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PubMed1998

Contributions of the entorhinal cortex, amygdala and hippocampus to human memory.

Recent studies have indicated that, in the monkey, the rhinal cortex (consisting of the entorhinal and perirhinal cortices) is more important to visual recognition memory than the hippocampus or amygdala. The present study investigated the role of the entorhinal cortex in humans using memory scores from surgical epilepsy patients classified according to their mesial temporal lobe pathology. The temporal lobe removals included 4-5 cm of neocortex, amygdala, rhinal cortex and 2-3 cm of the hippocampus and parahippocampal gyrus. Compared to autopsied control subjects, all of the patients showed significant gliosis in the amygdala, but they differed as to whether or not there were entorhinal and/or hippocampal abnormalities. Both preoperatively and one or more years postoperatively, the patients performed tests of verbal recall (Wechsler Memory Scale Logical Memory), visual recall (Rey Figure), verbal recognition and visual recognition (Warrington Recognition Memory Test: Words and Faces, respectively). Preoperatively, patients with hippocampal pathology showed deficits in visual recall. Postoperatively, a significant drop in verbal and visual recall was seen only for patients who lost intact hippocampal tissue, irrespective of the condition of the excised entorhinal cortex. Together, the results argue that the hippocampus is more important than the entorhinal cortex for the recall of newly learned information.

Adolescent↗

PubMed1998

Subthreshold membrane potential oscillations in neurons of deep layers of the entorhinal cortex.

Neuronal oscillations are important for information processing. The entorhinal cortex is one of the structures which is involved in generation of theta rhythm. The major role of the entorhinal cortex is to feed diverse sources of information both to and from the hippocampus. Far from simply being a funnel for this information it becomes clear that the entorhinal cortex has its own active properties that contribute to signal processing. Interestingly, stellate cells in layer II of the entorhinal cortex can intrinsically generate subthreshold, Na+-dependent membrane potential oscillations. Here, using intracellular and patch-clamp recordings, we report a similar phenomenon from neurons of the deep layers of the entorhinal cortex. In our in vitro slice preparation about two-thirds of recorded neurons were able to generate voltage-sensitive subthreshold membrane potential oscillations. At a membrane potential of about 50 mV the mean frequency of the voltage-oscillations was 8.1 Hz, whereby at slightly more positive potentials (-44 mV) the frequency of the membrane potential oscillations was 20 Hz and the oscillations became interrupted by clusters of non-adapting trains of spikes. Pharmacological experiments revealed that the oscillations were not affected by Cs+, but could be blocked by the fast Na+-channel blocker tetrodotoxin. We therefore conclude that voltage- and Na+-dependent subthreshold membrane potential oscillations are not only present in stellate cells of entorhinal cortex-layer II, but are also typical for neurons of the deep layers of the entorhinal cortex.

Animals↗

PubMed1995

Serotonin reduces synaptic excitation of principal cells in the superficial layers of rat hippocampal-entorhinal cortex combined slices.

The cells of the entorhinal cortex receive a dense innervation of serotonergic fibres from the Raphe nuclei and express a high density of 5-hydroxytryptamine 1A (5-HT1A) receptors. We investigated the effects of serotonin on excitatory synaptic transmission in principal cells from entorhinal cortex layers II and III within hippocampal-entorhinal cortex combined slices. Although serotonin had an effect upon the membrane conductance of some, but not all cells, its most pronounced action was to reduce stimulus evoked excitatory synaptic potentials and currents (EPSP/Cs). Both alpha-amino-3-hydroxy-5-methylisoxazole-4-propionic acid and N-methyl-D-aspartate receptor-mediated EPSPs were reduced to similar extents over a range of concentrations. Since the principal cells in layer II and layer III are the main projection cells of the entorhinal cortex, these inhibitory effects of serotonin may have implications for the transfer of information to the hippocampus.

Action Potentials↗

PubMed2000

Morphology of spiny neurons in the human entorhinal cortex: intracellular filling with lucifer yellow.

