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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↗

PubMed1987

The entorhinal cortex of the monkey: II. Cortical afferents.

The entorhinal cortex of the monkey is commonly viewed as the major link between the cerebral cortex and the other fields of the hippocampal formation. Until recently, however, little was known about the origins of the cortical projections to the entorhinal cortex, and most of the available information is still based on degeneration studies. We have carried out a systematic analysis of these connections by placing small injections of the retrograde tracer wheat germ agglutinin conjugated to horseradish peroxidase into each of the fields of the entorhinal cortex of the Macaca fascicularis monkey. Retrogradely labeled cells were observed in several areas of the frontal and temporal lobes, the insula, and the cingulate cortex. In the frontal lobe, the greatest number of labeled cells were observed in the orbital region and specifically in areas 13 and 13a: labeled cells were also seen in areas 14, 11, and 12. In the dorsolateral frontal cortex, labeled cells were observed mainly in the rostral half of area 46; occasionally cells were also seen in areas 9, 8, and 6. In the cingulate cortex, labeled cells were observed in area 25, area 32, and rostral levels of area 24; fewer cells were observed at caudal levels of area 24 or in area 23. The retrosplenial region (areas 30 and 29), including its caudal extension along the rostral calcarine sulcus and its ventral extension into the temporal lobe, contained numerous labeled cells. In the temporal lobe, retrogradely labeled cells were arranged in two rostrocaudally oriented bands. Rostral to the hippocampal formation, the first band encompassed the piriform and periamygdaloid cortices and areas 35 and 36; the labeling in area 36 was continuous to the temporal pole. At more caudal levels this band was located immediately lateral to the hippocampal formation and included areas 35 and 36 rostrally and areas TH and TF caudally. The second band was situated in the superior temporal gyrus where labeled cells were observed in several distinct cytoarchitectonic fields, including the parainsular cortex in the fundus of the inferior limiting sulcus. In the insula proper, retrogradely labeled cells were seen mainly in the rostral or agranular division; far fewer were observed in the dysgranular and granular insula. Whereas there is little available physiological information concerning many of the cortical regions that project to the entorhinal cortex, on anatomical grounds they may be generally characterized as polysensory associational regions.

Afferent Pathways↗

PubMed1998

Neuronal damage after the injection of aminooxyacetic acid into the rat entorhinal cortex: a silver impregnation study.

In rats, most neurons in layer III of the medial entorhinal cortex are exquisitely vulnerable to prolonged seizure activity. These neurons have also been shown to die preferentially in the entorhinal cortex of patients with temporal lobe epilepsy. This lesion can be duplicated in rats by a focal injection of the indirect excitotoxin aminooxyacetic acid into the entorhinal cortex. The present study was designed to examine the neuropathological consequences of an intra-entorhinal aminooxyacetic acid injection at various time-points with a sensitive silver staining method for the visualization of damaged neurons. After 3 h, affected cells with prominently stained processes were readily observed in the transition zone of the hippocampal CA1 field and the subiculum, but no silver-stained neurons were seen in the entorhinal cortex. Less consistently, damaged neurons were observed in the presubiculum, in the temporal and perirhinal cortices and in the lateral amygdaloid nucleus. At 6 h after an aminooxyacetic acid injection, numerous silver-stained neurons, which were typically devoid of processes, were also seen in layer III of the medial entorhinal cortex. This pattern of neurodegeneration remained similar at 12 and 24 h following the aminooxyacetic acid injection, though many silver-stained neurons were noted in layer II of the lateral entorhinal cortex as well. Notably, at five days, silver-stained neurons had disappeared. Instead, dendritic arbors, debris of degenerated neurons and reactive glial cells were present in lesioned brain regions. These data demonstrate the chronology and the extent of neuronal damage following an intra-entorhinal injection of aminooxyacetic acid. The results suggest that a detailed examination of the temporal sequence of neuronal death in the entorhinal cortex and in extra-entorhinal areas is likely to benefit our understanding of the pathophysiology of temporal lobe epilepsy.

Aminooxyacetic Acid↗

PubMed2000

Short- and long-term memory are differentially affected by metabolic inhibitors given into hippocampus and entorhinal cortex.

