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PubMed1999

Entorhinal cortex lesion in adult rats induces the expression of the neuronal chondroitin sulfate proteoglycan neurocan in reactive astrocytes.

The chondroitin sulfate proteoglycan neurocan is a major component of brain extracellular matrix during development. Neurocan is primarily synthesized by neurons and has the ability to interact with cell adhesion molecules involved in the regulation of cell migration and axonal growth. Within the first weeks postnatally, neurocan expression is strongly downregulated. To test whether neurocan is reexpressed in areas of axonal growth (sprouting) after brain injury, the time course of neurocan expression was analyzed in the denervated fascia dentata of the rat after entorhinal cortex lesion (12 hr; 1, 2, 4, and 10 d; 2 and 4 weeks; and 6 months after lesion). In the denervated zone, immunohistochemistry revealed neurocan-positive astrocytes by 2 d after lesion and a diffuse labeling of the extracellular matrix at all later time points. Electron microscopy confirmed the deposition of neurocan in the extracellular matrix compartment. In situ hybridization demonstrated a strong upregulation of neurocan mRNA within the denervated outer molecular layer 1 and 4 d after lesion. The combination of in situ hybridization with immunohistochemistry for glial fibrillary acidic protein demonstrated that the neurocan mRNA-expressing cells are astrocytes. These data demonstrate that neurocan is reexpressed in the injured brain. In contrast to the situation during development, astrocytes, but not neurons, express neurocan and enrich the extracellular matrix with this molecule. Similar to the situation during development, neurocan is expressed in an area of active axon growth, and it is suggested that neurocan acts to maintain the boundaries of the denervated fascia dentata after entorhinal cortex lesion.

Animals↗
PubMed2000

The over-expression of somatostatin in the gerbil entorhinal cortex induced by seizure.

In present study, we investigated the immunohistochemical distribution of somatostatin (SRIF) in the hippocampal complex of the Mongolian gerbil and its association with different sequelae of spontaneous seizures, in an effort to identify the roles of SRIF in the self-recovery mechanisms in these animals. In the dentate gyrus and subiculum, SRIF immunoreactive (SRIF(+)) cells were similar in both the seizure resistant and the pre-seizure group of seizure sensitive gerbils. Interestingly, SRIF immunoreactivity was markedly decreased until 12 h postictal. Twenty-four hours after the on-set of seizure, the distribution of SRIF immunoreactivity in these regions had slightly increased. In contrast, in the entorhinal cortex the population of SRIF(+) cells and their density were significantly elevated compared to pre-seizure group 30 min postictal. Twelve hours after the on-set of seizure, however, the population of SRIF(+) cells and their density declined, approximately 70-80% compared to the situation at 30 min postictal. These findings suggest that the enhancement of SRIF expression in gerbil entorhinal cortex may affect tissue excitability and have a role in modulating recurrent excitation following seizures.

Animals↗
PubMed2002

Loss of stimulatory effect of guanosine triphosphate on [(35)S]GTPgammaS binding correlates with Alzheimer's disease neurofibrillary pathology in entorhinal cortex and CA1 hippocampal subfield.

Heterotrimeric guanosine triphosphate (GTP)-binding proteins (G-proteins) couple many different cell surface receptor types to intracellular effector mechanisms. Uncoupling between receptors and G-proteins and between G-proteins and adenylyl cyclase (AC) and phospholipase C (PLC) has been described for Alzheimer's disease (AD) brain. However, there is little information on whether altered G-protein signaling in AD is just an end-stage phenomenon or is important for the progression of disease pathology. Here we used [(35)S]GTPgammaS autoradiography to study G-protein distribution in sections of entorhinal cortex and hippocampus from 23 cases staged for neurofibrillary changes and amyloid deposits according to Braak and Braak (Acta Neuropathol. [1991] 82:239-259). We also studied the effects of GTP, which has been found to increase [(35)S]GTPgammaS binding in an Mg(2+)-dependent manner. Results show that the ability of GTP (3 microM) to stimulate [(35)S]GTPgammaS binding declined significantly with staging for neurofibrillary changes in the entorhinal cortex (P < 0.05, ANOVA) and CA1 subfield of the hippocampus (P < 0.05, ANOVA). No significant changes were seen for [(35)S]GTPgammaS binding in the absence of GTP. Our results suggest a decrease in G-protein GTP hydrolysis, which correlates with the progression of AD neurofibrillary changes, in the regions most affected by this pathology. These alterations appear to occur prior to stages corresponding to clinical disease and could lead to an impaired regulation of several signaling systems in AD brain.

