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PubMed2000

Dopamine innervation of monkey entorhinal cortex: postsynaptic targets of tyrosine hydroxylase-immunoreactive terminals.

Dopamine (DA) has been demonstrated to play an important role in regulating cortical activity in both neocortical and periallocortical regions. However, marked differences between these two types of cortices in the laminar pattern of DA axons, the types and distribution of DA receptors, and the postnatal development of the DA innervation suggest that DA may have region-specific effects. Such regional specialization may also include the types of cortical cells apposed to DA terminals. In neocortical regions, such as the prefrontal and motor cortices, the majority of structures apposed to DA terminals appear to be the dendritic spines and shafts of pyramidal cells, and a minority are dendrites immunoreactive for gamma-amino butyric acid (GABA). However, the identity of the neural elements apposed to DA terminals in the entorhinal cortex, a periallocortical region, is unknown. In this study, we used immunocytochemical techniques and antibodies against tyrosine hydroxylase (TH) and GABA, visualized with preembedding immunoperoxidase and immunogold-silver labels, respectively, to examine DA terminals and their targets with electron microscopy. In the superficial layers of the monkey entorhinal cortex, TH-immunoreactive (IR) terminals varied greatly in size and formed thin, symmetric synapses. The majority of dendritic structures apposed to these TH-terminals were not GABA-IR, and included both dendritic shafts (64%) and spines (14%). A minority (22%) of the apposed dendrites were GABA-IR. A similar distribution of targets was observed for the subset of TH-IR terminals with identifiable synaptic specializations. In addition, the proportions of GABA-labeled and unlabeled dendrites apposed to TH terminals did not differ from those previously reported for monkey prefrontal cortex. These findings indicate that DA terminals provide direct input to both excitatory and inhibitory cells in the monkey entorhinal cortex and suggest that the effects of DA are mediated through a set of targets that are common to both neo- and periallocortex.

Animals↗

PubMed1994

Neurochemical development of the hippocampal region in the fetal rhesus monkey. II. Immunocytochemistry of peptides, calcium-binding proteins, DARPP-32, and monoamine innervation in the entorhinal cortex by the end of gestation.

Material for the study came from one 126 day-old rhesus monkey fetus and two 3 day-old neonates. The immunocytochemical detection of somatostatin, neurotensin (NT), parvalbumin, calbindin D-28K, DARPP-32 as well as tyrosine hydroxylase (TH), dopamine-beta-hydroxylase and serotonin (5-HT), was carried out on serial cryostat sections of the entorhinal cortex. The authors reported in a previous paper the precocious differentiation of the entorhinal cortex in rhesus monkey fetuses and featured the conspicuous expression of calbindin D-28K, somatostatin, neurotensin, and the monoaminergic innervation during the first half of gestation. The present study shows distinct temporal profiles of neurochemical development during the second half of gestation: the dense neuropeptidergic innervation remained a constant feature; the three aminergic systems gradually increased in density; parvalbumin, unlike calbindin D-28K, was primarily expressed during the last quarter of gestation. Three other prominent features of the last quarter of gestation are illustrated: the refinement of the modular neurochemical organization of the lamina principalis externa, the delayed chemoanatomical development of the rhinal sulcus area, and the establishment of a distinct rostrocaudal pattern of neurochemical distribution. In correspondence with the cluster-like organization of the lamina principalis externa, the authors observed in the olfactory, rostral, and intermediate fields of the neonate monkey entorhinal cortex, a particular subset of pyramidal-shaped neurons: located in layer III, they were characterized by fasciculated apical dendrites ascending between the cellular islands of the discontinuous layer II and the coexpression of calbindin D-28K and DARPP-32. Besides, most of the other chemical systems displayed a distinct, area-specific, patchy distribution, except for the homogeneously distributed noradrenergic innervation. In the olfactory and rostral fields, TH positive dopaminergic fibers accumulated on the neuronal islands of layers II-III, and parvalbumin labeled fibers on those of layer III, whereas patches of 5-HT and NT-like reactive terminals were segregated between the cellular islands, overlapping the DARPP-32/calbindin D-28 K labeled dendritic bundles. At the opposite, in the intermediate field, 5-HT positive terminals overlapped the cellular islands of layer II and thin fascicles of dopaminergic fibers ran in the inter island spaces. The somatostatin-LIR innervation was apparently too dense to reveal a patchy distribution that existed at earlier developmental stages. In the caudal field, the patchy pattern was replaced by a predominant bilaminar type of distribution of NT, 5-HT, and TH-like positive afferents.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗

PubMed2003

The perirhinal-entorhinal cortex, but not the hippocampus, is critical for expression of individual recognition in the context of the Coolidge effect.

