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PubMed2000

Hippocampus-entorhinal cortex loop and seizure generation in the young rodent limbic system.

Application of the convulsant 4-aminopyridine (4AP, 50 microM) to adult mouse combined hippocampus-entorhinal cortex (EC) slices induces interictal and ictal discharges originating from CA3 and EC respectively. In this model of limbic seizures, ictal discharges disappear over time and are reestablished after Schaffer collateral cut, a procedure that blocks interictal propagation from CA3 to EC. Here we tested whether this form of network plasticity is operant in hippocampus-EC slices obtained from young (10-25 day-old) mice. In these experiments 4AP elicited interictal (duration = 100-250 ms; interval = 0.7 +/- 0.2 s, mean +/- SD, n = 20) and ictal (duration = 267 +/- 37 s; interval = 390 +/- 37 s, n = 20) discharges in both CA3 and EC. However, in young mouse slices the ictal events occurred throughout the experiment, whereas Schaffer collateral cut abolished CA3-driven interictal discharges in EC without influencing ictal activity (n = 10). Perforant path lesion prevented the spread of EC-driven ictal events to CA3, where interictal and short ictal discharges (duration = 32 +/- 11 s; interval = 92 +/- 9.7 s, n = 8) continued to occur. Hence, two independent forms of ictal activity were seen in CA3 and in EC after separation of these structures. In intact hippocampus-EC slices, ictal discharges were reduced by an N-methyl-D-aspartate receptor antagonist (n = 10). Under these conditions, Schaffer collateral cut abolished ictal activity in EC, not in CA3 (n = 6). Thus the young mouse hippocampus-EC loop has different properties as compared with adult tissue. These differences, which include the inability of hippocampal outputs to control ictal discharge generation in EC and the ability of the loop to sustain ictal activity, may contribute to the low-seizure threshold seen in young individuals.

4-Aminopyridine↗
PubMed2006

Entorhinal cortex lesions disrupt fear conditioning to background context but spare fear conditioning to a tone in the rat.

Recent studies have shown that the integrity of the entorhinal cortex (EC) is not required for simple contextual conditioning. In background contextual conditioning, i.e., when a phasic cue is present during training, the involvement of the EC is still a matter of debate. Therefore, the present work further examines whether the EC is required for background contextual conditioning using a tone as the phasic cue. Rats sustaining either excitotoxic lesions of the EC or sham-lesions were trained with one of two procedures differing with respect to the predictive value of the tone: a paired procedure in which the tone perfectly predicts shock occurrence and overshadows context, and an unpaired procedure in which the predictive value of the tone is reduced. Conditioned fear was assessed by freezing responses during conditioning, reexposure to the training context, and reexposure to the tone in a new context. Postshock freezing was reduced in rats with entorhinal lesions. In all rats trained with the paired procedure, freezing to the context was low and freezing to the tone was high, suggesting that the tone has overshadowed the context during the conditioning session. The reverse pattern was observed with the unpaired procedure in sham-operated rats. In rats with entorhinal lesions trained with the unpaired procedure, freezing responses to the context was markedly reduced. In a new context, however, entorhinal-lesioned rats showed higher freezing scores than those of sham-lesioned rats. Freezing to the tone was unaffected by the lesion irrespective of the tone's predictive value. As a whole, these results support the notion that the EC is required for normal background contextual freezing.

Acoustic Stimulation↗
PubMed2003

Input and output stations of the entorhinal cortex: superficial vs. deep layers or lateral vs. medial divisions?

Based on the results of recent electrophysiological and anatomical studies, we argue that the classical division of the entorhinal cortex (EC) into a superficial layer input station and deep layer output station is no longer tenable. We point out that the anatomical data suggest that the medial and lateral divisions of EC are separate, and recent studies of the propagation of signals originating in the lateral olfactory tract and perirhinal cortex to the EC [J. Neurophysiol. 83 (2000) 1924-1931; Biella and de Curtis, 2000) indicate that the lateral division is the input station, and the medial division the output station for information processed in the hippocampus and subiculum.

Animals↗
PubMed1987

The entorhinal cortex of the monkey: III. Subcortical afferents.