Adult↗
PubMed2001

Conservation of neuronal number and size in the entorhinal cortex of behaviorally characterized aged rats.

Despite abundant evidence of behavioral and electrophysiological dysfunction of the rodent hippocampal formation with aging, the structural basis of age-related cognitive decline remains unclear. Recently, unbiased stereological studies of the mammalian hippocampus have found little evidence to support the dogma that cellular loss accompanies hippocampal aging, thereby supporting an alternative hypothesis that aging is marked by widespread conservation of neuronal number. However, to date, the effects of aging have not been reported in another key component of memory systems in the rodent brain, the entorhinal cortex. In the present study, we stereologically estimated total neuronal number and size (cross-sectional area and cell volume) in the subdivisions and cellular layers of the rat entorhinal cortex, using the optical fractionator and nucleator, respectively. Comparisons were made among Fischer 344 rats that were young, aged-impaired, and aged-unimpaired (based on functional analysis in the Morris water maze). No significant differences in cell number or size were observed in any of the entorhinal subdivisions or laminae examined in each group. Thus, aging is associated with widespread conservation of neuronal number, despite varying degrees of cognitive decline, in all memory-related systems examined to date. These data suggest that mechanisms of age-related cognitive decline are to be found in parameters other than neuronal number or size in the cortex of the mammalian brain.

Aging↗
PubMed1996

Effects of D2 dopamine receptor antagonists on Fos protein expression in the striatal complex and entorhinal cortex of the nonhuman primate.

Recent studies have reported that acute administration of dopamine D2 receptor antagonists increases expression of the immediate early gene c-fos in the rat striatal complex. There have been no corresponding studies of the effects of D2 antagonists in primate species. Since all clinically effective antipsychotic drugs share D2 receptor antagonism, it is important to define the extent to which these drugs may alter expression of c-fos or its protein product, Fos, in primates. We therefore examined the effects of administration of two D2 receptor antagonists, haloperidol and metoclopramide, on Fos expression in the striatum and temporal cortices of the vervet monkey. Metoclopramide does not appear to possess significant antipsychotic efficacy but potently produces extra-pyramidal side effects, while haloperidol is an effective antipsychotic drug that produces extrapyramidal side effects. Both drugs increased the number of Fos-like immunoreactive (Fos-li) neurons in the caudate nucleus and putamen; the numbers of Fos-li neurons in these regions were increased in both the patch and matrix compartments. Haloperidol but not metoclopramide increased the number of Fos-li neurons in the nucleus accumbens shell. Similarly, haloperidol but not metoclopramide increased the number of Fos-li neurons in the entorhinal cortex. Neither drug altered Fos expression in the inferior temporal cortex. These data suggest that the dorsolateral caudate nucleus and putamen may be sites at which D2 receptor antagonists elicit extrapyramidal side effects, and the nucleus accumbens shell and entorhinal cortex may be loci at which the therapeutic actions of antipsychotic drugs are manifested.

Animals↗
PubMed1989

Inhibition of protein synthesis in the dentate gyrus, but not the entorhinal cortex, blocks maintenance of long-term potentiation in rats.

