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At least 721 records · Page 40Linked to original sources
PubMed1987

Epileptiform activity induced by lowering extracellular [Mg2+] in combined hippocampal-entorhinal cortex slices: modulation by receptors for norepinephrine and N-methyl-D-aspartate.

Reduction of extracellular Mg2+ concentration induced spontaneous and evoked epileptiform activity in the entorhinal cortex (EC) and dentate gyrus (DG) of combined hippocampus (HC)-EC slices. Extracellular field potentials, as well as changes in extracellular Ca2+ and K+ concentrations, were measured in EC and DG with ion-selective/reference electrodes during both repetitive and single stimuli. In the EC, lowering extracellular [Mg2+] induces both spontaneous and single stimulus evoked ictal events consisting of extracellular negative potential shifts (up to 5 mV, 30 sec), decreases in [Ca2+]0 and increases in [K+]0. In the DG, spontaneous events were much shorter, but similar changes in [Ca2+]0, [K+]0 and field potentials (FPs) could be evoked by brief high-frequency stimulation. In both areas, the N-methyl-D-aspartate (NMDA) receptor antagonist 2-aminophosphonovalerate (2-APV) completely blocked spontaneous as well as stimulus evoked epileptiform events. The neurotransmitter norepinephrine (NE), which has previously been shown to modulate long-term potentiation in the DG, was found to exhibit differential modulation of epileptiform activity in the EC and DG. In the EC, NE, acting via alpha 1-receptors, completely blocked low Mg2+-induced epileptiform activity. In contrast, in the DG, NE exhibited a beta-receptor mediated prolongation of the low Mg2+-induced ictal events, and enhanced the stimulus-induced ionic and field potential changes. From these results, we conclude that lowering extracellular [Mg2+], acting in large part through the removal of the Mg2+ voltage-dependent blockade of NMDA receptors, leads to induction of epileptiform activity in both the EC and DG.(ABSTRACT TRUNCATED AT 250 WORDS)

2-Amino-5-phosphonovalerate↗
PubMed1986

Studies on retrograde and anterograde amnesia of olfactory memory after denervation of the hippocampus by entorhinal cortex lesions.

The effect of hippocampal denervation on olfactory memory in rats was tested after interrupting the lateral olfactory tract projections at the level of the entorhinal cortex. When lesioned animals were trained to learn new odors, they showed no evidence of retention 3 h after acquisition. These results confirm earlier data on rapid forgetting in rats after hippocampal deafferentation and are in parallel to the anterograde amnesia typically found in humans with hippocampal damage. On the other hand, preoperatively learned information was minimally impaired after hippocampal deafferentation even if it was acquired within less than 1 h before the lesion. This finding differs from reports on humans as well as monkeys with hippocampal damage where memories formed during a critical time span of months or even years before the lesion are found to be impaired. This may suggest that the consolidation process in humans and rodents has different time scales or that the roles of the human and the rat hippocampal structure in memory formation are somewhat different.

Amnesia↗
PubMed1987

Reinnervation of the dentate gyrus and recovery of alternation behavior following entorhinal cortex lesions.

Adult male rats were implanted with chronically indwelling recording electrodes in the dentate hilus of one hemisphere and bipolar stimulating electrodes in the contralateral entorhinal cortex (EC). Daily measurements were then made of the amplitude of responses, evoked through the crossed temporodentate (CTD) pathway, while the rats were unanesthetized and unrestrained. The implanted rats were also trained to alternate turns in a T-maze, with the use of a rewarded-alternation procedure. After reaching criterion performance in the alternation task, each rat was given a lesion of the EC ipsilateral to the recording electrode (n = 14) or a sham lesion (n = 5). Mean amplitudes of the evoked responses increased over Postlesion Days 4-11, probably due to reactive synaptogenesis in the CTD system, reaching a level that was significantly elevated above prelesion levels by Postlesion Day 6. Rats given EC lesions exhibited a transient impairment in alternation performance, with the mean alternation score significantly below prelesion levels on Postlesion Days 2-6. Although 2 EC-lesioned rats did not show a behavioral deficit, the electrophysiological increases and behavioral recovery were correlated in the remaining 12 cases (Pearson r = .73). These results are consistent with the interpretation that sprouting by the CTD system contributes to recovery of T-maze alternation performance following unilateral EC lesions.