The subcortical afferent connections of the entorhinal cortex of the Macaca fascicularis monkey were investigated by the placement of small injections of the retrograde tracer wheat germ agglutinin conjugated to horseradish peroxidase into each of its subdivisions. Retrogradely labeled cells were observed in several subcortical regions including the amygdaloid complex, claustrum, basal forebrain, thalamus, hypothalamus, and brainstem. In the amygdala, labeled cells were observed principally in the lateral nucleus, the accessory basal nucleus, the deep or paralaminar portion of the basal nucleus, and the periamygdaloid cortex. Additional retrogradely labeled cells were found in the endopiriform nucleus, the anterior amygdaloid area, and the cortical nuclei. Retrogradely labeled cells were observed throughout much of the rostrocaudal extent of the claustrum and tended to be located in its ventral half. In the basal forebrain, retrogradely labeled cells were observed in the medial septal nucleus, the nucleus of the diagonal band, and to lesser extent within the substantia innominata. Several of the cells in the latter region were large and located within the densely packed neuronal clusters of the basal nucleus of Meynert. Most of the labeled cells in the thalamus were located in the midline nuclei. Many were found in nucleus reuniens, but even greater numbers were located in the centralis complex. Additional labeled cells were located in the paraventricular and parataenial nuclei. In all cases, numerous retrogradely labeled cells were observed in the medial pulvinar. In the hypothalamus, most of the retrogradely labeled cells were located in the supramamillary area, though scattered cells were also observed in the perifornical region and in the lateral hypothalamic area. Caudal to the mamillary nuclei there were labeled cells in the ventral tegmental area. There were relatively few labeled cells in the brainstem and these were invariably located either in the raphe nuclei or locus coeruleus.

Amygdala↗
PubMed1990

Senile plaques: staining for acetylcholinesterase and A4 protein: a comparative study in the hippocampus and entorhinal cortex.

In 20 unselected autopsy cases tissue blocks from the hippocampus with adjacent entorhinal cortex and neocortex were stained for acetylcholinesterase (AChE). From five brains shown to have large numbers of senile plaques tissue, adjacent to that taken for AChE tissue blocks, was embedded in paraffin and sections were immunostained for the A4 protein. The morphological aspects were compared. Equivalent types of plaques and plaque-like structures were observed in the A4- and ACHE-stained sections. On selected tissue blocks from patients with many senile plaques two immediately adjacent cryostat sections were stained, one for AChE and one for A4 protein. The same individual plaques could be identified on the two sections. These findings suggest that high AChE activity is intimately associated with the process of A4 protein formation and accumulation in plaques and that this association already occurs at a very early stage of plaque formation.

Acetylcholinesterase↗
PubMed1988

Differential distribution of beta and theta EEG activity in the entorhinal cortex of the cat.

The basic characteristics of the electroencephalograms (EEGs) of the entorhinal cortex (EC) were compared to those of the olfactory bulb (OB) and prepiriform cortex (PPC) in the awake cat, using methods that take into account linear (coherence functions) and non-linear relationships (mutual information). The frequency spectra of EC signals differ from those of EEG signals recorded from OB or PPC, but in the beta frequency band (35-40 Hz) coherent activity between these latter two areas and the EC could be put in evidence. Taking the values of coherence as a measure of linear coupling between populations of neurons, this coupling is strong between PPC and the rostral part of the EC, and becomes weaker towards more lateral, caudal and medial areas. This decrease in coupling is confirmed by non-linear analysis methods. On the basis of intracortical depth profiles it was shown that the beta activity is locally generated in layer II of the EC. Another rhythmic activity was also recorded in EC in the theta frequency range. Theta rhythm is generated mainly in the caudal part of EC. This area has the strongest coupling with the hippocampal formation. These analyses lead to the conclusion that in the EC olfactory and limbic domains have different topographical distributions but with a certain degree of overlap.

Animals↗
PubMed1997

Systemic administration of the phencyclidine compound MK-801 affects stimulus-induced field potentials selectively in layer III of rat medial entorhinal cortex.