The Coolidge effect is a phenomenon in which males show renewed sexual interest in a novel female following copulation to satiety with another female. In golden hamsters, this phenomenon depends on the ability to recognize conspecifics using chemosensory cues processed through the main olfactory system. Here we tested whether olfactory targets in the hippocampal system support this natural form of recognition memory. Male hamsters received ibotenic acid lesions of the perirhinal-entorhinal cortex (PR-ENT) or hippocampus (H) and were allowed to copulate to satiety with a female conspecific, then were presented with two anesthetized females, the familiar mate and an unfamiliar female that copulated with another male. Sham-operated and H-lesioned subjects preferentially investigated the novel female, indicating intact recognition of individual identity. By contrast, PR-ENT-lesioned males failed to discriminate familiar and novel females, and this deficit could not be attributed to abnormal copulatory behavior during mating. All subjects were able to detect and discriminate between female odors when presented in isolation during a habituation-discrimination test, indicating that behavioral deficits shown by PR-ENT males were not due to anosmia or a general investigatory deficit. Thus, the perirhinal-entorhinal cortex, but not the hippocampus, is critical for the recognition of familiar conspecifics in this naturalistic situation. This study reveals an essential role for the perirhinal-entorhinal cortex, but not the hippocampus, in a natural form of recognition memory within the social behavior of hamsters. The findings show a strikingly similar pattern to the effects of selective damage to the same brain regions on performance in standard recognition memory tasks by rats and monkeys. Therefore, the present data extend our understanding of the differential role of structures of the hippocampal memory system, showing continuity across species and between formal laboratory tests and the function of memory in natural social behavior.

Animals↗

PubMed1997

The volume of the entorhinal cortex in schizophrenia: a controlled MRI study.

1. The entorhinal cortex (EC), part of the limbic temporal lobe, is a critical link between the cerebral cortex and the hippocampus, and is considered one of the most important cortical "association" areas. Several postmortem abnormalities in the EC have been reported. 2. Here, the authors report the first in vivo study of the volume of the EC in schizophrenia using magnetic resonance imaging (MRI) scans. 3. The authors compared 57 schizophrenic patients and 35 healthy controls. No overall difference in the mean EC volume was found between controls and schizophrenic patients, but there was a strong trend (p = .078) for the schizophrenic females to have a large mean EC than control females and for the early onset schizophrenia group to have a smaller (EC (p = .07) than late onset schizophrenia subjects. 4. The implications of the findings are discussed.

Adolescent↗

PubMed2005

Effects of early-life stress on behavior and neurosteroid levels in the rat hypothalamus and entorhinal cortex.

Recent evidence support the hypothesis that exposure to stress or trauma during early childhood may disturb the formation of functional brain pathways, in particular, of the limbic circuits. We examined the effects of exposure to early life trauma (juvenile stress) on emotional and cognitive aspects of behavior in adulthood as well as on dehydroepiandrosterone (DHEA) and its sulfate ester (DHEAS) levels in relevant brain regions. Quantitative assessment of the effects of exposure to juvenile stress was made 1 month post-stress, and obtained by measuring: emotional (utilizing an open field and a startle response tests) and cognitive (Morris water-maze task) functions, as well as neurosteroids concentration (DHEA and its sulfate ester, DHEAS) in the hypothalamus and entorhinal cortex. We report here that an exposure to juvenile stress led to elevated levels of anxiety 1 month post-stress. Moreover, in a spatial learning task, the juvenile stress group performed poorer than the control group. Finally, an exposure to juvenile stress increased DHEAS but not DHEA concentrations both in the hypothalamus and the entorhinal cortex. These findings indicate that an exposure to juvenile stress has long-lasting effects on behavior and DHEAS levels in the hypothalamus and the entorhinal cortex. These effects may be of relevance to our understanding of early life stress-related disorders such as PTSD and major depression.

Affective Symptoms↗

PubMedDate not supplied

[Effect of xymedone on high-voltage-activated Ca2+ currents in pyramidal neurons of the entorhinal cortex].

The effect of xymedon on Ca2+ currents in entorhinal cortex LIII pyramidal neurons was studied using brain slices from 10-17-day old rats, which were analyzed by means of the infrared video assisted whole cell patch clamp recording. The sample slices were superfused with artificial cerebrospinal fluid containing tetrodotoxin, 4-aminopyridine, and tetraethylammonium for the blocking of Na+ and K+ channels, respectively. Xymedone was added to artificial cerebrospinal fluid and to all extracellular solutions. The slices were exposed to different concentrations of xymedone for 3 hours followed by patch-clamp recordings. Control recordings were run with the vehicle. Xymedone in a concentration of 0.01 mM decreased the maximum voltage-dependent Ca2+ current amplitude by 39.8 %, while 1 mM of xymedone inhibited the Ca2+ currents almost completely. The obtained data showed for the first time that xymedone exhibits a calcium channel blocker activity in neurons. Possible neuroprotective mechanisms of xymedone are discussed.