Animals↗
PubMed1980

Immunohistochemical localization of serotonin nerve terminals in the lateral entorhinal cortex of the rat: demonstration of two separate patterns of innervation from the midbrain raphe.

The distribution of serotonin (5-hydroxytryptamine, 5HT) containing nerve terminals in the lateral entorhinal cortex (LEC) has been studied using antibodies against 5-HT in combination with fluorescence histochemistry. Thin, varicose, branching fibers were found to be distributed in a relatively even, diffuse pattern throughout all layers of the LEC. The largest amount of this type of 5HT innervation was in Layer I. This diffuse pattern of 5-HT terminals was supplemented by a dense network of 5HT terminals restricted to Layer III of a small (approximately 1 mm) strip of the LEC. The fibers in this layer were thicker and more convoluted and contained larger varicosities than fibers in any other layer. The existence of a distinct innervation by 5-HT terminals of only a small portion of the LEC demonstrates a hitherto unrecognized and important principle of heterogeneity in 5-HT innervation of cortex. It suggests that 5-5HT neurons in the raphe can selectively influence specific, narrow regions of the lateral perforant path system, which, in turn, affect the intrinsic hippocampal circuits.

Animals↗
PubMed1986

Chronic epileptogenesis induced by kindling of the entorhinal cortex: the role of the dentate gyrus.

The role of the dentate gyrus (DG) in the development and maintenance of kindling induced by periodic electrical stimulation of the entorhinal cortex (EC) was evaluated in rats. Colchicine, a selective neurotoxin for granule cells of the DG, was injected into the DG: prior to kindling and after the development of kindling. Prior destruction of the DG delayed the development of afterdischarge (AD) induced by EC stimulation, but kindling proceeded at normal rates after the first AD was induced. Destruction of the DG after kindling did not abolish the kindled seizures. Thus, the DG was not required for either the development or maintenance of kindling by EC stimulation, but an intact perforant path input from the EC to DG facilitated the emergence of epileptogenesis by kindling of the EC. The results suggest that kindling develops and is maintained in a network of multiple pathways which are related to the site of stimulation. The DG appears to be the site of a temporally specific alteration which facilitates the development of kindling by EC stimulation.

Animals↗
PubMed1991

Corticosterone differentially regulates the bilateral response of astrocyte mRNAs in the hippocampus to entorhinal cortex lesions in male rats.

This study examined the effect of adrenalectomy (ADX) and corticosterone (CORT) replacement on the levels of two astrocyte mRNAs during responses to unilateral entorhinal cortex lesions (ECL) to identify molecular mechanisms involved in glucocorticoid modulation of astrocyte activation following deafferentation. Both glial fibrillary acidic protein (GFAP) and sulfated glycoprotein-2 (SGP-2) mRNA were increased in the ipsilateral hippocampus 4 days following unilateral ECL. In unlesioned ADX rats CORT replacement decreased both messages in the hippocampus. CORT replacement suppressed the ECL-induced increase of GFAP mRNA in the contralateral, but not ipsilateral hippocampus of ADX rats. In contrast, CORT decreased SGP-2 mRNA both ipsi- and contralaterally. It is clear that several regulatory mechanisms are responsible for maintaining a physiological balance of astrocyte activity in the adult brain, and that changes in circuit integrity and the endocrine milieu can alter this balance.

Adrenalectomy↗
PubMed1994

Differences in voltage-dependent sodium currents exhibited by superficial and deep layer neurons of guinea pig entorhinal cortex.

1. Sodium currents were studied using whole-cell voltage-clamp techniques in neurons acutely isolated from superficial (II/III) and deep (V/VI) layers of guinea pig entorhinal cortex. 2. Sodium currents were larger (peak amplitude) in superficial than in deep layer cells under the same conditions: -1939 +/- 780 (SD) pA (N = 6) versus -307 +/- 257 pA (N = 6). Specific membrane conductance was calculated to be 12.3 +/- 9.6 mS/cm2 for superficial layer cells and 1.4 +/- 0.9 mS/cm2 for deep layer cells. 3. Sodium currents could be activated in superficial layer cells from potentials as depolarized as -20 mV, whereas no significant currents could be activated in deep neurons from potentials more depolarized than about -50 mV. Using a protocol consisting of a 25-ms prepulse and a 20 ms test pulse, the inactivation curves for superficial layer cells were found to be shifted toward more depolarized potentials by an average of 15 mV (V50 = -59.8 +/- 3.8 mV compared with -75.7 +/- 12.0 mV for deep cells). This produced a region of overlap with the activation curves for superficial cells. 4. Over a range of about -50 to -20 mV in superficial layer cells, the region of overlap of the activation and inactivation curves, a sodium current could be activated, which did not fully inactivate during the test pulse (average peak amplitude: -89.5 +/- 48.7 pA; crossover voltage: -39.2 +/- 2.0 mV). Voltage steps to more depolarized potentials, outside the voltage "window", permitted complete inactivation of the sodium current.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1993