The present study was designed to investigate the morphology of spiny neurons in the human entorhinal cortex. Coronal entorhinal slices (n = 67; 200 microm thick) were obtained from autopsies of three subjects. Spiny neurons (n = 132) filled with Lucifer Yellow were analysed in different subfields and layers of the entorhinal cortex. Based on the shape of the somata and primary dendritic trees, spiny neurons were divided into four morphological categories; (i) classical pyramidal, (ii) stellate, (iii) modified stellate, and (iv) horizontal tripolar cells. The morphology of filled neurons varied more in different layers than in the different subfields of the entorhinal cortex. In layer II, the majority (81%) of spiny neurons had stellate or modified stellate morphology, but in the rostromedial subfields (olfactory subfield and rostral subfield) there were also horizontal tripolar neurons. Dendritic branches of layer II neurons extended to layer I (94%) and to layer III (83%). Unlike in layer II, most (74%) of the filled neurons in layers III, V and VI were classical pyramidal cells. The majority of pyramidal cells in the superficial portion of layer III had dendrites that extended up to layer II, occupying the space between the neuronal clusters. Some dendrites reached down to the deep portion of layer III. Apical dendrites of layer V and VI pyramidal cells traveled up to the deep portion of layer III.Our data indicate that the morphology of spiny neurons in different layers of the human entorhinal cortex is variable. Vertical extension of dendritic branches to adjacent layers supports the idea that inputs terminating in a specific lamina influence target cells located in various entorhinal layers. There appears to be more overlap in the dendritic fields between superficial layers II and III than between the superficial (II/III) and deep (V/VI) layers, thus supporting the idea of segregation of information flow targeted to the superficial or deep layers in the human entorhinal cortex.

Entorhinal Cortex↗

PubMed1999

Subfield- and layer-specific changes in parvalbumin, calretinin and calbindin-D28K immunoreactivity in the entorhinal cortex in Alzheimer's disease.

The entorhinal cortex, which is involved in neural systems related to memory, is selectively degenerated in early Alzheimer's disease. Here, we examined neuropathological changes in the eight entorhinal subfields in post mortem Alzheimer's disease subjects using Thionin and Bielschowsky stains and parvalbumin, calretinin and calbindin-D28k immunohistochemistry. Both histological stains revealed the most dramatic cell loss and neurofibrillary tangle formation to be in layers II and V of the lateral, intermediate and caudal subfields. In accordance, immunohistochemical staining showed that neurons and fibres that contain calcium-binding proteins were also more frequently altered in these subfields than in the rostromedial subfields. Detailed analysis further revealed that non-principal cells containing parvalbumin or calbindin-D28k showed morphological alterations early in the entorhinal pathology of Alzheimer's disease, whereas non-principal neurons containing calretinin were better preserved even in Alzheimer's disease patients with severe entorhinal pathology. The degeneration of parvalbumin-immunoreactive neurons and basket-like networks and calbindin-positive non-principal neurons was observed mainly in layer II, where the calretinin-positive non-principal neurons formed aggregates especially at late stages of the disease. The pyramidal-shaped neurons containing either calretinin or calbindin-D28k were often preserved, although morphological alterations were observed. Our findings indicate that specific subfields of the entorhinal cortex involving neurons that contain distinct calcium-binding proteins are differentially vulnerable in Alzheimer's disease. This could have an impact on the topographically organized inputs and outputs of the entorhinal cortex in Alzheimer's patients.

Aged↗

PubMed2001

Loss and atrophy of layer II entorhinal cortex neurons in elderly people with mild cognitive impairment.

Layer II of the entorhinal cortex contains the cells of origin for the perforant path, plays a critical role in memory processing, and consistently degenerates in end-stage Alzheimer's disease. The extent to which neuron loss in layer II of entorhinal cortex is related to mild cognitive impairment without dementia has not been extensively investigated. We analyzed 29 participants who came to autopsy from our ongoing longitudinal study of aging and dementia composed of religious clergy (Religious Orders Study). All individuals underwent detailed clinical evaluation within 12 months of death and were categorized as having no cognitive impairment (n = 8), mild cognitive impairment (n = 10), or mild or moderate Alzheimer's disease (n = 11). Sections through the entorhinal cortex were immunoreacted with an antibody directed against a neuron-specific nuclear protein (NeuN). Stereological counts of NeuN-immunoreactive stellate cells, their volume, and the volume of layer II entorhinal cortex were estimated. Cases exhibiting no cognitive impairment averaged 639,625 +/- 184,600 layer II stellate neurons in the right entorhinal cortex. Individuals with mild cognitive impairment (63.5%; p < 0.0003) and mild or moderate Alzheimer's disease (46.06%; p < 0.0017) displayed significant losses of layer II entorhinal cortex neurons relative to those with no cognitive impairment but not relative to each other (p > 0.33). There was also significant atrophy of layer II entorhinal cortex neurons in individuals with mild cognitive impairment (24.1%) and Alzheimer's disease (25.1%). The volume of layer II was also reduced in individuals with mild cognitive impairment (26.5%), with a further reduction in those with Alzheimer's disease (46.4%). The loss and atrophy of layer II entorhinal cortex neurons significantly correlated with performance on clinical tests of declarative memory. Atrophy of layer II entorhinal cortex and the neurons within this layer significantly correlated with performance on the Mini Mental Status Examination. These data indicate that atrophy and loss of layer II entorhinal cortex neurons occur in elderly subjects with mild cognitive impairment prior to the onset of dementia and suggests that these changes are not exacerbated in early Alzheimer's disease.

