiform layer. The periamygdaloid cortex and the endopiriform nucleus also project to the same part of the subiculum, but these fibers terminate in the outer part of the plexiform layer. None of these projections extend into the dorsal part of the subiculum. The posterior division of the basolateral nucleus also projects to the posterodorsal part of the parasubiculum ("parasubiculum a" of Blackstad, '56). These fibers end in the deeper part of the plexiform layer and the superficial part of the cellular layer.

Afferent Pathways↗