Entorhinal cortex long-term potentiation evoked by theta-patterned stimulation of associative fibers in the isolated in vitro guinea pig brain.

Long-term potentiation (LTP) induced in the lateral entorhinal cortex by theta-patterned tetanic stimulation of the piriform cortex was analyzed in the isolated guinea pig brain maintained in vitro. Monosynaptic excitatory postsynaptic potentials (EPSPs) evoked by stimulation of the piriform cortex are composed of an early and late component selectively blocked by non-N-methyl-D-aspartate (non-NMDA) and NMDA receptor antagonists, respectively. LTP induction was dependent on NMDA receptor activation, being blocked by perfusing the preparation with 2-amino-5-phosphonovalerate (AP-5). LTP was expressed through synaptic enhancement of both early non-NMDA and late, possibly NMDA receptor-mediated responses.

2-Amino-5-phosphonovalerate↗
PubMed1994

Long-lasting transneuronal dendritic changes of GABAergic neurons in the monkey dentate gyrus following entorhinal cortex lesion.

This study analyses dendritic changes of GABAergic neurons in the dentate gyrus of the African green monkey Cercopithecus aethiops upon lesioning of their main afferents, i.e., fibers originating form the entorhinal cortex (EC). Monkeys received a unilateral EC lesion (ECL) under visual control. Four, 10 and 365 days after surgery, GABAergic dentate neurons were immunostained for parvalbumin (PV). In comparison to the contralateral side, immunolabeled dendrites ipsilateral to the lesion appeared to be retracted from the outer portions of the molecular layer at all survival times. Dendritic changes were further analysed using an interactive neuron-tracing system. Whereas immunoreactive cell bodies were not reduced in number, the relative extension of dendrites throughout the dentate molecular layer was reduced by 40% 10 days postlesion (dpl) and recovered only up to 80% 365 dpl when compared with the control side. This was reflected by a decrease of the mean segment length, which included proximal dendrites and was apparent even after 365 dpl. The spread of the dendritic field was initially diminished by 50% and seemed to exhibit a long-lasting reduction. The findings are in line with previous results obtained in the rat, thus, indicating that similar transneuronal changes after ECL occur in the primate dentate gyrus. This may be of importance, since the EC appears to be a very early target area of affection in human neurodegenerative disorders, such as Alzheimer's disease.

Afferent Pathways↗
PubMed1989

Subthreshold Na+-dependent theta-like rhythmicity in stellate cells of entorhinal cortex layer II.

The oscillation of membrane potential in mammalian central neurons is of interest because it relates to the role of oscillations in brain function. It has been proposed that the entorhinal cortex (EC), particularly the stellate cells of layer II (ECIIscs), plays an important part in the genesis of the theta rhythm. These neurons occupy a key position in the neocortex-hippocampus-neocortex circuit, a crucial crossroad in memory functions. Neuronal oscillations typically rely on the activation of voltage-dependent Ca2+ conductances and the Ca2+ -dependent K+ conductance that usually follows, as seen in other limbic subcortical structures generating theta rhythmicity. Here we report, however, that similar oscillations are generated in ECIIscs by a Na+ conductance. The finding of a subthreshold, voltage-gated, Na+ -dependent rhythmic membrane oscillation in mammalian neurons indicates that rhythmicity in heterogeneous neuronal networks may be supported by different sets of intrinsic ionic mechanisms in each of the neuronal elements involved.

Afferent Pathways↗
PubMed1992

Histamine H3 receptors modulate the release of [3H]-acetylcholine from slices of rat entorhinal cortex: evidence for the possible existence of H3 receptor subtypes.