Aged↗

PubMed1997

Prolonged inhibitory potentials in layer III projection cells of the rat medial entorhinal cortex induced by synaptic stimulation in vitro.

The entorhinal cortex projects via layer III neurons directly to the hippocampal area CA1 and the subiculum. We studied the functional properties of the medial entorhinal cortex projection cells in horizontal hippocampal-entorhinal cortex combined slices. These cells displayed, upon single-shock synaptic stimulation, an excitatory postsynaptic potential followed by a fast and/or slow inhibitory postsynaptic potential. Short train repetitive stimulation subthreshold for generation of action potentials induced a slow hyperpolarization of up to 20 s. Pharmacological analysis shows that the slow hyperpolarization could be divided into three components: i) the first component, which lasted 1 s, was sensitive to GABA(B) receptor antagonists; ii) the second component lasting for about 6 s was sensitive to atropine, suggesting muscarinic acetylcholinergic nature of these responses; iii) a late component lasting for up to 20 s was sensitive to naloxone, suggesting a role for opioids in its generation. The finding that layer III projection neurons to the hippocampus proper develop long-lasting hyperpolarizations suggests possible control mechanisms for the output functions of the entorhinal cortex.

Animals↗

PubMed1992

Rat hippocampal lactate efflux during electroconvulsive shock or stress is differently dependent on entorhinal cortex and adrenal integrity.

The role of the entorhinal cortex and the adrenal gland in rat hippocampal lactate formation was assessed during and after a short-lasting immobilization stress and electroconvulsive shock (ECS). Extracellular lactate was measured on-line using microdialysis and enzyme reactions (a technique named lactography); in some rats, unilateral lesions of the entorhinal cortex were made or the bilateral adrenal glands were removed. The stress-evoked increase in hippocampus lactate was not altered either ipsi- or contralateral to an entorhinal cortex lesion. The response to ECS was attenuated only in the hippocampus ipsilateral to the entorhinal cortex lesion. Removal of bilateral adrenal glands caused some delay in the increase in hippocampal lactate after ECS and a major reduction in the stress-evoked lactate response. These results indicate that (1) the entorhinal cortex is activated by ECS, thereby activating hippocampal lactate efflux and presumably metabolism, and (2) the adrenal gland is essential in the response to stress and, to a minor extent, in the ECS-altered hippocampal metabolism.

Adrenal Glands↗

PubMed1997

Converging inputs to the entorhinal cortex from the piriform cortex and medial septum: facilitation and current source density analysis.