Rats were implanted with cannulae in the CA1 area of the dorsal hippocampus or in the entorhinal cortex and trained in one-trial step-down inhibitory avoidance. Two retention tests were carried out in each animal, one at 1.5 h to measure short-term memory (STM) and another at 24 h to measure long-term memory (LTM). The purpose of the present study was to screen the effect on STM of various drugs previously shown to affect LTM of this task when given posttraining at the same doses that were used here. The drugs and doses were the guanylyl cyclase inhibitor LY83583 (LY, 2.5 microMg), the inhibitor of Tyr-protein kinase at low concentrations and of protein kinase G (PKG) at higher concentrations lavendustin A (LAV, 0.1 and 0.5 microMg), the PKG inhibitor KT5823 (2.0 microMg), the protein kinase C (PKC) inhibitor staurosporin (STAU, 2.5 microMg), the inhibitor of calcium/ calmodulin protein kinase II (CaMKII) KN62 (3.6 microMg), the protein kinase A (PKA) inhibitor KT5720 (0.5 microMg), and the mitogen-activated protein kinase kinase (MAPKK) inhibitor PD098059 (PD, 0.05 microMg). PD was dissolved in saline; all the other drugs were dissolved in 20% dimethyl sulfoxide. In all cases the drugs affected LTM as had been described in previous papers. The drugs affected STM and LTM differentially depending on the brain structure into which they were infused. STM was inhibited by KT5720, LY, and PD given into CA1 and by STAU and KT5720 given into the entorhinal cortex. PD given into the entorhinal cortex enhanced STM. LTM was inhibited by STAU, KN62, KT5720, KT5823, and LAV (0.5 microMg) given into CA1 and by STAU, KT5720, and PD given into the entorhinal cortex. The results suggest that STM and LTM involve different physiological mechanisms but are to an extent linked. STM appears to require PKA, guanylyl cyclase, and MAPKK activity in CA1 and PKA and PKC activity in the entorhinal cortex; MAPKK seems to play an inhibitory role in STM in the entorhinal cortex. In contrast, LTM appears to require PKA and PKC activity in both structures, guanylyl cyclase, PKG, and CaMKII activity in CA1, and MAPKK activity in the entorhinal cortex.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed1996

Ethosuximide specifically antagonizes the effect of pentylenetetrazol in the rat entorhinal cortex.

This study tested two related hypotheses. The first is that the entorhinal cortex has an important role in synchronization and spread of epileptiform activity into the dentate gyrus. The second is that ethosuximide acts by antagonizing the action of pentylenetetrazol (PTZ) in the entorhinal cortex. Experiments were carried out in urethane anesthetized rats. Recording electrodes were placed in the dentate gyrus and stimulating electrodes were placed in the angular bundle. Administration of PTZ reduced the time to onset of maximal dentate activation, which is a marker for synchronized reverberatory seizure activity in the hippocampal-parahippocampal circuits. Since PTZ facilitates the spread of epileptiform activity in, or through, the entorhinal cortex, these results support the hypothesis that the entorhinal cortex can influence the spread of seizure activity from the entorhinal cortex into the hippocampus. Ethosuximide specifically, and dose-dependently, reduced the polysynaptic response in the dentate gyrus that is initiated by PTZ, while having no effect on the response in the dentate gyrus to ipsilateral angular bundle stimulation. These results support the hypotheses that ethosuximide can antagonize this effect of PTZ.

Animals↗

PubMed1997

Serotonin blocks different patterns of low Mg2+-induced epileptiform activity in rat entorhinal cortex, but not hippocampus.

