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PubMed1993

Entorhinal cortex lesion induces differential responses in [125I]insulin-like growth factor I, [125I]insulin-like growth factor II and [125I]insulin receptor binding sites in the rat hippocampal formation.

The hippocampus can be induced by deafferentation to selectively reorganize its neuronal input. Entorhinal cortex lesion, which causes degeneration of the perforant pathway, evokes sprouting of septal afferents as well as glutamatergic commissural/associational fibers in the deafferentated zone of the molecular layer of the dentate gyrus. Although the process of reactive synaptogenesis that follows deafferentation has been extensively studied, at present little is known about its molecular basis and the mechanism of initiation. In this study, following unilateral lesion of the entorhinal cortex, the time-course of possible alterations of insulin-like growth factors I and II, and insulin binding sites were evaluated by in vitro quantitative receptor autoradiography. [125I]Insulin-like growth factor I receptor binding sites did not exhibit any significant variation between the contralateral and ipsilateral hippocampal formation at any time periods following lesion except in the molecular layer of the dentate gyrus (P < 0.05) at day 8. However, when compared with the unlesioned animals, a differential time-dependent response of [125I]insulin-like growth factor I binding sites was noted in selective layers of the hippocampus. [125I]Insulin-like growth factor II receptor binding sites showed a significant decrease (P < 0.05) in the ipsilateral granular cell layer of the dentate gyrus only at day 14 post lesion. Interestingly, compared to controls, a dramatic bilateral increase (P < 0.05) in [125I]insulin-like growth factor II binding was evident between days 1 and 8 in most layers of the hippocampal formation. A lesion-induced bilateral increase (P < 0.05) in [125I]insulin binding sites was evident in all layers of the hippocampus between two to eight days and at 30 days post lesion. In selective layers, however, a significant increase (P < 0.05) in [125I]insulin binding sites was also observed at days 1 and 14 after lesion. These results, which are compatible with the process of degeneration and/or sprouting of the terminal fibers, suggest possible involvement of insulin-like growth factors and insulin in the sequence of molecular events that occur to facilitate neuronal repair and to promote neuronal survival following entorhinal cortex lesion.

Afferent Pathways↗
PubMed1999

GM1 produces attenuation of short-term memory deficits in Hebb-Williams maze performance after unilateral entorhinal cortex lesions.

The Hebb-Williams maze was used to examine spatial abilities of adult male Sprague-Dawley rats with unilateral electrolytic entorhinal cortex lesions. The injured rats were treated for 14 days with either saline or ganglioside GM1. Testing was begun 7 weeks following injury, and involved 12 maze problems with independent configurations, with immediate starting replacement used for the six trials per problem. Compared to sham-operated counterparts, the rats with lesion plus saline treatment were impaired in total number of errors, initial entry errors, and repeat errors over 12 consecutive problems. GM1-treated rats showed improved performance, making significantly fewer total and repeat errors, indicating that this substance may be potentially useful as therapy after entorhinal cortex injury.

Analysis of Variance↗
PubMed1994

Pentylenetetrazol elicits epileptiform activity in the dentate gyrus of the urethane anesthetized rat by activation of the entorhinal cortex.

Pentylenetetrazol is a chemical convulsant, often used to generate experimental seizures, that is thought to act as a GABA antagonist. In the urethane anesthetized rat, pentylenetetrazol produces a characteristic epileptiform discharge in the dentate gyrus. The hypothesis that this discharge is generated by activity in the entorhinal cortex was examined in this study. Recording electrodes were placed in the dentate gyrus bilaterally and neuronal activity was recorded after administration of pentylenetetrazol. A laminar analysis of the convulsant-induced activity was compared to responses evoked by angular bundle stimulation (n = 6). Both convulsant-induced and evoked activity were negative-going in the molecular layer of the dentate gyrus. In other animals tetrodotoxin (TTX) was injected into the right entorhinal cortex before the onset of epileptiform activity (n = 5). The TTX prevented epileptiform activity in the right dentate gyrus. Injection of TTX after the onset of epileptiform activity caused the epileptiform activity to cease on the side of injection (n = 5). These experiments support the hypothesis that pentylenetetrazol specifically activates the entorhinal cortex to produce the epileptiform activity recorded in the dentate gyrus. This selective activation suggests that the mechanism of action of pentylenetetrazol, as a convulsant, is not simply as an antagonist of GABA receptors.

Anesthesia↗
PubMed1998

Laminar organization of epileptiform discharges in the rat entorhinal cortex in vitro.