1. The effect of agents which interact with the histamine H3 receptor on potassium-stimulated tritium release from slices of rat entorhinal cortex preloaded with [3H]-choline is described. We have examined the effects of the selective H3 receptor agonist, (R)-alpha-methylhistamine (RAMH), and a number of H3 receptor antagonists, including the selective compound thioperamide, on the potassium-stimulated release of tritium. 2. In the presence of mepyramine and ranitidine, RAMH (0.01-10 microM) inhibited potassium-stimulated tritium release in a concentration-dependent manner, EC50 = 0.11 microM. The maximum inhibition was approximately 50%. 3. Thioperamide displaced the RAMH concentration-response curve to the right yielding a pKB value of 8.4. There was no change in the maximum response to RAMH. 4. Other H3 receptor antagonists, including impromidine and burimamide, also caused rightwards displacement of the linear portion of the RAMH concentration-response curve. However, phenylbutanoylhistamine and betahistine, which are reported to be relatively potent H3 receptor antagonists, showed very low affinity. 5. Thioperamide (0.001-1 microM) alone enhanced the potassium-stimulated release of tritium in a concentration-dependent manner. Maximum effects were observed at 0.1-1 microM thioperamide, enhancing release by approximately 20%. 6. Results are discussed in terms of the regulatory role of H3 receptors on acetylcholine release and the possible existence of H3 receptor subtypes.

Acetylcholine↗
PubMed1992

Synthesis and transport of GAP-43 in entorhinal cortex neurons and perforant pathway during lesion-induced sprouting and reactive synaptogenesis.

Metabolic labeling and quantitative 2D gel autoradiography were used to assess changes in the synthesis and transport of GAP-43 in entorhinal cortex (EC) neurons and perforant pathway during lesion-induced sprouting and reactive synaptogenesis. In normal adult rats, there is a high constitutive level of GAP-43 synthesis and transport in EC neurons projecting to the hippocampus. Following unilateral EC lesions, there is a 2-fold (100%) increase in the transport of newly synthesized GAP-43 to the contralateral or 'sprouting' hippocampus. The timing of this upregulation (between 6 and 15 days) suggests that changes in GAP-43 expression occur in response to the growth of presynaptic terminals during sprouting.

Animals↗
PubMedDate not supplied

Long lasting changes in the spontaneous activity of hippocampal neurons following stimulation of the entorhinal cortex.

The spontaneous activity of hippocampal and denate units was investigated in acute and chronic experiments on adult rats. Spontaneous unitary discharges from both regions were measured before and after brief tetanic stimulation of the entorhinal cortex. An increase in the frequency of spontaneous unit activity was obtained in units recorded from the dentate gyrus and CA3 field of the hippocampus for up to 20 min following stimulation. In chronic recordings of physiologically identified dentate units from freely moving rats similar results were obtained. The findings are discussed with reference to long lasting potentiation of synaptic activity in the perforant path-dentate granule cell connection.

Action Potentials↗
PubMed1983

Ganglioside treatment improves recovery of alternation behavior after unilateral entorhinal cortex lesion.

Exogenous gangliosides have been reported to enhance neurite formation in vitro and in vivo after damage to peripheral nerves. We report here the effects of ganglioside treatment on the course of recovery of alternation behavior that follows a unilateral lesion of the rat entorhinal cortex. The recovery of this function is known to parallel rapid synaptic reinnervation (collateral sprouting) into the partially denervated dentate gyrus of the hippocampus which previously received afferent input from the entorhinal region. Rats trained on an alternation behavior were subjected to a unilateral entorhinal lesion and subsequently given daily injections of total ganglioside (50 mg/kg, i.m.). Testing of the behavior continued for 2 weeks to assess the extent of behavioral impairment and the rate of recovery. Rats treated with gangliosides showed reduced behavioral impairment, accelerated recovery of the learned behavior, and final performance levels greater than controls. We hypothesize that the gangliosides may be interacting with regenerating neuronal membranes, either acting as receptors for trophic growth factors or altering membrane structure itself.

Animals↗
PubMed1994

Changes in nerve growth factor immunoreactivity following entorhinal cortex lesions: possible molecular mechanism regulating cholinergic sprouting.