Low Mg2+-induced epileptiform activity in the entorhinal cortex is characterized by an initial expression of seizure-like events followed by late recurrent discharges. Both these forms of activity as well as the transition between them were blocked by serotonin. In contrast, serotonin had little effect upon the epileptiform activity in areas CA3 and CA1 of the hippocampus. Both forms of epileptiform activity in the entorhinal cortex are sensitive to N-methyl-D-aspartate receptor antagonists and it is shown here that serotonin blocked both types of epileptiform activity through an effective concentration-dependent reduction of N-methyl-D-aspartate receptor-mediated excitatory postsynaptic potentials in deep layer entorhinal cortex cells. Serotonin also prolonged or even prevented the transition between the two types of epileptiform activity and we suggest that this may be through activation of the Na+/K+-ATPase. The resistance of epileptiform activity in CA1 and CA3 to serotonin was most likely related to the inability of serotonin to reduce Schaffer collateral-evoked excitatory postsynaptic potentials. Given the strong serotonergic inputs to both the hippocampus and entorhinal cortex, the differential sensitivity of the two regions to serotonin suggests functional differences. In addition since the late recurrent discharges in the entorhinal cortex are resistant to all clinically used anticonvulsants, serotonin may open new avenues for the development of novel anticonvulsant compounds.

Animals↗

PubMed1994

Topographic organization of the reciprocal connections between the monkey entorhinal cortex and the perirhinal and parahippocampal cortices.

The perirhinal and parahippocampal cortices constitute the major sources of cortical input to the monkey entorhinal cortex. Neuropsychological studies have shown that these three cortical regions contribute in an important way to normal memory function. We have investigated the topographic and laminar organization of the reciprocal projections between the entorhinal cortex and these two adjacent cortical areas by placing anterograde and retrograde tracers in all three regions. There were three major findings. First, the perirhinal and parahippocampal cortices have distinct but partially overlapping interconnections with the entorhinal cortex. The perirhinal cortex tends to be interconnected with the rostral two-thirds of the entorhinal cortex while the parahippocampal cortex tends to be interconnected with approximately the caudal two-thirds of the entorhinal cortex. Second, the degree of reciprocity of the interconnections of the entorhinal cortex with the perirhinal and parahippocampal cortices differs. The parahippocampal/entorhinal connections have a high degree of reciprocity. In contrast, the degree of reciprocity of the perirhinal/entorhinal interconnections varies depending on the mediolateral position within the perirhinal cortex; medial portions of the perirhinal cortex exhibit a higher degree of reciprocity with the entorhinal cortex than lateral portions. Third, the projections from the perirhinal and parahippocampal cortices to the entorhinal cortex resemble a feedforward projection, while the projections from the entorhinal cortex to the perirhinal and parahippocampal cortices resemble a feedback projection pattern.

Animals↗

PubMed1981

An autoradiographic study of the efferent connections of the entorhinal cortex in the rat.

The longer connections of the entorhinal cortex have been studied autoradiographically in a series of rats, each of which received a small injection of 3H-amino acids in one of the various cytoarchitectonic subfields of the entorhinal cortex. The major findings can be summarized as follows. Whereas the projection of the lateral entorhinal area (LEA) to the dentate gyrus is broad in its longitudinal extent, the medial entorhinal area (MEA), and especially the ventral portion of this zone, projects in a more lamellar fashion. In the transverse plane the LEA preferentially projects to the inner (dorsal) blade of the dentate gyrus, while the MEA innervates both blades equally. Within the radial dimension, the entorhinal cortex projects to the dentate gyrus according to a medial to lateral gradient, with lateral portions of the LEA projecting along the pial surface and successively more medial portions of the entorhinal projecting closer to the granule cells. The commissural entorhinal to dentate projections are similar to the ipsilateral projections in location; however, they are considerably reduced in septotemporal extent and do not arise from cells in the ventral half of either LEA or the intermediate entorhinal area (IEA). The projection of the entorhinal cortex to Ammon's horn reflects the same longitudinal characteristics as the dentate projections. An alvear input which extends only to the pyramidal cells at the CA1-subicular junction was most noticeable at ventral hippocampal levels. Finally the extrahippocampal projections have been analyzed. These arise predominantly from cells in the LEA and project forward along the angular bundle to the piriform and periamygdaloid cortices, as well as the endopiriform nucleus, the lateral, basolateral, and cortical amygdaloid nuclei, the nucleus of the lateral olfactory tract, the olfactory tubercle, the anterior olfactory nucleus, the taenia tecta, and the indusium griseum. These extrinsic projections are to a large extent reciprocal to the major extrinsic inputs to the LEA.