1. Interictal and ictal epileptiform discharges induced by 4-aminopyridine (4AP, 50 microM) were studied in the rat lateral entorhinal cortex with field potential and intracellular recordings in an in vitro slice preparation. Both types of discharge disappeared in layer II, but continued to occur in layers IV-VI after a knife cut separation was made at approximately 600 micro(m) from the pia (n = 4 slices). 2. Interictal depolarizations recorded in layer IV-VI cells (amplitude, 29.4 +/- 8.6 mV; duration, 386 +/- 177.4 ms, means +/- s.d.; n = 17) were capped by action potential bursts, while smaller interictal depolarizations in layer II cells (amplitude, 11.7 +/- 5.8 mV; duration, 192.6 +/- 47.9 ms; n = 10) were associated with single action potentials and were terminated by a hyperpolarization. Ictal discharges were initiated by an interictal discharge; they were characterized by a depolarization of 31.5 +/- 6.2 mV (n = 12) in layer IV-VI and 11.6 +/- 3.5 mV (n = 7) in layer II neurones. 3. Slow, presumptive Ca2+-mediated spikes occurred in layer II (n = 4) and IV-VI (n = 6) cells loaded with the Na+ channel blocker QX-314 (50 mM). These events were synchronized with population spikes during interictal and ictal discharges, and were abolished by Ni2+ (1 mM, n = 4 cells) along with the 4AP-induced synchronous activity. 4. The N-methyl-D-aspartate (NMDA) receptor antagonist 3, 3-(2-carboxypiperazine-4-yl)-propyl-1-phosphonate (CPP, 10 microM) abolished ictal discharges and reduced interictal depolarizations in layer IV-VI neurones (n = 4). The non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX, 10 microM) abolished both interictal and ictal activity (n = 4 cells). 5. These findings provide evidence for a role played by NMDA-mediated mechanisms in the generation of epileptiform discharges in the entorhinal cortex. Lack of an NMDA-mediated component along with presence of inhibition in layer II neurones results in attenuation of epileptiform activity at this site. Moreover Ca2+-mediated spikes may contribute to the appearance of epileptiform discharges in this model.

4-Aminopyridine↗
PubMed2006

Bilateral entorhinal cortex lesions impair acquisition of delayed spatial alternation in rats.

Entorhinal cortex lesions induce significant reorganization of several homotypic and heterotypic inputs to the hippocampus. This investigation determined whether surviving heterotypic inputs after bilateral entorhinal lesions would support the acquisition of a learned alternation task. Rats with entorhinal lesions or sham operations were trained to acquire a spatial alternation task. Although the sham-operated rats acquired the task within about 3 weeks postsurgery, rats with bilateral entorhinal lesions failed to learn the task after 12 consecutive weeks of training despite heterotypic sprouting of the cholinergic septodentate pathway and the expansion of the commissural/associational fiber plexus within the dentate gyrus. Thus, heterotypic sprouting failed to ameliorate significantly the effects of bilateral entorhinal lesions. Rather, entorhinal lesions produced a persistent impairment of spatial memory, characterized by a mixture of random error production and perseverative responding.

Animals↗
PubMed2000

Ventral subicular lesion alters rhythmical slow wave activity (theta) of CA1 area of hippocampus and entorhinal cortex.

The present study demonstrates the effect of ibotenic acid lesioning of ventral subiculum on the theta activity of CA1 area of hippocampus and the entorhinal cortex during REM sleep. Ibotenic acid lesioning of ventral subiculum, has increased the absolute power with no noticeable change in the relative power of theta of the CA1 area. In contrast, it has decreased both the absolute and relative power of entorhinal cortical theta. Subicular output may serve to modulate the synchronous neuronal activity of entorhinal cortex and CA1 pyramidal cells during REM sleep.

Animals↗
PubMed1983

Functional dissociation between lateral and medial entorhinal cortex in memory processes in mice.

The effects of lesions of the medial or the lateral entorhinal cortex in mice were examined on acquisition, retention and extinction of an operant-conditioning task in a Skinner box. Compared with the control animals, lesions in the medial entorhinal had no behavioral effects whereas lesions in the lateral entorhinal enhanced retention and increased resistance to extinction but did not change acquisition of this task. These results suggest a functional dissociation between the two parts of the entorhinal cortex.

Animals↗
PubMedDate not supplied

Net dendritic stability of layer II pyramidal neurons in F344 rat entorhinal cortex from 12 to 37 months.