We examined whether the critical protein synthesis for maintenance of perforant path long-term potentiation (LTP) takes place in the dentate gyrus or the entorhinal cortex. Field potential recordings were made of responses in the dentate gyrus to stimulation of the perforant path in urethane-anaesthetized rats. Anisomycin (10 micrograms) injected into the dentate gyrus, but not the entorhinal cortex, 1 h prior to tetanization led to nearly complete decay of perforant path LTP of the excitatory postsynaptic potential (EPSP) within 3 h. Intra-dentate injection of neither actinomycin D (a mRNA synthesis inhibitor) nor boiled anisomycin affected LTP maintenance over 6 h. These results suggest that the proteins necessary for the maintenance of LTP over 6 h are synthesized in the dentate gyrus from already existing mRNA without involving protein synthesis in the cell bodies of the afferent fibres.

Action Potentials↗
PubMed1989

A columnar arrangement of dendritic processes of entorhinal cortex neurons revealed by a monoclonal antibody.

Immunohistochemical screening of the cat limbic system using a panel of monoclonal antibodies (MAbs) revealed that MAb R2D5 specifically labeled a subset of layer 3 cells in the entorhinal cortex, while leaving layer 2 cells unlabeled. The apical dendrites of the R2D5-positive layer 3 cells tended to gather and formed columnar structures which penetrated layer 2 and climbed to the surface of entorhinal cortex.

Animals↗
PubMed1984

Localization of entorhinal cortex neurons projecting to the dorsal hippocampal formation--a stereotaxic tool in three dimensions.

After topical injection of horseradish peroxidase into the dorsal hippocampal formation, the distribution of retrogradely labelled neurons of the entorhinal cortex was investigated. The distribution of these cells, which are projecting to the dorsal hippocampal formation, is demonstrated by drawings representing series of frontal, sagittal and horizontal sections and including stereotaxic coordinates. These drawings can be used as a morphological and stereotaxic tool in neurobiological research. Controversial opinions as to the dividing of the entorhinal cortex into subfields are discussed.

Afferent Pathways↗
PubMed1995

Spatial location learning in mice with ibotenate lesions of entorhinal cortex or subiculum.

This study examined the effects of ibotenate lesions of either the entorhinal cortex (EC) or the subiculum (SUB) on the ability of mice to memorize a single spatial location (initial discrimination), and on their capacity to switch to a new location (transfer) following the initial learning in an eight-arm radial maze. Results indicated that mice with ibotenate lesions of the EC or SUB were impaired in postoperative acquisition of the spatial discrimination task, making more reference, but not working memory, errors and displaying fewer first correct response trials than sham-operated control mice. Furthermore, additional damage to the ventral hippocampus exacerbated the impairment of performance induced by lesions of the SUB alone. In addition, all mice, except for the combined lesion group, exhibited similar performance levels when they were trained to choose another arm of the maze that had not previously been baited (transfer). These findings suggest that both the EC and the SUB play important roles in spatial information processing in mice.

Animals↗
PubMed2002

Calcium currents in rat entorhinal cortex layer II stellate and layer III pyramidal neurons in acute brain slice.

The entorhinal cortex (EC) is an essential relay station in neocortical - hippocampal information transfer and memory functions. Layer II stellate and layer III pyramidal neurons show specific damage in Alzheimer's disease and epilepsy, respectively. Using whole cell patch clamp recording in rat brain slices we here demonstrate that high voltage activated Ca(2+)-currents (I(Ca)(2+)) are about 1.6-fold bigger in stellate cells than in pyramidal neurons while current density is equal in both cell types. In stellate cells I(Ca)(2+) shows stronger inactivation with depolarization, block of I(Ca)(2+) by Ni(2+) (300 and 600 microM) is more effective, and this block decreases more for currents evoked from a less negative holding potential than in layer III pyramidal neurons. These data indicate distinct molecular composition of Ca(2+)-channels and can partially explain stronger increases of [Ca(2+)](i) during 10 Hz firing activity in EC pyramidal versus stellate neurons.

Animals↗
PubMed1997

Developmental changes of inward rectifier currents in neurons of the rat entorhinal cortex.

