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At least 1,621 records · Page 90Linked to original sources
PubMed1999

Spatial and temporal relationships between C-Fos expression and kindling of audiogenic seizures in Wistar rats.

In a strain of Wistar rats selected in our laboratory, audiogenic seizures (AS), characterized by a wild running phase followed by a tonic seizure, can be elicited by exposure to sound. In these animals repeated daily stimulations induce permanent changes which reflect the extension of seizure activity from the brainstem to the forebrain. C-Fos immunoreactivity was used to further characterize the sound-susceptibility of the strain and to specify the spatiotemporal relationships between c-Fos expression and development of AS kindling. AS susceptible rats appeared to be more sensitive to a subthreshold sound as compared to controls. Sound-evoked wild running induced a similar pattern of c-Fos as a full AS in naive rats, confirming the epileptic nature of this early component. AS-induced c-Fos labeling in the auditory pathways of the brainstem extended to the forebrain with repetition of AS and marked increases in c-Fos expression sequentially occurred in the amygdala and perirhinal cortex, followed by the frontoparietal cortex, the piriform cortex, and finally the hippocampus and entorhinal cortex. These results show that the kindled AS preferentially propagate from the brainstem, through the amygdala and the perirhinal cortex, to the motor cortex, with the piriform cortex and hippocampus as secondary targets. No more c-Fos expression was detected 24 h after an AS. A down-regulation of cortical c-Fos induction was observed 1 and 2 days after daily exposure to kindled AS, with full recovery of c-Fos expression after a 5-day seizure-free period. This suggests a regulatory function of c-Fos expression in development of kindling.

Acoustic Stimulation↗
PubMed1992

Localization of gene expression of calreticulin in the brain of adult mouse.

The localization of gene expression of calreticulin, a calcium-binding protein in the endoplasmic reticulum, was examined throughout the entire brain of adult mice by in situ hybridization. Calreticulin mRNA is expressed widely and heterogeneously in discrete neurons throughout the brain, but the white matters expressed it weekly or faintly. In the olfactory bulb, the mRNA is expresses moderately in the mitral cells, but weakly in the periglomerular cells and internal granule cells. In the cerebrum, the gene is expressed intensely in the piriform cortex, but weakly in neocortex, the entorhinal cortex and the amygdaloid nuclei. In the hippocampal formation, calreticulin mRNA is expressed intensely in the CA1-CA3 regions but less intensely in the granule cells of the dentate gyrus. The caudate-putamen, thalamic and hypothalamic nuclei, and mammillary nuclei express the mRNA weakly or faintly. In the mesencephalon, pons and medulla, moderate expression of the mRNA is detected in the pontine nuclei and the locus ceruleus. Weak expression of the mRNA is detected in several discrete nuclei and zones such as the substantia nigra, the superior colliculus and the central gray. Expression signals of calreticulin mRNA are faint in the inferior olive. In the cerebellum, calreticulin mRNA is expressed moderately in the Purkinje cells whereas no significant expression is detected in the granule cells. The plexus choroideus of the lateral, third and fourth ventriculi express calreticulin mRNA intensely although no distinct expression of the mRNA is discerned in the ependyma.

Animals↗
PubMed1992

Distribution of neurofibrillary tangles and senile plaques in the cerebral cortex in postencephalitic parkinsonism.

Postencephalitic parkinsonism is characterized neuropathologically by severe loss of pigmented neurons in the substantia nigra and the presence of high densities of neurofibrillary tangles in several brainstem structures. In 5 cases of postencephalitic parkinsonism, we observed that the neurofibrillary tangle distribution in the cerebral cortex predominated in the hippocampus and entorhinal cortex. In the prefrontal and inferior temporal cortex, neurofibrillary tangles were preferentially localized in layers II and III. This pattern contrasts with the neurofibrillary tangle distribution observed in neocortical areas of Alzheimer's disease cases, where neurofibrillary tangles are denser in layer V than in layer III. These results suggest that specific elements of the cortical circuitry might be differentially affected in postencephalitic parkinsonism as compared to Alzheimer's disease, and that cortical involvement is likely to be a common feature of this condition.

Aged↗
PubMed1998

Central 5-HT3 receptors in P and in AA alcohol-preferring rats: An autoradiographic study.