Amino Acids↗

PubMedDate not supplied

Abnormal cholecystokinin mRNA levels in entorhinal cortex of schizophrenics.

Limbic cortical regions, including anterior cingulate cortex (ACC), prefrontal cortex (PFC) and entorhinal cortex (ERC), have been implicated in the neuropathology of schizophrenia. Glutamate projection neurons connect these limbic cortical regions to each other, as well as to the terminal fields of the striatal/accumbens dopamine neurons. Subsets of these glutamate projection neurons, and of the GABA interneurons in cortex, contain the neuropeptide cholecystokinin (CCK). In an effort to study the limbic cortical glutamate projection neurons and GABA interneurons in schizophrenia, we have measured CCK mRNA with in situ hybridization histochemistry in postmortem samples of dorsolateral (DL)PFC, ACC and ERC of seven schizophrenics, nine non-psychotic suicides and seven normal controls. CCK mRNA is decreased in ERC (especially layers iii vi) and subiculum in schizophrenics relative to controls. Cellular analysis indicates that there is a decrease in density of CCK mRNA in labelled neurons. In so far as ERC CCK mRNA is not reduced in rats treated chronically with haloperidol, this decrease in schizophrenics does not appear to be related to neuroleptic treatment. In contrast, in DLPFC, where schizophrenics do not differ from normals, the suicide victims have elevated CCK mRNA (especially in layers v and vi), and increased cellular density of CCK mRNA, relative to both normals and schizophrenics. These results lend further support for the involvement of ERC and hippocampus in schizophrenia, suggesting that neurons that utilize CCK may be particularly important. Similarly, an increase in CCK mRNA levels in the PFC of suicides adds to a growing body of evidence implicating this structure in this pathological state. In so far as CCK is co-localized with GABA or glutamate in cortical neurons, both of these neuronal populations need to be studied further in schizophrenia and suicide.

Animals↗

PubMed1997

Effects of entorhinal cortex lesions on memory in different tasks.

Lesions of the entorhinal cortex produce retrograde memory impairment in both animals and humans. Here we report the effects of bilateral entorhinal cortex lesions caused by the stereotaxic infusion of N-methyl-D-aspartate (NMDA) in rats at two different moments, before or after the training session, on memory of different tasks: two-way shuttle avoidance, inhibitory avoidance and habituation to an open field. Pre- or post-training entorhinal cortex lesions caused an impairment of performance in the shuttle avoidance task, which agrees with the previously described role of this area in the processing of memories acquired in successive sessions. In the inhibitory avoidance task, only the post-training lesions had an effect (amnesia). No effect was observed on the open field task. The findings suggest that the role of the entorhinal cortex in memory processing is task-dependent, perhaps related to the complexity of each task.

Alzheimer Disease↗

PubMed1991

Some cytoarchitectural abnormalities of the entorhinal cortex in schizophrenia.

The cytoarchitecture of the entorhinal cortex was examined in the brains of six patients with a diagnosis of schizophrenia and in 16 controls. All six brains of schizophrenic patients showed abnormalities of the rostral and intermediate portions of the entorhinal cortex. The abnormalities included aberrant invaginations of the surface, disruption of cortical layers, heterotopic displacement of neurons, and paucity of neurons in superficial layers. These changes suggest disturbed development. Because the entorhinal cortex is pivotal for neural systems that mediate corticohippocampal interactions, early disruption of its structure could lead to important neuropsychological changes during development and in adult life and could contribute to the symptomatology of schizophrenia.

Adult↗

PubMed1996

Histological evidence for cholinergic alteration in the hippocampus following entorhinal cortex lesion.

The initial stage of Alzheimer's disease is characterized by neuropathological alteration in the entorhinal cortex. To model one aspect of the neurodegeneration observed and to investigate anatomical changes of the hippocampus associated with unilateral entorhinal cortex lesion, excitotoxin ibotenic acid was used to produce selective unilateral neuronal loss in rat entorhinal cortex. Histological and morphometrical analyses confirmed excitotoxic lesion of the entorhinal cortex after 3 months and showed a decrease of acetylcholineste-rase-stained fibers in the stratum moleculare of the dentate gyrus and the stratum radiatum of the CA3 field. This study demonstrates the importance of the entorhinal cortex in the hippocampal cholinergic function which appears to be important to memory and learning, and raises the possibility that memory deficit in Alzheimer's disease may be associated with partial neuronal loss in the entorhinal cortex.