A slice preparation was used to investigate inward rectifier currents (I(H)) of entorhinal cortex (EC) neurons. Using the whole-cell configuration of the patch-clamp technique, I(H) was studied in pyramidal cells from layer IV of the rat EC and in stellate cells from layer II of the EC. Inward rectifier currents were analyzed in neurons of newborn (P1-3), juvenile (P8-14) and adult (>P28) rats. Pyramidal cells of juvenile rats possessed a significantly larger current density of I(H) than pyramidal cells of newborn rats, whereas no differences in the current density of I(H) were found between pyramidal neurons of juvenile and of adult animals. In contrast, the current density of I(H) of stellate cells was significantly increased in juvenile rats compared with newborn rats as well as in adult rats compared with juvenile rats. Moreover, in adult rats the current density of I(H) was larger in stellate cells than in pyramidal cells, whereas opposite data were obtained in juvenile animals.

Age Factors↗
PubMed2003

Learning associations between places and visual cues without learning to navigate: neither fornix nor entorhinal cortex is required.

Rats with fornix transection, or with cytotoxic retrohippocampal lesions that removed entorhinal cortex plus ventral subiculum, performed a task that permits incidental learning about either allocentric (Allo) or egocentric (Ego) spatial cues without the need to navigate by them. Rats learned eight visual discriminations among computer-displayed scenes in a Y-maze, using the constant-negative paradigm. Every discrimination problem included two familiar scenes (constants) and many less familiar scenes (variables). On each trial, the rats chose between a constant and a variable scene, with the choice of the variable rewarded. In six problems, the two constant scenes had correlated spatial properties, either Allo (each constant appeared always in the same maze arm) or Ego (each constant always appeared in a fixed direction from the start arm) or both (Allo + Ego). In two No-Cue (NC) problems, the two constants appeared in randomly determined arms and directions. Intact rats learn problems with an added Allo or Ego cue faster than NC problems; this facilitation provides indirect evidence that they learn the associations between scenes and spatial cues, even though that is not required for problem solution. Fornix and retrohippocampal-lesioned groups learned NC problems at a similar rate to sham-operated controls and showed as much facilitation of learning by added spatial cues as did the controls; therefore, both lesion groups must have encoded the spatial cues and have incidentally learned their associations with particular constant scenes. Similar facilitation was seen in subgroups that had short or long prior experience with the apparatus and task. Therefore, neither major hippocampal input-output system is crucial for learning about allocentric or egocentric cues in this paradigm, which does not require rats to control their choices or navigation directly by spatial cues.

Animals↗
PubMed2006

Parvalbumin neurons in the entorhinal cortex of subjects diagnosed with bipolar disorder or schizophrenia.

BACKGROUND: Growing evidence indicates that the entorhinal cortex (ECx) might be affected in schizophrenia (SZ) and bipolar disorder (BD). To test whether distinct interneuronal subpopulations might be altered, numbers of parvalbumin-immunoreactive (PVB-IR) neurons were measured in the ECx of BD and SZ subjects. These neurons play a pivotal role within ECx intrinsic circuits. METHODS: Numbers, numerical density, and soma size of PVB-IR neurons were measured in the ECx of normal control (n = 16), BD (n = 10), and SZ (n = 10) subjects. The volume of the ECx was measured in Nissl-stained sections. RESULTS: In BD, decreases of total numbers (p = .02) and numerical densities (p = .01) of PVB-IR neurons were detected in the ECx. Within distinct subregions, reductions were detected in the superficial layers of the lateral (p = .02), intermediate (p = .04), and caudal (p = .01) ECx. In SZ, total numbers and numerical densities were not altered. A reduction of soma size was present in the intermediate ECx (p = .01). Volume was unaffected in either disorder. CONCLUSIONS: In BD, a decrease of PVB-IR neurons may alter intrinsic inhibitory networks within the superficial layers of the ECx. The likely consequence is a disruption of integration and transfer of information from the cerebral cortex to the hippocampus.

Adult↗
PubMed1988

Topographical relationship between the entorhinal cortex and the septotemporal axis of the dentate gyrus in rats: II. Cells projecting from lateral entorhinal subdivisions.