Converging inputs to the entorhinal cortex from the piriform cortex and medial septum: facilitation and current source density analysis. J. Neurophysiol. 78: 2602-2615, 1997. The entorhinal cortex receives sensory inputs from the piriform cortex and modulatory inputs from the medial septum. To examine short-term synaptic facilitation effects in these pathways, current source density (CSD) analysis was used first to localize the entorhinal cortex membrane currents, which generate field potentials evoked by stimulation of these afferents. Field potentials were recorded at 50-micron intervals through the medial entorhinal cortex in urethan-anesthetized rats and the one-dimensional CSD was calculated. Piriform cortex stimulation evoked a surface-negative, deep-positive field potential component in the entorhinal cortex with mean onset and peak latencies of 10.4 and 18.4 ms. The component followed brief 100-Hz stimulation, consistent with a monosynaptic response. CSD analysis linked the component to a current sink, which often began in layer I before peaking in layer II. A later, surface-positive field potential component peaked at latencies near 45 ms and was associated with a current source in layer II. Medial septal stimulation evoked positive and negative field potential components which peaked at latencies near 7 and 16 ms, respectively. A weaker and more prolonged surface-negative, deep-positive component peaked at latencies near 25 ms. The early components were generated by currents in the hippocampal formation, and the late surface-negative component was generated by currents in layers II to IV of the entorhinal cortex. Short-term facilitation effects in conscious animals were examined using electrodes chronically implanted near layer II of the entorhinal cortex. Paired-pulse stimulation of the piriform cortex at interpulse intervals of 30 and 40 ms caused the largest facilitation (248%) of responses evoked by the second pulse. Responses evoked by medial septal stimulation also were facilitated maximally (59%) by a piriform cortex conditioning pulse delivered 30-40 ms earlier. Paired pulse stimulation of the medial septum caused the largest facilitation (149%) at intervals of 70 ms, but piriform cortex evoked responses were facilitated maximally (46%) by a septal conditioning pulse 100-200 ms earlier. Frequency potentiation effects were maximal during 12- to 18-Hz stimulation of either the piriform cortex or medial septum. Occlusion tests suggested that piriform cortex and medial septal efferents activate the same neurons. The CSD analysis results show that evoked field potential methods can be used effectively in chronically prepared animals to examine synaptic responses in the converging inputs from the piriform cortex and medial septum to the entorhinal cortex. The short-term potentiation phenomena observed here suggest that low-frequency activity in these pathways during endogenous oscillatory states may enhance entorhinal cortex responsivity to olfactory inputs.

Animals↗

PubMed1994

Hippocampal-entorhinal relationships: electrophysiological analysis of the ventral hippocampal projections to the ventral entorhinal cortex.

The hippocampal output to the ventral entorhinal area was studied in the guinea-pig by field potential analysis. Perforant path volleys, synaptically elicited by stimulation of dorsal psalterium fibers, were used to obtain activation of the lamellar circuit of the dorsal hippocampal formation and the subsequent activation, through intrahippocampal longitudinal connections, of pyramidal neurons in the ventral hippocampus. The latter activation was obtained by low-frequency (0.1-2.0/s) repetitive dorsal psalterium stimulation. A response occurred in the ventral entorhinal area only following low-frequency (0.1-2.0/s) repetitive stimulation. The ventral entorhinal response occurred both in the medial and lateral divisions of the ventral entorhinal area. It consisted of a negative wave with associated unit firing in all cellular layers of the medial and lateral ventral entorhinal area. The latency of the entorhinal response increased moving from the deep to the superficial layers. These findings suggest the generation of excitatory synaptic effects in temporal sequence in the deep and then in the superficial layers of the entorhinal cortex. The ventral entorhinal response showed longer latency and a higher threshold than the ventral hippocampal response, and was eliminated by interruption of the caudally directed ventral hippocampal projections. These data suggest that the ventral entorhinal response was mediated by projections from the ventral hippocampus. The results show that the ventral hippocampal output evokes excitatory synaptic effects in all cellular layers of the medial and the lateral ventral entorhinal area. The massive involvement of the entorhinal area, together with the widespread distribution of the entorhinal projections, support the idea that the entorhinal cortex represents a crucial link between the hippocampus and the other brain regions.

Animals↗

PubMed2001

Entorhinal cortex of the mouse: cytoarchitectonical organization.

The present study describes the cytoarchitectonical and chemoarchitectonical organization of the entorhinal cortex of the mouse (C57BL/6J strain). The entorhinal cortex is medially bordered by the parasubiculum, and laterally by the perirhinal cortex; rostrally and medially it is bordered by the piriform cortex, whereas caudally and dorsally it is bordered by the postrhinal cortex. The entorhinal cortex is divided into two main areas, i.e., the lateral entorhinal area (LEA) and the medial entorhinal area (MEA). Both entorhinal areas are further divided into subfields, i.e., LEA is divided into DLE (dorsolateral entorhinal field), DIE (dorsal intermediate entorhinal field), and VIE (ventral intermediate entorhinal field), whereas MEA is divided into CE (caudal entorhinal field) and ME (medial entorhinal field). Cytoarchitectonically, the main difference between LEA and MEA is displayed by layer II neurons: while these are in a dense layer in LEA, they are more dispersed in MEA. Further, in LEA there is a relatively cell-free zone between layers II and III; this zone is not present in MEA. Histochemically, in acetylcholinesterase (AChE)-stained material, MEA is characterized by darker-stained bands in the superficial layer (i.e., layer I) and in the lamina dissecans, in contrast to LEA, which is more evenly stained for AChE. Further, both the border with the perirhinal cortex and the border with the parasubiculum are characterized by dark-stained bands of AChE. The border between the entorhinal cortex and perirhinal cortex is also easily distinguished in parvalbumin-stained material; while the entorhinal cortex is darkly stained, the perirhinal cortex is lightly stained. In contrast, in sections stained for calretinin, the entorhinal cortex is more lightly stained than the parasubiculum, which has a darkly stained superficial layer, and a densely stained group of neurons in layer III.