Considerable evidence exists for an involvement of serotonergic mechanisms in the control of alcohol consumption. In the present study, an extensive 5-hydroxytryptamine (5-HT3) receptor autoradiographical investigation was performed using two genetically selected rat strains, alcohol preferring (P) and Alko alcohol (AA) alcohol-preferring rats, as well as the corresponding alcohol nonpreferring (NP) and Alko nonalcohol (ANA) alcohol-nonpreferring rats. The aim was to determine if there are any differences in 5-HT3 binding levels that may illuminate mechanisms of alcohol preference in these animals. For quantitating 5-HT3 binding sites, [3H]S(-)zacopride (0.5 nM) was used. Non-specific binding was measured in the presence of granisetron 10(-6) M. The [3H]S(-)zacopride binding density was measured in two subregions of the amygdaloid nucleus, frontal cortex, piriform cortex, cingulate laminae, parietal anterior cortex, parietal medial cortex, hippocampus CA1, hippocampus CA3, and entorhinal cortex. In all the brain areas investigated, the results showed no differences between AA and ANA rats. In P rats, compared to NP controls, there was a 30% lower 5-HT3 binding level in the lateral nucleus and the posteromedial cortical nucleus of the amygdala. These findings suggest that the expression of high alcohol preference in genetically selected P and AA rats is not associated with a general alteration of central 5-HT3 receptors, although a lower 5-HT3 receptor level in the amygdala of P rats may contribute to the phenotype of this strain of animals.

Alcohol Drinking↗
PubMed2004

Immunohistochemical studies concerning the neuronal cell cycle of the cat using PCNA, Ki-67 and p53 markers.

Recent studies about parvovirus replication in mature neurones of cats indicate that even feline neurones do not seem to be terminally differentiated. For further determination of the proliferative capability of feline neurones, an immunohistochemical study investigating the neuronal expression of the cell cycle-related proteins, proliferating cell nuclear antigen (PCNA), Ki-67 and p53 was initiated. Brains of 50 cats of different age and gender, dying of various diseases, were examined. Strong PCNA clone PC10 expression could be observed in neurones of the cerebellar cortex and the vestibular nuclei, whereas entorhinal cortex, lateral geniculate nucleus and cerebral cortex revealed only weak immunolabelling. The PCNA clone 19F4 labelled numerous neurones in vestibular nuclei and some Purkinje cells of the cerebellum. Nuclear expression of Ki-67 was sporadic in the vestibular nuclei, but p53 expression could not be detected anywhere in the feline brain. However, the presence of nuclear PCNA and Ki-67 expression indicates that certain feline neurones are capable of re-entering the cell cycle.

Animals↗
PubMed1977

Progressive brain damage accelerates axon sprouting in the adult rat.

An entorhinal cortical lesion causes undamaged fibers in the deafferented hippocampus to sprout and form new connections within 4 to 7 days after the lesion was made. When a partial lesion of the entorhinal cortex precedes a second, more complete entorhinal lesion by a few days, the rate of axon sprouting is accelerated so that the response to the second lesion occurs within only 2 days. This priming effect is present within 4 days, lasts for a few weeks, and eventually subsides. This acceleration may explain, in part, the faster recovery and reduced deficits seen in behavioral studies that have followed serial lesion paradigms.

Acetylcholinesterase↗
PubMed2002

Selective entorhinal and nonselective cortical-hippocampal region lesions, but not selective hippocampal lesions, disrupt learned irrelevance in rabbit eyeblink conditioning.

Prior experiments, as well as computational models, have implicated the hippocampal region in mediating the influence of nonreinforced stimulus preexposure on subsequent learning. Learned irrelevance (LIRR) is a preexposure task in which uncorrelated preexposures to the conditioned stimulus (CS) and the unconditioned stimulus (US) produce a retardation of subsequent CS-US conditioning. In the work presented here, we report the results of tests of LIRR in eyeblink conditioning in rabbits with sham lesions, nonselective cortical-hippocampal region lesions, selective hippocampal lesions, and selective entorhinal lesions. Sham-lesioned rabbits that had been preexposed to the CS and the US exhibited slower acquisition of conditioned response, as compared with context-preexposed controls. Nonselective cotical-hippocampal region lesions disrupted LIRR, whereas selective hippocampal lesions had no detrimental effect on LIRR. Selective entorhinal lesions disrupted LIRR. These findings fit other recent empirical findings and theoretical predictions that some classical conditioning tasks previously thought to depend on the hippocampus depend, rather, on the entorhinal cortex.

Animals↗
PubMed1999

Cerebral amyloid induces aberrant axonal sprouting and ectopic terminal formation in amyloid precursor protein transgenic mice.