Projections from the rat lateral entorhinal cortex (area 28-l) to the dentate gyrus were traced and then interpreted according to a parcellation scheme that recognized four cytoarchitectonic subdivisions of area 28-l: areas dorsolateral (dl), ventrolateral (vl), ventromedial (vm), and TR. Following lesions of area 28-l, anterograde degeneration was traced with the Fink-Heimer method. In parallel experiments iontophoretic injections of horseradish peroxidase (HRP) were made in the lateral perforant path terminal zone of the dentate molecular layer. Retrograde neuronal labeling patterns within area 28-l were charted following dorsal, midseptotemporal (mid ST), and ventral dentate injections. In two additional cases HRP was deposited in the ventral subiculum. Lesions of area dl (which lies entirely on the posterolateral cortex) produced terminal degeneration that was confined to the dorsal one-half of the dentate gyrus. Lesions involving primarily areas vl and vm (which lie on the posteroinferior cortex) caused a complementary pattern of degeneration; silver grains predominated in the ventral dentate gyrus. Injections of HRP into the outer dentate molecular layer labeled layer II neurons within area 28-l. Deposits of HRP in the dorsal one-third of the dentate gyrus labeled a rostrocaudal strip of neurons within the dorsal one-third of area dl; no other subdivisions of area 28-l contained labeling. After mid-ST deposits of HRP, a rostrocaudally oriented strip of labeled cells appeared in the ventral one-third of area dl. Mid-ST injections also labeled neurons in the caudolateral quadrant of area vl. Injection of HRP into the ventral dentate gyrus labeled neurons in the caudomedial quadrant of area vl as well as a few neurons in caudal area vm. No labeled cells were ever found in area dl following ventral dentate HRP deposits. Neurons within area TR were never retrogradely labeled from injections of HRP into the dentate perforant path zone. However, ventral subicular injections of HRP labeled a few cells in the posterior part of area TR, as well as hundreds of neurons throughout the rostrocaudal extent of area vl. The results indicate a highly organized innervation of the dentate gyrus by several subdivisions of area 28-l. In area dl, rostrocaudal strips of layer II neurons innervate distinct segments of the dorsal ST axis. The posterior half of areas vl and vm innervates the ventral half of the ST axis; a lateromedial gradient there corresponds to increasingly ventral terminations along the dentate ST axis.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed2001

Localization of two major GABA(A) receptor subunits in the dentate gyrus of the rat and cell type-specific up-regulation following entorhinal cortex lesion.

GABA(A) receptor subunits show a specific regional distribution in the CNS during development and in the adult animal. In the hippocampal formation, individual subsets of GABAergic interneurons are highly immunoreactive for the alpha1-subunit, whereas granule and pyramidal cells show a strong expression of the alpha2-subunit. Using confocal microscopy and digital image analysis, we demonstrate that in the dentate gyrus the alpha1-subunit immunolabeling appears in differently sized clusters. The large clusters, which are confined to dendrites of interneurons, show no alpha2 labeling, whereas the smaller ones coincide with alpha2-subunit-positive clusters. In the molecular layer, the clusters of both alpha-subunits co-localize with the anchoring protein gephyrin. In the granule cell layer and hilus, we found alpha1- and alpha2-subunit-positive clusters which were devoid of gephyrin labeling. Lesions of the medial entorhinal cortex led to the deafferentation of dendrites in the middle molecular layer of the dentate gyrus. This resulted in a significantly increased concentration of alpha2-subunit-positive clusters. We also observed an increase of alpha1-subunit immunolabeling in the deafferented area. We found no change in the co-localization between alpha1 and alpha2, and no significant change in the number of large alpha1-positive clusters along individual dendritic segments of interneurons. In a previous study, we demonstrated that calbindin-immunoreactive dendrites of granule cells revealed a significant increase in gephyrin immunoreactivity following lesion, whereas parvalbumin-positive dendrites showed no such alterations. The predominant localization of small gephyrin clusters in dendrites of granule cells, which was also described in this study, leads to the conclusion that the increase of the alpha2-subunit-positive clusters, demonstrated in the present study, indicates that, following entorhinal cortex lesion, new GABAergic synapses may be formed and that they contact predominantly granule cell dendrites.