Dendritic extent of Golgi-Cox stained layer II entorhinal cortex pyramidal neurons was quantified in five groups of male F344 rats aged 12, 20, 27, 30 and 37 months. Over the age range studied, neither the apical nor the basal dendritic trees showed any statistically significant change in total dendritic length, numbers of segments or average segment length. This finding of average stability of the dendritic tree does not imply absence of remodelling of connections, but does require that if remodeling does occur, retraction and proliferation of dendrites must, on average, be equal. We hypothesized that in groups of animals with similar genetic and environmental histories neighbor neuron death provides the major stimulus for dendritic proliferation. Since we found dendritic stability in the cells reported here, we would predict that there should be no age-related loss of layer II pyramidal neurons in the entorhinal cortex of the normally aging F344 male rat between 12 and 37 months. This hypothesis may be tested by counting neurons within this region.

Aging↗
PubMed1992

Theta rhythms in the rat medial entorhinal cortex in vitro: evidence for involvement of muscarinic receptors.

Slice preparation obtained from the rat were used to study cholinergically induced field potentials in the medial entorhinal cortex. Perfusion of slices containing medial entorhinal cortex with acetylcholine, muscarine and eserine induced theta-like activity in a frequency range of 3-10 Hz and an amplitude of 200-300 microV. Nicotine, in contrast, did not produce any rhythmical slow waveforms. The cholinergically induced theta-like oscillations were abolished by perfusion of the muscarinic antagonists atropine sulphate and scopolamine but were unaffected by the nicotine blockers hexamethonium and mecamylamine.

Acetylcholine↗
PubMed2004

Subthreshold resonance explains the frequency-dependent integration of periodic as well as random stimuli in the entorhinal cortex.

Neurons integrate subthreshold inputs in a frequency-dependent manner. For sinusoidal stimuli, response amplitudes thus vary with stimulus frequency. Neurons in entorhinal cortex show two types of such resonance behavior: stellate cells in layer II exhibit a prominent peak in the resonance profile at stimulus frequencies of 5-16 Hz. Pyramidal cells in layer III show only a small impedance peak at low frequencies (1-5 Hz) or a maximum at 0 Hz followed by a monotonic decrease of the impedance. Whether the specific frequency selectivity for periodic stimuli also governs the integration of non-periodic stimuli has been questioned recently. Using frozen-noise stimuli with different distributions of power over frequencies, we provide experimental evidence that the integration of non-periodic subthreshold stimuli is determined by the same subthreshold frequency selectivity as that of periodic stimuli. Differences between the integration of noise stimuli in stellate and pyramidal cells can be fully explained by the resonance properties of each cell type. Response power thus reflects stimulus power in a frequency-selective way. Theoretical predictions based on linear system's theory as well as on conductance-based model neurons support this finding. We also show that the frequency selectivity in the subthreshold range extends to suprathreshold responses in terms of firing rate. Cells in entorhinal cortex are representative examples of cells with resonant or low-pass filter impedance profiles. It is therefore likely that neurons with similar frequency selectivity will process input signals according to the same simple principles.

Action Potentials↗
PubMed2002

Low levels of estrogen significantly diminish axonal sprouting after entorhinal cortex lesions in the mouse.

This study tested the hypothesis that estrogen enhances axonal sprouting in the hippocampal formation in the female mouse. The entorhinal cortex was unilaterally lesioned with ibotenic acid in control mice and in ovariectomized mice that were treated with a high dose of, a moderate dose of, or zero estrogen supplementation pellets. Four weeks later the density of staining for synaptophysin immunoreactivity and acetylcholinesterase (AChE) histochemistry was measured in the molecular layer of the dentate gyrus. In control mice, lesions of the lateral part of the entorhinal cortex increased synaptophysin and acetylcholinesterase staining (i.e., indicative of axonal sprouting) in the outer one-third of the molecular layer of the dentate gyrus. Mice receiving high and moderate estrogen supplementation displayed the same sprouting response; however, in ovariectomized mice the sprouting response was significantly reduced (to nearly nothing). Thus, in ovariectomized compared with control mice the lesion-induced sprouting response is severely blunted, and this effect is reversed by estrogen supplementation. Together, these findings suggest that estrogen plays a prominent role in promoting neuronal plasticity and remodeling in the dentate gyrus.

Acetylcholinesterase↗
PubMed1998

Lesion-induced transneuronal plasticity of the cholinergic innervation in the adult rat entorhinal cortex.