Phencyclidine and related compounds such as MK-801 produce psychotic symptoms, which closely resemble schizophrenia. MK-801 causes lesions in different corticolimbic regions including the medial entorhinal cortex (mEC). Using electrophysiological recordings in brain slices we tested whether several hours of systemic administration of MK-801 affect stimulus-induced field potentials (FPs) in the mEC. Stimulus-induced FPs were selectively reduced in layer III, but not in layers II and V of the mEC. In contrast, MK-801 applied acutely over the bath in low concentration had no significant effect on evoked FPs. Since the principal cells of layer III project directly to area CA1 and the subiculum, the selective effects of MK-801 may have implications for the transfer of information to the hippocampus.

Animals↗
PubMed2006

Mechanism of graded persistent cellular activity of entorhinal cortex layer v neurons.

Working memory is an emergent property of neuronal networks, but its cellular basis remains elusive. Recent data show that principal neurons of the entorhinal cortex display persistent firing at graded firing rates that can be shifted up or down in response to brief excitatory or inhibitory stimuli. Here, we present a model of a potential mechanism for graded firing. Our multicompartmental model provides stable plateau firing generated by a nonspecific calcium-sensitive cationic (CAN) current. Sustained firing is insensitive to small variations in Ca2+ concentration in a neutral zone. However, both high and low Ca2+ levels alter firing rates. Specifically, increases in persistent firing rate are triggered only during high levels of calcium, while decreases in rate occur in the presence of low levels of calcium. The model is consistent with detailed experimental observations and provides a mechanism for maintenance of memory-related activity in individual neurons.

Action Potentials↗
PubMed1994

Circumscribed malformation and nerve cell alterations in the entorhinal cortex of schizophrenics. Pathogenetic and clinical aspects.

A postmortem histological comparison of 5 selected cases of schizophrenia with 5 non-schizophrenic controls showed a circumscribed malformation of the entorhinal cortex. The cortical alterations consisted mainly of a lack or a change of the characteristic island formations in layer II pre-alpha. Further, there were atypical neurons in layers II and III showing a conspicuous decrease of volume, often a change of the shape. They lay either in clusters or in columnar formations. These cells were considered "young neurons". The changes varied considerably from case to case and sometimes extended to all entorhinal layers. In one case the extension of the changes is described by means of serial sections in steps which extend over the whole rostral entorhinal region. Here, the striking architectural changes were formed in an exactly circumscribed sector and did not extend to the rostral hippocampal formation. On the whole, the changes are regarded as local migrational disturbances that occur during the second trimester of brain development. Neuronal displacements like these could give rise to various aberrant connections within the limbic system and related structures (e.g. the central position of the entorhinal region in circuits such as the entorhino-hippocampal loop, entorhinol-insula and entorhino-orbitofrontal reciprocal connections). Whereas alterations of the genetic programming of cell migrations may be suspected, various environmental influences (e.g. viral infections during the months III-V of pregnancy) appear to play a significant role. The malformations may be a decisive vulnerability factor for the later manifestation of the illness.

Adult↗
PubMed2004

Enhanced locomotor activity in rats with excitotoxic lesions of the entorhinal cortex, a neurodevelopmental animal model of schizophrenia: behavioral and in vivo microdialysis studies.

In order to examine the construct validity of rats with excitotoxic damage of the left entorhinal cortex (EC) as an animal model of schizophrenia, we measured dopamine (DA)-related behaviors and methamphetamine (MAP)-induced DA release in the accumbens nucleus (NAC) in these animals. Quinolinic acid (lesion group) or phosphate buffer (sham group) was infused into the left EC of adolescent (postnatal 7 weeks) male Wistar rats. On the 14th and 28th postoperative day, spontaneous and MAP (1 mg/kg, i.p.)-induced locomotor activities, as well as MAP-induced stereotypy, were measured. The lesioned rats exhibited significantly greater spontaneous or MAP-induced locomotor activity on both of the postoperative days than did sham-operated animals, while EC lesions did not affect MAP-induced stereotypy on either occasion. MAP (1 mg/kg, i.p.)-induced DA release in NAC was measured by in vivo microdialysis on the 28th postoperative day. Lesioned rats did not show a significant change in MAP (1 mg/kg, i.p.)-induced DA release in NAC compared to sham-operated animals. These results suggest that excitotoxic damage of the left EC produces behavioral changes consistent with altered mesolimbic dopaminergic transmissions, possibly mediated by postsynaptic supersensitivity.