Animals↗

PubMed1995

Preservation of topography in the connections between the subiculum, field CA1, and the entorhinal cortex in rats.

In order to examine whether the entorhinal-hippocampal-entorhinal circuit is reciprocal and topographic, the connections between the subiculum, the CA1 field, and the entorhinal cortex were studied with the carbocyanine dye (Dil), which moves in both retrograde and anterograde directions. We investigated the organization of reciprocal connections revealed by injections of Dil in the entorhinal cortex along the rhinal sulcus. Anterograde fluorescent labeling showed the same pattern reported in previous studies of the dorsal hippocampus. When the injection site of DiI extended into the deep layers (IV-VI) of the same cortical column, the anterograde labeling of the perforant path was accompanied by retrograde labeling of the subicular neurons and the CA1 neurons. The distribution of labeled cells overlapped the distribution of labeled fibers, and the distribution of labeled cells paralleled that of the labeled fibers in the CA1 field. DiI injection into the medial entorhinal cortex revealed fewer retrogradely labeled subicular neurons than injection into the lateral entorhinal cortex, whereas the number of labeled CA1 neurons was not dependent on the injection site. The number of labeled CA1 neurons was always several times greater than the number of subicular neurons. Thus, the amount of information conveyed by the CA1 projection might be higher than that conveyed by the subicular projection. These results indicate that the entorhinal cortex, CA1, and the subiculum are connected reciprocally and topographically. We believe that the framework of the major hippocampal circuit proposed in previous studies should be reconsidered. We propose that the CA1 projection, rather than the subicular projection, is the main projection that feeds back information from the hippocampus to the entorhinal cortex.

Afferent Pathways↗

PubMedDate not supplied

Effects of entorhinal cortex lesions on sensory integration and spatial learning.

BACKGROUND: The entorhinal cortex provides sensory information to the hippocampus for memory and learning. Damage to the entorhinal cortex is common in patients who experience traumatic brain injury, stroke, and Alzheimer's disease. Entorhinal damage is assumed to interfere with sensory integration; however, substantive knowledge of behavioral patterns is lacking. OBJECTIVES: To describe specific behavioral deficits associated with entorhinal cortex injury related to special senses identification, sensory integration, and spatial learning. METHOD: Adult male rats received bilateral entorhinal cortex damage (n = 19) or sham surgery (n = 11) with a subset randomized to participate in special senses identification, exploration, and sensory integration testing. Spatial learning was examined using a water maze. RESULTS: Lesion and control animals were similar in special senses identification testing. Sensory integration was markedly impaired in lesion animals over 3 days for all integration tasks; however, travel deficit persisted for 4 days. By day 5 sensory integration ability was equal. Lesion animals were significantly impaired across all days of spatial learning for swim time (p = .0001) and directional heading error (p = .03). Control animals exposed to sensory testing demonstrated significantly more efficient learning (p = .005) on swim days 2 and 3 versus control animals not exposed to sensory testing. CONCLUSIONS: Early and prolonged behavioral changes are evident following entorhinal cortex damage including sensory integration deficits and persistent spatial learning impairment.

Alzheimer Disease↗

PubMed1999

Progressive unilateral damage of the entorhinal cortex enhances synaptic efficacy of the crossed entorhinal afferent to dentate granule cells.

Progressive injury to the mammalian CNS often reduces the severity of lesion-induced deficits or spares the behavior from deficits altogether. The mechanism(s) underlying this behavioral sparing is not clearly understood, but axonal sprouting is a likely candidate. To test this possibility, unilateral, two-stage (progressive) lesions of the entorhinal cortex, which are known to accelerate sprouting by the crossed temporodentate pathway and spare spatial memory function, were made in rats. We examined the changes in synaptic efficacy (as measured by the amplitude and slope of evoked population EPSPs) of the crossed temporodentate projection after either one-stage or progressive unilateral lesions of the entorhinal area. Whereas the synaptic efficacy of the one-stage group did not differ significantly from the control group at 4, 6, or 8 d after the lesion, the synaptic efficacy of the crossed temporodentate pathway in the progressive lesion group significantly increased above the control values as early as 4 d after the lesion and remained stable thereafter. Axonal sprouting thus may provide a mechanism by which to account for behavioral sparing after progressive brain damage.