A characteristic feature of Alzheimer's disease (AD) is the formation of amyloid plaques in the brain. Although this hallmark pathology has been well described, the biological effects of plaques are poorly understood. To study the effect of amyloid plaques on axons and neuronal connectivity, we have examined the axonal projections from the entorhinal cortex in aged amyloid precursor protein (APP) transgenic mice that exhibit cerebral amyloid deposition in plaques and vessels (APP23 mice). Here we report that entorhinal axons form dystrophic boutons around amyloid plaques in the entorhinal termination zone of the hippocampus. More importantly, entorhinal boutons were found associated with amyloid in ectopic locations within the hippocampus, the thalamus, white matter tracts, as well as surrounding vascular amyloid. Many of these ectopic entorhinal boutons were immunopositive for the growth-associated protein GAP-43 and showed light and electron microscopic characteristics of axonal terminals. Our findings suggest that (1) cerebral amyloid deposition has neurotropic effects and is the main cause of aberrant sprouting in AD brain; (2) the magnitude and significance of sprouting in AD have been underestimated; and (3) cerebral amyloid leads to the disruption of neuronal connectivity which, in turn, may significantly contribute to AD dementia.

Amyloid beta-Protein Precursor↗
PubMedDate not supplied

Exploratory activity and a conditioned fear response: correlation with cortical and subcortical binding of the alpha4beta2 nicotinic receptor agonist [3H]-epibatidine.

Rat behavior in the open field and the conditioned fear response test was correlated with specific binding of the alpha4beta2 nicotinic acetylcholine receptor (nAChR) agonist, [3H]-pibatidine, assayed in different brain structures by autoradiography. A significant positive correlation was found between the ligand binding in the frontal cortex (r = 0.529, p < 0.011), the entorhinal cortex (r = 0.603, p < 0.003), and CA1 layer of the hippocampus (r = 0.465, p < 0.029), and the conditioned freezing reaction in the contextual fear conditioning test. In the frontal cortex, there was also a significant positive correlation between [3H]-epibatidine binding and preconditioned freezing reaction (r = 0.469, p < 0.028), and a negative correlation with rat motility (r = -0.452, p < 0.035). Rat motor activity correlated in a negative way with preconditioned freezing reaction (r = -0.436, p < 0.043), and in a positive way with the number of entries into the central sector of the open field (r = 0.690, p < 0.001). The neophobia-related parameter of the open field behavior (the number of central entries) did not correlate with the [3H]-epibatidine binding. Factor analysis confirmed these findings and showed that rat behavioral parameters measured in the tests of neophobia and conditioned freezing were loading on different factors, thus, pointing to separate central mechanisms operating in both behavioral models of anxiety. Furthermore, factor analysis showed that rat conditioned freezing behavior and [3H]-epibatidine binding in the CA1 layer of the hippocampus and enorhinal cortex, represented similar central processes. These findings suggest that rat emotional reactions evoked by different stressors (neophobia vs. conditioned fear) are differently regulated by the central cholinergic system. The presented data indicate also a significant, structure dependent correlation between rat conditioned emotional reaction and the alpha4beta2 nAChR ligand binding, in the rat cortical forebrain structures.

Animals↗
PubMedDate not supplied

Resistance of the hippocampus in Creutzfeldt-Jakob disease.

Creutzfeldt-Jakob disease (CJD) belongs to the group of subacute spongiform encephalopathies of animals and man. Their pathogenesis is certainly related to the formation and deposition in the brain of an amyloid-type specific protein, named PrPres (prion protein-resistant). The neuropathological topography of CJD does generally admit that archicortex is relatively spared, but only a few papers have been devoted to this issue. A neuropathological study of CJD cases divided in sporadic, familial, and iatrogenic forms of the disease has been carried out, taking into consideration the archipallial lesions in relation to different clinical and neuropathological parameters. The pyramidal cell layer of CA1 of all CJD cases did not show any major loss of neurons in comparison to that observed in other cortical fields of the limbic cortex (mainly in the presubicular and entorhinal cortex) and of the neocortex. Spongiogliotic reaction was observed only in the stratum radiatum and molecularis lacunosum in a iatrogenic case of the disease. The findings observed in the pyramidal cell layer of CA1 were neither related to the clinical duration of the disease nor to the severity of the lesions found in other limbic and neocortical areas. The results of this study support the view of no close relationships between the demential syndrome typically related to the clinical onset and progression of CJD, and the structural damage of the hippocampus classically involved in the pathogenetic mechanism of the amnestic syndrome related to the clinical presentation and course of more common forms of dementias, such as Alzheimer's disease.

Adult↗
PubMed1997

Collateral projections of single neurons in the posterior thalamic region to both the temporal cortex and the amygdala: a fluorescent retrograde double-labeling study in the rat.