The present experiments were designed to determine the effect that lesions of the basal forebrain cholinergic system exert on cholinergic interneurons within the entorhinal cortex (EC) in the rat. Unilateral infusion of 192 IgG-saporin into the nucleus of the horizontal diagonal band of Broca (HDB) decreased the number of ipsilateral choline acetyltransferase immunoreactive (ChAT-ir) neurons by 54%. Two-four weeks after the lesion, the ipsilateral EC exhibited a moderate but significant loss of ChAT-ir fibres and interneurons. Adjacent sections revealed a parallel loss of vasoactive intestinal polypeptide (VIP) immunoreactivity. Cell counts in the cingulate cortex were unaffected, suggesting that this effect was indeed specific to the main target area for HDB neurons. Ibotenic acid lesions also induced a significant 36% decrease in the number of cholinergic neurons in the ipsilateral HDB, and disappearance of ChAT terminals in the EC, whereas the number of ChAT-ir neurons in the EC was unchanged. Since ibotenic acid affects all cells and not only cholinergic ones, our results suggest that the specific degeneration of cholinergic neurons in the HDB after 192 IgG-saporin treatment could be inducing transsynaptic effects on their targets. Injections of 192 IgG-saporin directly into the EC also lesioned the cholinergic projection from the HDB, but had no effect on the intrinsic population. Eight weeks after immunolesion, the number of interneurons immunoreactive for ChAT and VIP in the EC had returned to normal values, and persisted for as long as 6 months after the lesion. By contrast, ChAT-ir neurons in the HDB were permanently lost. Our results suggest that the transient down-regulation of the cholinergic phenotype in entorhinal cortex interneurons could be a manifestation of activity-dependent plasticity, and that the loss of cholinergic innervation from the basal forebrain could be responsible for these effects through an imbalance of inputs. We hypothesize that the recovery of the phenotypic expression of entorhinal interneurons could be due to a recovery in their innervation, perhaps from sprouting axons in the same fields, belonging to surviving cholinergic neurons in the basal forebrain.

Animals↗
PubMed1983

Modification of membrane-bound proteins of the hippocampus and entorhinal cortex by change in behavior in rats.

Rats were trained in an instrumental task for 2 X 25 min during 1 day and 4 days and compared with active controls with respect to membrane-bound proteins solubilized by chloral hydrate and fractionated on polyacrylamide gels. Then 30-micrograms samples of the hippocampus and entorhinal cortex were labeled by 14C- and 3H-valine. The distribution of the stained electrophoretogram was recorded by microdensitometry. The results show that the 1-day training induced an increased synthesis of a membrane protein fraction of 50,000 mol wt already present in the brain membrane proteins of active controls. Training for 4 days resulted in an overall stimulation of the hippocampal membrane protein fractions, especially in the higher-molecular-weight range. The entorhinal cortex showed two stimulated membrane protein fractions, 50,000 and 120,000 mol wt. Together with previous studies, this study makes it probable that training to establish a new behavior induces a modulation of both soluble and membrane-bound protein patterns in the hippocampus and the entorhinal cortex with a time phase retardation for the latter.

Animals↗
PubMed2000

Sparse colocalization of somatostatin- and GABA-immunoreactivity in the entorhinal cortex of the rat.

We studied the regional and laminar distribution of neurons expressing immunoreactivity with antibodies against the neuropeptide somatostatin (SOM) in the entorhinal cortex of colchicine-treated rats. We further determined whether these neurons also express immunoreactivity with antibodies against the neurotransmitter gamma-aminobutyric acid (GABA). Frontally and horizontally cut brain sections were subjected to double immunofluorescence histochemistry and investigated in a two-laser confocal laser scanning fluorescence microscope. The exact position of each single- or double-labeled cell was obtained via the preparation of large-scale digital fluorescence images superimposed on a brightfield digital image obtained postscanning after decoverslipping and staining with cresyl violet. Three types of SOM-positive cells were found: big multipolar cells (10-15% of the SOM-positive cells), oval cells (15-20%), and small spherical cells (majority of SOM-positive cells). Most cells were seen in layer III. In addition, we found immunoreactive cells in the other layers, with the fewest cells in layers I and IV (lamina dissecans). Of the SOM-positive cells, 18% also expressed GABA immunoreactivity; of the GABA-positive cells, 8% were also immunoreactive for SOM. Double-labeled cells were mostly small spherical cells and, infrequently, multipolar. These data indicate that in the entorhinal cortex, a large proportion of the cells belonging to the SOM population do not express GABA. We speculate that there may be several subpopulations of SOM cells, of which the largest may consist of non-GABAergic, excitatory interneurons.

Animals↗
PubMed2000

Effects of retigabine (D-23129) on different patterns of epileptiform activity induced by low magnesium in rat entorhinal cortex hippocampal slices.