Animals↗
PubMed2002

Induction of homosynaptic long-term depression in entorhinal cortex.

Prolonged low frequency stimulation (1 Hz, 15 min) induced significant long-term depression (LTD) in hippocampal CA1 region and superficial, but not deep, layers of rat medial entorhinal cortex (EC) in vitro. In the presence of D-AP5, significant LTD was induced in EC superficial layers, but not in CA1 or EC deep layers. These results show differences in characteristics of LTD induction across CA1, EC superficial layers, and EC deep layers.

2-Amino-5-phosphonovalerate↗
PubMed1996

A comparison of spontaneous EPSCs in layer II and layer IV-V neurons of the rat entorhinal cortex in vitro.

1. We have compared the characteristics of spontaneous excitatory postsynaptic currents (sEPSCs) in neurons of layer IV-V and layer II of the rat entorhinal cortex (EC) using whole cell voltage-clamp recordings in a slice preparation. 2. The frequency of sEPSCs was similar in the two layers, but the events in layer IV-V had a larger mean amplitude, faster rise time, and were faster to decay. The difference in amplitude could be attributed to the presence of a population of larger events in the layer IV-V neurons that were not present in layer II. 3. Electrotonic length was greater in layer II neurons, suggesting that the difference in kinetics of the sEPSCs may be explained partly by electrotonic attenuation. 4. The frequency of sEPSCs in both layers was reduced by tetrodotoxin (TTX) to a similar extent (15-20%). However, the amplitude distribution was unchanged in layer II, whereas in layer IV-V TTX abolished most of the larger amplitude sEPSCs. 5. 6-cyano-7-nitroquinoxaline-2,3-dione or 6-nitro-7-sulphamoylbenzo (f)-quinoxaline-2,3-dione, abolished most of the sEPSCs in neurons of both layers. However, even at negative holding potentials, a population of slower time-course sEPSCs remained in the presence of these antagonists. 6. The slow sEPSCs were more frequent in layer IV-V but had similar characteristics in both layers, being increased in amplitude at more positive holding potentials or in Mg2+-free medium, and blocked by 2-amino-5-phosphonovalerate (AP5). 7. AP5 alone (i.e., without addition of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid antagonists) reduced the peak amplitude and decay phase of sEPSCs in layer IV-V neurons but appeared to have little effect on amplitude and only a weak effect on decay phase in layer II. 8. Thus both layer IV-V and layer II neurons of the EC suffer continuous spontaneous excitation. However, layer IV-V neurons exhibit larger amplitude sEPSCs, probably mediated by release of multiple quanta of neurotransmitter. In addition, although both types of neurons display spontaneous excitation mediated by N-methyl-D-aspartate receptors, this component appears more pronounced in the deeper layers.

Animals↗
PubMed1994

The entorhinal cortex and a delayed non-matching-to-place task in mice: emphasis on preoperative training and presentation procedure.

This study examined the effects of ibotenate lesions of the entorhinal cortex (EC) on performance of a spatial recognition memory task, the delayed non-matching-to-place task (DNMTP), varying in level of difficulty according to the number of interpolated arm visits between sample-place presentation and subsequent recognition in mice. Results of experiment 1, designed to test the rate of acquisition of the task, showed that experimental animals were impaired in the basic non-matching task. However, with further training they were able to learn the task. Impairments were also observed when the amount of interpolating information inserted was gradually increased, and then all problem difficulties were pseudorandomly tested. There was no measurable recovery of function over time when the animals were retested on the task approximately 1 month later. Experiment 2 showed that the animals that received extensive training on the task prior to lesions of the EC were only transiently impaired in the DNMTP task. These data suggest that the EC plays an important role in acquisition rather than retention of the spatial recognition memory task.

Animals↗
PubMed1998

Increased apolipoprotein E mRNA in the hippocampus in Alzheimer disease and in rats after entorhinal cortex lesioning.

The distribution of apolipoprotein E (ApoE) mRNA was characterized in the hippocampus of humans with Alzheimer disease (AD) and in rats with experimental lesions (unilateral ablation of the entorhinal cortex) that model selected features of AD. In both AD and the lesion model, we observed a shift in the location of astrocytes containing prevalent ApoE mRNA from the neuropil to regions with densely packed neurons. The increased abundance of ApoE mRNA in astrocytes close to neuron cell bodies could be indicative of lipid uptake in regions where neurons are degenerating or where synaptic remodeling is taking place.