Afferent Pathways↗

PubMed1998

Entorhinal cortex of the rat: organization of intrinsic connections.

Two sets of experiments were carried out to examine the organization of associational connections within the rat entorhinal cortex. First, a comprehensive analysis of the areal and laminar distribution of intrinsic projections was performed by using the anterograde tracers Phaseolus vulgaris-leuocoagglutinin (PHA-L) and biotinylated dextran amine (BDA). Second, retrograde tracers were injected into the dentate gyrus and PHA-L and BDA were injected into the entorhinal cortex to determine the extent to which entorhinal neurons that project to different septotemporal levels of the dentate gyrus are linked by intrinsic connections. The regional distribution of intrinsic projections within the entorhinal cortex was related to the location of the cells of origin along the mediolateral axis of the entorhinal cortex. Cells located in the lateral regions of the entorhinal cortex gave rise to intrinsic connections that largely remained within the lateral reaches of the entorhinal cortex, i.e., within the rostrocaudally situated entorhinal band of cells that projected to septal levels of the dentate gyrus. Cells located in the medial regions of the entorhinal cortex gave rise to intrinsic projections confined to the medial portion of the entorhinal cortex. Injections made into mid-mediolateral regions of the entorhinal cortex mainly gave rise to projections to mid-mediolateral levels, although some fibers did enter either lateral or medial portions of the entorhinal cortex. These patterns were the same regardless of whether the projections originated from the superficial (II-III) or deep (V-VI) layers of the entorhinal cortex. This organizational scheme indicates, and our combined retrograde/anterograde labeling studies confirmed, that laterally situated entorhinal neurons that project to septal levels of the dentate gyrus are not in direct communication with neurons projecting to the temporal portions of the dentate gyrus. These results suggest that entorhinal intrinsic connections allow for both integration (within a band) and segregation (across bands) of entorhinal cortical information processing.

Amidines↗

PubMed1993

Neurochemical development of the hippocampal region in the fetal rhesus monkey. I. Early appearance of peptides, calcium-binding proteins, DARPP-32, and monoamine innervation in the entorhinal cortex during the first half of gestation (E47 to E90).

Although the entorhinal cortex is a key structure connecting the hippocampal formation with the rest of the cerebral cortex, little is known about its early chemoanatomical development in primates. In the present study, a cytoarchitectonic analysis and immunocytochemical detection of somatostatin, neurotensin, parvalbumin, calbindin-D 28K, DARPP-32, as well as tyrosine hydroxylase, dopamine-beta-hydroxylase, and serotonin, were carried out on serial sections of the entorhinal cortex of six rhesus monkey fetuses aged E47 to E90 (gestation period 165 days). At E56 the cortical plate of the entorhinal cortex already exhibited a sublamination; at E64 the lamina dissecans was partly formed, allowing the emergence of the lamina principalis externa and interna, and at E83 most of the regional and laminar subdivisions characteristic of the adult cortex could be identified, except for the rhinal sulcus restricted to a small dimple. The neurochemical development paralleled the early cytoarchitectonic differentiation, both largely preceding that of the neighboring cortical areas. The somatostatin-like immunoreactive innervation, first detected at E56, was very dense as early as E64 and displayed by E83 a laminar distribution similar to that found in the adult. Labeled neurons indicated an intrinsic origin for this innervation but an extrinsic connection might be present as labeled fibers in the subplate of the entorhinal cortex were in continuity with positive fibers in the intermediate zone of the hippocampal formation. A faint neurotensin-like immunoreactivity first detected at E64 became prominent at E83 in the entorhinal cortex but stopped abruptly at the anlage of the rhinal sulcus. The lack of neurotensin-labeled neurons contrasted with their presence in other parts of the hippocampal region and suggested a precocious extrinsic connection. Only rare parvalbumin-LIR neurons were detected at midgestation, whereas calbindin-D 28K was expressed from E47 on in Cajal-Retzius cells and from E56 on in various types of neurons in the cortical plate and subplate. Most characteristic was a category of medium-sized, deeply stained calbindin-LIR neurons, present only in the lamina principalis externa and possibly corresponding to the population of large neurons described by Kostovic et al. (1990, Soc Neurosci Abstr 16:846) in early developing entorhinal cortex of human fetuses. These and probably other neurons were also DARPP-32-positive, suggesting the possibility of an early dopaminergic regulation. Indeed, the monoaminergic innervation of the entorhinal cortex was detected from E56 on and gradually increased in density, displaying areal and laminar differences in the distribution of the dopaminergic, noradrenergic, and serotoninergic afferents.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed1991