PURPOSE: The objective of this study was to evaluate the effect of a new antiseizure drug, retigabine (D-23129; N-(2-amino-4-[fluorobenzylamino]-phenyl) carbamic acid ethyl ester) on low-Mg2+-induced epileptiform discharges in rat in vitro. METHODS: Three types of epileptiform discharges (recurrent short discharges in the hippocampus, seizure-like events, and late recurrent discharges in the entorhinal cortex) were elicited in rat combined entorhinal cortex-hippocampal slices by perfusion with low-Mg2+-artificial cerebrospinal fluid (ACSF). The antiepileptic properties of retigabine were evaluated as effect on the frequency and amplitude of the epileptiform activities as well as time of onset of the effect in the entorhinal cortex (EC) and in hippocampal area CA1 (CA1) by using extracellular recording techniques. RESULTS: Retigabine (20 microM) reversibly suppressed the recurrent short discharges otherwise sensitive only to high doses of valproate (VPA) but insensitive to standard antiepileptic drugs (AEDs) in CA1, whereas 10 microM reduced the frequency of discharges by 34+/-18.8%, with no significant effect on the amplitude. In EC, retigabine (50 microM) reversibly suppressed the seizure-like events, whereas 20 microM blocked seizure-like events in 71.5% of the slices. The seizure-like events were also sensitive to standard AEDs. Late recurrent discharges in EC that are not blocked by standard AEDs were reversibly suppressed by retigabine (100 microM), whereas 50 microM reduced the frequency of the discharges by 94.4+/-7.7%, and 20 microM, by 74.2+/-18.0%, with no significant effect on the amplitude. CONCLUSIONS: Retigabine is an effective AED with suppressive effects on recurrent short discharges and on late recurrent discharges normally insensitive to standard AEDs.

Animals↗
PubMedDate not supplied

Behavioral correlates of denervation and reinnervation of the hippocampal formation of the rat: recovery of alternation performance following unilateral entorhinal cortex lesions.

Following unilateral lesions of the entorhinal cortex (E.C.) of the rat, cells in the dentate gyrus which have been deprived of their normal ipsilateral input are reinnervated in part by axons from the contralateral E.C. The proliferation of this crossed projection occurs largely between 8 and 12 days postlesion. The present experiments analyze changes in alternation behavior which occur during this period of afferent proliferation. Rats were trained to alternate responses (L-R) in a T-maze for food reward. Bilateral E.C. lesions resulted in a persistent deficit in alternation performance which did not recover after over 50 days of postoperative testing. Unilateral E.C. lesions, however, resulted in a transient deficit in alternation which recovered over time to preoperative levels. For example, animals permitted a 10-day recovery before the initiation of postlesion testing exhibited no more of a performance deficit than following a 10-day no-training period alone. However, animals permitted only a 3-day postoperative recovery were impaired in the alternation task until 10-12 days postlesion, despite daily training. Thus, recovery of performance following unilateral lesions was dependent on postlesion time rather than the amount of testing/retraining. Since bilateral lesions resulted in a persistent performance deficit while unilateral lesions resulted in a deficit with recovery, we hypothesize that behavioral recovery might be related to the reinnervation of the dentate gyrus by the contralateral E.C. To test this hypothesis, secondary lesions were placed in operated-recovered animals. Secondary lesions of the surviving E.C. resulted in a deficit in alternation performance similar to that following one stage bilateral lesions. In addition, secondary lesions of the dorsal psalterium (the fiber tract which carries the corssed E.C.-dentate projections) also disrupted performance in operated-recovered animals. Primary lesions of the dorsal psalterium alone had only slight and transient effects on alternation performance, however. Thus, the time course of the recovery, the results following bilateral lesions, and the results of secondary lesions are all consistent with the hypothesis that recovery of alternation performance following unilateral E.C. lesions may depend upon the reinnervation of the dentate gyrus by the contralateral E.C.

Afferent Pathways↗
PubMed1972

Cortical afferents to the entorhinal cortex of the Rhesus monkey.

Although the entorhinal cortex is a major contributor of afferents to the hippocampus and dentate gyrus, knowledge of its own afferents has been vague. Regions of both the frontal and temporal lobes were found to contribute afferents to this region of the brain. These afferents form probable multisynaptic links in pathways connecting the classical sensory areas of the cortex and the limbic system.

Animals↗
PubMed1980

[Autoradiography of transneural substance transport in the entorhino-hippocampal system after [3H] proline injection into the entorhinal cortex in rat (author's transl)].

The entorhinal afferences to Fascia dentata and Stratum lacunoso-moleculare of CA1 could be visualised by means of anterograde axoplasmic transport 5 days after L-[5-3H]-proline injection into the entorhinal cortex. Furthermore, the macromolecule-bound tracer was found in the perikarya of granule cells and mossy fibres as well as in the cell bodies of the CA1 pyramids. These findings indicate that labelled material, released from the axonal terminals of the perforant pathway, is taken up by these neurons.

Afferent Pathways↗