It has been reported that the acoustic thalamus of the rat sends projection fibers to both the temporal cortical areas and the lateral amygdaloid nucleus to mediate conditioned emotional responses to an acoustic stimulus. In the present study, fluorescent retrograde double labeling with Fast Blue and Diamidino Yellow has been used in the rat to examine whether single neurons in the posterior thalamic region send axon collaterals to both the temporal cortical areas and lateral amygdaloid nucleus. One of the tracers was injected into the lateral amygdaloid nucleus and the other into the temporal cortical areas close to the rhinal sulcus. Neurons double-labeled with both tracers were found mainly in the posterior intralaminar nucleus and suprageniculate nucleus, and to a lesser extent in the subparafascicular nucleus and medial division of the medial geniculate nucleus. No double-labeled neurons were seen in either the dorsal or ventral division of the medial geniculate nucleus. When one of the tracers was injected into the lateral amygdaloid nucleus and the other into either the dorsal portion of the temporal cortex, the dorsal portion of the entorhinal cortex, or the posterior agranular insular cortex, no double-labeled neurons were found in the posterior thalamic region. The present results indicate that a substantial number of single neurons in the acoustic thalamus project to both the limbic cortical areas and lateral amygdaloid nucleus by way of axon collaterals. These neurons may be implicated in affective and autonomic components of responses to multi-sensory stimuli, including acoustic ones.

Amygdala↗
PubMed2003

Lewy body densities in the entorhinal and anterior cingulate cortex predict cognitive deficits in Parkinson's disease.

Previous studies reported an association between cortical Lewy body (LB) formation and dementia in Parkinson's disease (PD). However, it is unclear whether cognitive decline in this disorder is related to specific patterns of LB distribution within the cerebral cortex. Moreover, the prediction of cognitive status based on concomitant assessment of LB and Alzheimer's disease lesions has led to conflicting results. We performed a clinicopathological study in 22 elderly PD patients in whom parkinsonism preceded cognitive decline by at least 3 years. Cognitive status was assessed prospectively using the clinical dementia rating scale (CDR); quantitative assessment of LB, neurofibrillary tangles (NFT), and senile plaques (SP) was performed in Brodmann areas 9, 21, 24, 40 and the entorhinal cortex. Statistical analysis was performed using both correlation coefficients and logistic regression models. There was a highly significant correlation between CDR scores and regional LB scores in the entorhinal cortex and area 24. LB and SP densities in the entorhinal cortex accounted for 36.2% and 19.3% of the variability in CDR scores. LB densities in area 24 could explain 25.2% of this variability. NFT densities did not predict cognitive status. In multivariate models only LB densities in the entorhinal cortex and anterior cingulate cortex were significantly associated with CDR scores. These results imply that an assessment of LB pathology limited to the entorhinal cortex and area 24 may be sufficient to predict cognition in PD. They also suggest that LB formation in limbic areas may be crucial for the development of PD dementia.

Age Distribution↗
PubMed1999

Development of afferent fiber lamination in the infrapyramidal blade of the rat dentate gyrus.

In the rat dentate gyrus, the lateral perforant path, the medial perforant path, and the major part of the hilar projection to the molecular layer share the lamination domain, mainly in the outer one-third of the molecular layer, the middle one-third, and the inner one-third, respectively. To reveal the order of the afferent fiber lamination and to have an indication of how the synaptic sites on dendrites are determined, we investigated the ontogeny of afferent fiber lamination in the dorsal hippocampus by injecting 1, 1'-dioctodecyl-3,3,3',3'-tetramethylindocarbocyanine perchlorate (DiI) into the entorhinal cortex and hippocampus in vivo. Fibers from the contralateral hilar region were found under the pia mater of the infrapyramidal blade at postnatal day 3 (P3), whereas the entorhinal afferent fibers were absent in the infrapyramidal blade. Then the medial and the lateral perforant path appeared under the pia mater in the infrapyramidal blade as riding on top of the preexisting laminae by P7 and by P11, respectively. Based on the established knowledge that most entorhinal layer II neurons simultaneously innervate both the suprapyramidal blade and infrapyramidal blade by branching, it is assumed that the medial and lateral perforant path in the suprapyramidal blade await an appropriate timing for sprouting of interstitial branches into the infrapyramidal blade. The granule cells in the infrapyramidal blade had dendritic growth cones by P11. Calretinin immunohistochemistry revealed Cajal-Retzius cells in the infrapyramidal blade even at P14. Under the pia mater, axon growth cones of ingrowing afferent fibers may interact with the dendritic growth cones or the Cajal-Retzius cells, and determines the synaptic sites on the granule cell dendrites.