To assess the possible role of trophic factors in lesion-induced plasticity, we have used a sensitive immunohistochemical technique to evaluate changes in nerve growth factor (NGF) staining in the hippocampal formation 3, 8, 16, and 30 days following entorhinal cortex lesions. Our results indicate that a band of NGF immunoreactivity appears in the outer molecular layer of the ipsilateral dentate gyrus following entorhinal ablation. The distribution of the NGF-immunoreactive band exactly coincides with the distribution of sprouting cholinergic terminals revealed by acetylcholinesterase histochemistry or NGF-receptor immunostaining. Increased NGF-immunoreactivity is detectable at 3 days postlesion, is most intense at 8 days, and decreases to near control levels by 30 days. Lesion-induced increases in NGF immunostaining also occur in animals in which septohippocampal fibers had been removed by prior destruction of the fimbria-fornix. Increases in NGF-immunoreactivity, however, are substantially reduced in animals receiving intraventricular injections of colchicine, which presumably blocks NGF release. These results indicate that 1) increases in NGF immunostaining, which occur following entorhinal lesions, precede any changes in cholinergic sprouting parameters and are greatest during the period of maximal cholinergic sprouting; 2) increased NGF-immunoreactivity is not due to NGF binding by septohippocampal fibers; and 3) increased NGF-immunoreactivity appears to depend on the release of NGF by neurons that produce it. We hypothesize that, following entorhinal lesions, NGF immunostaining within the hippocampal formation may represent NGF "anchored" within the tissue and that NGF accumulation by such a mechanism may direct the sprouting response of NGF-sensitive cholinergic neurons.

Acetylcholinesterase↗
PubMed1982

The sprouting of septal afferents to the dentate gyrus after lesions of the entorhinal cortex in adult rats.

The projection of the septum to the dentate gyrus has been demonstrated autoradiographically and the pattern of acetylcholinesterase (AChE) staining in the dentate gyrus has been mapped histochemically, in a series of normal young adult rats and in a group of animals in which the entorhinal cortex had been ablated or its efferents to the dentate gyrus interrupted, some weeks earlier. It is clear from this material that the normal disposition of the septal projection to the dentate gyrus differs significantly from the pattern of AChE staining; however, in the denervated region of the molecular layer in the experimental animals there is a marked increase in the density of the septal projection which precisely coincides with the zone of intensification of AChE staining. It follows from this that although the distribution AChE does not accurately reflect the organization of the septo-dentate projection in normal animals, the intensification of AChE staining provides a good indication of the reorganization which occurs in this pathway following entorhinal deafferentation.

Acetylcholinesterase↗
PubMed1996

Reverberation of chloride-dependent synaptic potentials in the rat entorhinal cortex in vitro.

The spontaneous activity generated by rat entorhinal neurons during application of 4-aminopyridine (4AP; 50 microM) was studied with intracellular and extracellular field-potential recordings in an vitro slice preparation. Long-lasting depolarizations (LLDs) with amplitudes of 15 +/- 7.6 mV (mean +/- SD; n = 14) and durations of 1.65 +/- 0.77 s (n = 14) occurred at 0.036 +/- 0.01/s (n = 14). Each LLD was followed by a rhythmic sequence of depolarizing potentials (up to 22 events) with amplitudes of 4-30 mV, durations of 40-500 ms and frequency of 0.9 +/- 0.2/s (n = 14). These intracellular potentials were mirrored by negative-going field potentials, suggesting that they represented synchronous events. Membrane input resistance decreased by 79-86% during both LLDs and subsequent rhythmic depolarizations. Intracellular injection of steady depolarizing or hyperpolarizing current modified the amplitude of these potentials in a similar manner: the reversal potential of the LLDs and of the rhythmic depolarizations was -66.4 +/- 4 mV and -67.9 +/- 3.2 mV, respectively (n = 7). Intracellular injection of Cl- increased the amplitude of both types of potentials. Spontaneous LLDs continued to occur during application of the non-N-methyl-D-aspartate (NMDA) receptor antagonist 6-cyano-7-nitro-quinoxaline-2,3-dione (10 microM), a procedure that abolished the subsequent rhythmic depolarizations (n = 3). LLDs were blocked by further addition of the gamma-aminobutyric acid (GABA)A receptor antagonist bicuculline methiodide (10 microM, n = 3). Our findings demonstrate that during 4AP application entorhinal neurons generate glutamatergic-independent LLDs as well as synchronous, Cl(-)-dependent depolarizations that reverberate through non-NMDA-mediated excitatory circuits.

4-Aminopyridine↗