Acetylcholinesterase↗

PubMed2001

Entorhinal cortex atrophy in epilepsy patients exhibiting normal hippocampal volumes.

OBJECTIVE: To determine whether MRI volumetric measurement of the entorhinal cortex could detect structural damage and lateralize the seizure focus in patients with temporal lobe epilepsy in whom no measurable hippocampal abnormalities were found. BACKGROUND: A reduction in the volume of the entorhinal cortex ipsilateral to the seizure focus in patients with intractable temporal lobe epilepsy and hippocampal atrophy was recently shown. METHODS: MRI volumetric analysis of the entorhinal cortex was performed using a T1-weighted three-dimensional gradient echo sequence in 24 control subjects and 22 patients with temporal lobe epilepsy and normal hippocampal volumes. Thirteen patients underwent surgery, with a mean postoperative follow-up of 36 months. RESULTS: Group analysis (multivariate analysis of variance) showed a reduction in the volume of the entorhinal cortex ipsilateral to the seizure focus in patients with left (p < 0.0001) and right temporal lobe epilepsy (p < 0.0001). Lateralization of the seizure focus could be done in 14 of 22 patients (64%) based on entorhinal cortex volumetry. CONCLUSION: Entorhinal cortex atrophy ipsilateral to the seizure focus supports the presence of structural damage in the mesial temporal lobe in patients with temporal lobe epilepsy and normal hippocampal volumes and emphasizes the participation of the entorhinal cortex in the pathogenesis of this disorder.

Adult↗

PubMed1994

Effect of the infusion of the GABA-A receptor agonist, muscimol, on the role of the entorhinal cortex, amygdala, and hippocampus in memory processes.

Rats were bilaterally implanted with cannulae in the entorhinal cortex, amygdala, and hippocampus; after recovery, they were trained in a step-down inhibitory avoidance task and tested for retention 24 h later. Muscimol (0.03 microgram) or D-amino-5-phosphonovalerate (5.0 micrograms) infused in the entorhinal cortex 20 min prior to training inhibited the amnestic effect of the same dose of muscimol infused into this area 100 min after training. Thus, memory-relevant information must be processed by the entorhinal cortex at the time of training in order that this cortex may play a late post-training role in memory processing. Pretraining intraentorhinal muscimol administration did not affect the amnestic effect of the post-training infusion of muscimol into the amygdala and hippocampus, or the inhibition of memory expression induced by a pretest infusion of CNQX into the amygdala and hippocampus or into the entorhinal cortex. Pretest intraentorhinal muscimol also did not influence the effect of pretest intra-amygdala and intrahippocampal CNQX administration. These data indicate that the cells of the entorhinal cortex that are sensitive to pretraining muscimol are not part of the inputs that lead to post-training processing by the amygdala and hippocampus, or to the intervention of the amygdala, hippocampus, and entorhinal cortex in memory expression. The present findings are compatible with the possibility that, instead, the entorhinal cortex may be an output of the amygdala and hippocampus at the time of memory expression.

2-Amino-5-phosphonovalerate↗

PubMed2000

Cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus of the rat.

Effects of cholinergic agents on synaptic transmission and plasticity were examined in entorhinal cortex and hippocampus. Bath application of carbachol (0.25-0.75 microM) induced transient depression of field potential responses in all cases tested (24/24 in layer III of medial entorhinal cortex slices and 24/24 in CA1 of hippocampal slices; 11.0+/-1.9% and 7.8+/-2.5%, respectively) and long-lasting potentiation in some cases (4/24 in entorhinal cortex and 12/24 in hippocampus; 33.7+/-3.7% and 32.1+/-9.9%, respectively, in successful cases). Carbachol (0.5 microM) induced transient depression, but not long-lasting potentiation, of N-methyl-D-aspartate receptor-mediated responses in entorhinal cortex. At 5 microM, carbachol induced transient depression only (55. 9+/-4.7% in entorhinal cortex and 41.4+/-2.9% in hippocampus), which was blocked by atropine. Paired-pulse facilitation was not altered during carbachol-induced potentiation but enhanced during carbachol-induced depression. These results suggest that the underlying mechanisms of carbachol-induced depression and potentiation are decreased transmitter release and selective enhancement of non-N-methyl-D-aspartate receptor-mediated responses, respectively. Long-term potentiation could be induced in the presence of 10 microM atropine by theta burst stimulation. The magnitude was significantly lower (15.2+/-5.2%, n=9) compared with control (37.2+/-6.1%, n=8) in entorhinal cortex, however. These results demonstrate similar, but not identical, cholinergic modulation of synaptic transmission and plasticity in entorhinal cortex and hippocampus.