Animals↗
PubMed2003

Reelin-immunoreactive Cajal-Retzius cells: the entorhinal cortex in normal aging and Alzheimer's disease.

Alzheimer's disease (AD) is a disorder of brain self organization associated with morphodysregulation at the synaptic level. Disturbances follow a hierarchical spatio-temporal pattern throughout the cortex and involve the re-activation of developmental molecular programs. The large glycoprotein reelin, synthesized by Cajal-Retzius (CR) cells, is an important component of a signaling pathway involved in embryonic development and modulation of synaptic circuitry, but is also implicated in the pathogenetic cascade in AD. Although the majority of CR cells sequentially disappears from the postnatal cortical layer I, a few of them persist in the normal adult brain. They continue to produce reelin, express a variety of other proteins, and are characterized by a typical morphology. Recently, CR cells have been reported to be altered in number and morphology in a variety of neurological and psychiatric diseases linked to maldevelopment. In the present study we show that reelin-positive CR cells persist in the layer I of the entorhinal cortex in normal senescent brains and are also preserved in AD. The majority of CR cells in AD is morphologically and cytochemically-as revealed by double labeling with calcium-binding proteins-indistinguishable from normal cases, suggesting that they are not dramatically altered in the entorhinal cortex of AD patients. Nevertheless, CR cells seem to be partially affected by the formation of paired helical filaments, indicating subtle changes that are suggested to be a result rather than a cause of the pathogenetic cascade of AD.

Aged↗
PubMed2004

Effects of phencyclidines on signal transfer from the entorhinal cortex to the hippocampus in rats.

The information transfer from the superficial layers of the entorhinal cortex (EC) to the hippocampus is regulated in a frequency dependent manner. Phencyclidine and related compounds such as MK-801 produce psychotic symptoms that closely resemble schizophrenia. We studied the effects of systemic administration of MK-801 on the signal transfer from the EC layer III to the hippocampal area CA1. High frequency (above 10 Hz) activation of the bi-synaptic entorhinal input in control animals results in a strong suppression of the field potentials in the stratum lacunosum-moleculare of the area CA1. In contrast, in MK-801 pretreated rats the field response was less reduced. The field potential responses evoked in these two groups of animals by high-frequency activation of the monosynaptic input were similar suggesting selective alterations in layer III of the medial EC. We suggest, that MK-801 causes disinhibition of layer III projection cells and, therefore, may cause strong, pathological activation of direct layer III-CA1 pathway.

Action Potentials↗
PubMed1992

Tracing of axonal connections by rhodamine-dextran-amine in the rat hippocampal-entorhinal cortex slice preparation.

In order to demonstrate axonal connections preserved in rat temporal cortex slices the authors used rhodamine-dextran-amine as a tracer. The slices contained the neocortical areas Te2 and Te3, the medial and lateral entorhinal cortices (MEC and LEC), the subicular regions, and the dentate gyrus and hippocampus proper. Rhodamine-dextran-amine crystals were placed by microinjection into a given area. Following this local lesioning the dye was permitted to diffuse and migrate intraaxonally in antero- and retrograde directions for about 8 hours. The slices were then formaldehyde-fixed and analyzed by fluorescence microscopy. Most of the known connections within and between the entorhinal cortex and the hippocampus and dentate gyrus were preserved in the slice preparation, provided that the slices were cut with a near horizontal orientation corresponding to plates 99-108 in Paxinos and Watson (1986). Only the lateral perforant path between the LEC and the hippocampus could not be followed to its full extent. The authors conclude that most aspects of the intrinsic synaptic organization of the temporal lobe can be reliably studied in hippocampal-entorhinal cortex slice preparations.

Animals↗