Entorhinal cortex of the monkey: V. Projections to the dentate gyrus, hippocampus, and subicular complex.

The topographic and laminar organization of entorhinal projections to the dentate gyrus, hippocampus, and subicular complex was investigated in the Macaca fascicularis monkey. Injections of 3H-amino acids were placed at various positions within the entorhinal cortex and the distribution of anterogradely labeled fibers and terminals within the other fields of the hippocampal formation was determined. Injections of the retrograde tracers Fast blue, Diamidino yellow, and wheat germ agglutinin-horseradish peroxidase (WGA-HRP) were also placed into the dentate gyrus, hippocampus, and subicular complex, and the distribution of retrogradely labeled cells in the entorhinal cortex was plotted using a computer-aided digitizing system. The entorhinal cortex gave rise to projections that terminated in the subiculum, in the CA1, CA2, and CA3 fields of the hippocampus, and in the dentate gyrus. Projections to the dentate gyrus, and fields CA3 and CA2 of the hippocampus, originated preferentially in layers II and VI of the entorhinal cortex whereas projections to CA1 and to the subiculum originated mainly in layers III and V. Anterograde tracing experiments demonstrated that all regions of the entorhinal cortex project to the outer two-thirds of the molecular layer of the dentate gyrus and to much of the radial extent of the stratum lacunosum-moleculare of CA3 and CA2. While the terminal distributions of entorhinal projections to the dentate gyrus, CA3, and CA2 were not as clearly laminated as in the rat, projections from rostral levels of the entorhinal cortex preferentially innervated the outer portion of the molecular layer and stratum lacunosum-moleculare, whereas more caudal levels of the entorhinal cortex projected relatively more heavily to the deeper portions of the entorhinal terminal zones. The entorhinal projection to the CA1 field of the hippocampus and to the subiculum followed a transverse rather than radial gradient of distribution. Rostral levels of the entorhinal cortex terminated most heavily at the border of CA1 and the subiculum. More caudal levels of the entorhinal cortex projected to progressively more distal portions of the subiculum (towards the presubiculum) and more proximal portions of CA1 (towards CA2). Lateral portions of the entorhinal cortex projected to caudal levels of the recipient fields and more medial parts of the entorhinal cortex projected to progressively more rostral portions of the fields.

Animals↗

PubMed1997

Evidence for recovery of spatial learning following entorhinal cortex lesions in mice.

The influence of entorhinal cortex lesions on behaviour and concommitant changes in synaptophysin immunoreactivity (IR) in the denervated dentate gyrus was assessed. Male, C57/B6 mice received either bilateral (BI), unilateral (UNI), or no lesion (SHAM) to the entorhinal cortex. At various stages post-lesion the animals were evaluated in tests to examine neurological and cognitive (spatial and cued learning, Morris water maze) function. UNI lesioned animals from 6-36 days post-lesion showed no neurological nor marked cued learning deficit, yet a profound spatial learning deficit. However by 70 days post-lesion, spatial learning ability was clearly evident. In contrast, BI lesioned animals showed severe spatial learning deficits throughout the test period (6-70 days), cued learning was also impaired. In parallel groups of UNI lesioned mice, 6-36 days post-lesion there was a marked reduction (-40%) in synaptophysin IR in the dentate gyrus molecular layer. However by 70 days post-lesion a clear increase in this measure was noted. Changes in the expression of the growth associated protein, GAP43, were also noted over this period. Taken together, the present results suggest some recovery of spatial learning following unilateral entorhinal cortex lesions in mice. This behavioural recovery of a hippocampally dependant task may be associated with a recovery of function related to the synaptic remodelling and elevation of synapse number in the denervated hippocampus, as evidenced by changes in synaptophysin and GAP43 IR.

Animals↗