Alzheimer Disease↗
PubMed2003

Reduced inhibition and increased output of layer II neurons in the medial entorhinal cortex in a model of temporal lobe epilepsy.

Temporal lobe epilepsy is the most common type of epilepsy in adults, and its underlying mechanisms are unclear. To investigate how the medial entorhinal cortex might contribute to temporal lobe epilepsy, we evaluated the histology and electrophysiology of slices from rats 3-7 d after an epileptogenic injury (pilocarpine-induced status epilepticus). Nissl staining, NeuN immunocytochemistry, and in situ hybridization for GAD65 mRNA were used to verify the preferential loss of glutamatergic neurons and the relative sparing of GABAergic interneurons in layer III. From slices adjacent to those that were used for anatomy, we obtained whole-cell patch recordings from layer II medial entorhinal cortical neurons. Recordings under current-clamp conditions revealed similar intrinsic electrophysiological properties (resting membrane potential, input resistance, single spike, and repetitive firing properties) to those of controls. Spontaneous IPSCs were less frequent (68% of controls), smaller in amplitude (57%), and transferred less charge (51%) than in controls. However, the frequency, amplitude, and rise time of miniature IPSCs were normal. These findings suggest that after epileptogenic injuries the layer II entorhinal cortical neurons receive less GABA(A) receptor-mediated synaptic input because presynaptic inhibitory interneurons become less active. To investigate the possible consequences of reduced spontaneous inhibitory input to layer II neurons, we recorded field potentials in the dentate gyrus, their major synaptic target. At 5 d after pilocarpine-induced status epilepticus the spontaneous field potentials recorded in vivo were over three times more frequent than in controls. These findings suggest that an epileptogenic injury reduces inhibition of layer II neurons and results in excessive synaptic input to the dentate gyrus.

Animals↗
PubMed1999

Effects of glutamate uptake blockers on stimulus-induced field potentials in rat entorhinal cortex in vitro.

L-Glutamic acid (Glu) is a key excitatory transmitter in the central nervous system. Excessive amounts of Glu are highly toxic to neurons and particularly the entorhinal cortex (EC) exhibits a remarkable loss of cells in the superficial layers in acute brain injury. The accumulation of Glu is limited by a family of high-affinity Glu transporters. Using extracellular potential recordings in rat brain slices we tested whether application of the Glu uptake blockers dihydrokainate and L-trans-pyrrolidine-2,4-dicarboxylate (L-trans-2,4-PDC) affect stimulus-induced field potentials (FPs) in superficial layer III and deep layer V of the medial EC. We found that a high concentration (400 microM) of the uptake blockers significantly reduces stimulus-induced FPs in both layers. At lower concentration (200 microM), only dihydrokainate is efficient. The data show that Glu uptake is involved in the control of extracellular Glu levels during synaptic excitation of layers III and V of the medial EC.

Amino Acid Transport System X-AG↗
PubMed2004

Inhibition of dopamine synthesis with alpha-methyl-p-tyrosine abolishes the enhancement of methamphetamine-induced extracellular dopamine levels in the amygdala of rats with excitotoxic lesions of the entorhinal cortex.

This study was performed to investigate the mechanisms underlying the augmentation of methamphetamine (MAP)-induced dopamine (DA) release in the entorhinal cortex-lesioned rats. Quinolinic acid or phosphate buffered saline was infused into the left entorhinal cortex of adolescent rats (postnatal day 7 weeks). After 4 weeks of lesioning, acute MAP (2 mg/kg, i.p.)-induced DA release in the amygdala was significantly enhanced in lesioned rats compared to sham operated rats. Inhibition of DA synthesis by alpha-methyl-p-tyrosine, an inhibitor of catecholamine synthesis, resulted in abolishment of the enhancement of MAP (2 or 5 mg/kg, i.p.)-induced DA release in the amygdala of lesioned rats. These results suggest that excessive DA pool in nerve terminals underlies the augmentation of MAP-induced DA release in the amygdala of the lesioned rats.

Amygdala↗