Afferent Pathways↗
PubMedDate not supplied

Proposal to revise the morphologic criteria for the diagnosis of Alzheimer's disease.

Ten years have passed since the drafting of the original National Institute on Aging/American Association of Retired Persons or Khatchaturian criteria for the neuropathologic diagnosis of Alzheimer's disease. In that time, much progress has been made in the study of this disorder. It is clear that although the Khatchaturian criteria have been useful, advances in our understanding of the morphologic substrate of the disease needs to be incorporated in any newly proposed diagnostic criteria. We propose diagnostic criteria to be employed in establishing the diagnosis of Alzheimer's disease in a research setting. Here, we require that a level of density and distribution of senile plaques and neurofibrillary tangles be identified and that other superimposed conditions, such as major cerebral infarcts and/or Parkinson's disease changes, are absent. We also propose separate criteria for diagnosing individuals who die in the early stages of the disease. These latter cases are of extreme research interest and are characterized by a distribution of neurofibrillary tangles that remains primarily restricted to the entorhinal cortex and hippocampus.

Aged↗
PubMed2005

Major dissociation between medial and lateral entorhinal input to dorsal hippocampus.

Hippocampal place cells are a model system of how the brain constructs cognitive representations and of how these representations support complex behavior, learning, and memory. There is, however, a lack of detailed knowledge about the properties of hippocampal afferents. We recorded multiple single units from the hippocampus and the medial and lateral entorhinal areas of behaving rats. Although many medial entorhinal neurons had highly specific place fields, lateral entorhinal neurons displayed weak spatial specificity. This finding demonstrates a fundamental dissociation between the information conveyed to the hippocampus by its major input streams, with spatial information represented by the medial and nonspatial information represented by the lateral entorhinal cortex.

Animals↗
PubMed1983

Benzodiazepine receptor declines in hippocampal formation following limbic seizures.

Electrolytic lesions of entorhinal cortex have previously been shown to consistently produce limbic seizures. We report a bilateral and symmetrical decline in benzodiazepine receptor number in dentate gyrus of the hippocampal formation in unilateral entorhinal cortex-lesioned animals. We think this decline is caused by seizures since phenobarbital pretreatment prevented the appearance of limbic seizures and blocked the receptor decline. We postulate that these receptor declines may contribute to decreased endogenous recurrent inhibition (a presumed GABAergic synapse) of dentate granule cells which could lead to their repetitive firing. Thus these benzodiazepine receptor declines may be a consequence of limbic seizures yet increase the likelihood of subsequent seizures.

Afferent Pathways↗
PubMed2001

Exacerbation of pain by anxiety is associated with activity in a hippocampal network.

It is common clinical experience that anxiety about pain can exacerbate the pain sensation. Using event-related functional magnetic resonance imaging (FMRI), we compared activation responses to noxious thermal stimulation while perceived pain intensity was manipulated by changes in either physical intensity or induced anxiety. One visual signal, which reliably predicted noxious stimulation of moderate intensity, came to evoke low anxiety about the impending pain. Another visual signal was followed by the same, moderate-intensity stimulation on most of the trials, but occasionally by discriminably stronger noxious stimuli, and came to evoke higher anxiety. We found that the entorhinal cortex of the hippocampal formation responded differentially to identical noxious stimuli, dependent on whether the perceived pain intensity was enhanced by pain-relevant anxiety. During this emotional pain modulation, entorhinal responses predicted activity in closely connected, affective (perigenual cingulate), and intensity coding (mid-insula) areas. Our finding suggests that accurate preparatory information during medical and dental procedures alleviates pain by disengaging the hippocampus. It supports the proposal that during anxiety, the hippocampal formation amplifies aversive events to prime behavioral responses that are adaptive to the worst possible outcome.

Adult↗
PubMed2003

Differential associations between entorhinal and hippocampal volumes and memory performance in older adults.

Magnetic resonance imaging-derived entorhinal and hippocampal volumes were measured in 14 nondemented, community-dwelling older adults. Participants were selected so that memory scores from 2 years prior to scanning varied widely but were not deficient relative to age-appropriate norms. A median split of these memory scores defined high-memory and low-memory groups. Verbal memory scores at the time of imaging were lower, and entorhinal and hippocampal volumes were smaller, in the low-memory group than in the high-memory group. Left entorhinal cortex volume showed the strongest correlation (r= .79) with immediate recall of word lists. Left hippocampal volume showed the strongest correlation (r= .57) with delayed paragraph recall. These results suggest that entorhinal and hippocampal volumes are related to individual differences in dissociable kinds of memory performance among healthy older adults.

Aged↗