6-Cyano-7-nitroquinoxaline-2,3-dione↗

PubMed1983

Evidence for a direct projection from the superior temporal gyrus to the entorhinal cortex in the monkey.

During the course of a larger study of the afferent and efferent connections of the entorhinal cortex in the macaque monkey we have found evidence for a hitherto undescribed projection to the entorhinal cortex from the superior temporal gyrus. The evidence is derived principally from experiments in which small volumes of wheat germ agglutinin-conjugated horseradish peroxidase (WGA-HRP) were injected into different parts of the entorhinal cortex, but has been confirmed by 3H-amino acid autoradiography. After WGA-HRP injections into the entorhinal cortex, retrogradely labeled neurons have been seen mainly in layer III, but also to some extent in layer VI, throughout much of the superior temporal gyrus. The projection appears to be topographically organized in the sense that the ventral insular cortex and the adjoining temporal operculum have been found to project to the periamygdaloid cortex and the lateral division of the entorhinal cortex; the convexity of the superior temporal gyrus and the cortex along the dorsal bank of the superior temporal gyrus project further caudally to the medial division of the entorhinal cortex; and the cortex surrounding the fundus of the superior temporal sulcus projects to the perirhinal cortex. Following an injection of 3H-amino acids into the convexity of the superior temporal gyrus, terminal labeling has been seen over layers I and II of the entorhinal cortex and over layer I in the most lateral portion of the presubiculum. While the distribution of retrogradely labeled cells in our WGA-HRP experiments encompasses several cytoarchitectonically distinguishable areas in the superior temporal gyrus, the most heavily labeled field appears to coincide with what Gross and his colleagues have termed the 'superior temporal polysensory area' on the dorsal bank of the superior temporal sulcus.

Afferent Pathways↗

PubMed1992

Parvalbumin and calbindin D-28K in the human entorhinal cortex. An immunohistochemical study.

Research is here reported on the distribution of immunoreactivities of the calcium-binding proteins parvalbumin and calbindin D-28K in the entorhinal cortex of normal human brains. Topographically, parvalbumin immunoreactive neurons were only seen in the lateral portion of the rostral entorhinal cortex, in continuity with the adjacent perirhinal cortex. The intermediate and caudal portions gave positive results along the mediolateral extension of the entorhinal cortex. The laminar distribution of parvalbumin immunoreactive neurons was similar throughout the entorhinal cortex. Heavy immunostaining, largely coincident with cell islands, was observed in cells and fibers in layer II, being densest in the deep half of layer III and more sparsely distributed in layers V and VI. Calbindin D-28K immunoreactivity was found throughout the entorhinal cortex. In contrast to parvalbumin immunoreactivity, calbindin D-28K was present from layer I up to upper layer III, the neurons being most numerous in the cell islands of layer II. These results show that rostromedial portions of the human entorhinal cortex contain calbindin immunoreactivity, but not parvalbumin, while the lateral, intermediate and caudal portions of the entorhinal cortex contain both calcium-binding proteins. As it is known that these two proteins belong to a subset of GABAergic neurons, we suggest that a topographical diversity in some of the cells may be responsible for inhibitory effects in the human entorhinal cortex. This proposed diversity might be relevant to the processing of information that the entorhinal cortex conveys to the dentate gyrus and receives from various components of the hippocampus, the subicular complex and other cortical and subcortical sources.

Calbindins↗