Animals↗

PubMed1985

Physiological evidence for an excitatory pathway from entorhinal cortex to amygdala in the rat.

We studied the responses of amygdala neurons to entorhinal cortex stimulation in anaesthetized rats. Intracellular and extracellular data were obtained in a total of 16 cells located throughout the amygdaloid complex and two cells in adjacent piriform cortex. In addition, antidromic responses to amygdala stimulation were obtained in 7 cells of the entorhinal or perirhinal cortex. All recordings in the amygdala showed orthodromic excitatory responses (spikes or EPSPs), with a mean latency of 8 ms. These were succeeded by IPSPs with a mean latency of 15 ms. Two cells in piriform cortex responded to entorhinal stimulation with inhibition alone. A cell in the region of the basomedial nucleus showed characteristics of an inhibitory interneuron. Cells in entorhinal and perirhinal cortex responding antidromically to amygdala stimulation were found primarily in layers III-V. Axons of one such cell, which was injected with HRP, were seen to course rostrally to the region of the amygdala within the fiber tract of the external capsule. Three entorhinal cells (layer III) responded antidromically to both amygdala and hippocampal formation stimulation. A neuronal circuit diagram accounting for our findings is presented.

Amygdala↗

PubMed2004

Effects of neonatal excitotoxic lesions of the entorhinal cortex on cognitive functions in the adult rat.

The entorhinal cortex (EC) is involved in a variety of cognitive functions by virtue of its neuronal input from the neocortex and projection to the hippocampal formation and the limbic-striatal system. Neonatal lesions are increasingly considered useful models for disconnection syndromes such as schizophrenia. Therefore, we investigated the effects of neonatal EC lesions on adult rat behavior. Neonatal (postnatal day 7) lesions were inflicted by bilateral injections of ibotenate into the EC. Sham-lesioned (vehicle injection) and naive (unoperated) rats served as controls. Locomotor activity was measured in prepubertal and young adult rats. Adult rats were then tested for spatial learning in an eight-arm radial maze (reinforced delayed alternation) and for motivation (progressive ratio schedule of operant behavior). Finally, prepulse inhibition (PPI) of the acoustic startle reflex and locomotor activity were investigated with and without apomorphine (APO) challenge. Brain tissue damage was assessed using Nissl-staining. The total volume of the adult rat EC was reduced after neonatal ibotenate-injection. Neonatal EC-lesions increased perseveration only in a delayed task in the radial maze and induced a leftward-shift of breakpoints in operant responding. Lesions did not alter baseline locomotor activity, but enhanced the locomotor stimulating effect of APO. PPI was not affected by neonatal lesions of the EC with and without APO challenge. Neonatal lesions of the EC impaired the ability to hold information during delays and reduced motivation during operant behavior which reflects a state of anhedonia. Thus, they may serve as an animal model for certain aspects of schizophrenia.

Aging↗

PubMed1997

Further evidence of abnormal cytoarchitecture of the entorhinal cortex in schizophrenia using spatial point pattern analyses.

Previous studies have reported cytoarchitectural abnormalities in superficial laminae of rostral portions of the entorhinal cortex in schizophrenia, including decreased densities of neurons, poorly formed layer II neuron islands, and apparent displacement of layer II-type neurons deep into layer III; however, findings have been controversial, given the qualitative nature of the descriptions and the normal heterogeneity of cytoarchitecture of the region. The x, y coordinates of Nissl-stained neurons were mapped in layers II, III, and V of entorhinal subdivision ER in 8 prospectively accrued patients with schizophrenia and 8 nonneuropsychiatric controls. Indices of neuron dispersion, nearest neighbor distances, and effective radius were determined. An abnormally clustered dispersion of neurons in layer III was present in schizophrenics compared to controls along with a reduced neuron effective radius, whereas the mean nearest-neighbor distance was normal. In layer II, there was a significantly increased effective radius, whereas other indices were normal. No between-group differences were noted in layer V for any variable. These data provide further evidence for subtle aberrant cytoarchitecture in superficial laminae of the entorhinal cortex in schizophrenia and are consistent with neurodevelopmental models of abnormal neuronal pruning, "miswiring," and/or migration in the illness.

Aged↗

PubMed1994

Differential expression of metabotropic glutamate receptors in the hippocampus and entorhinal cortex of the rat.

Metabotropic glutamate receptors (mGluRs) have been implicated in a number of hippocampal functions including learning and memory. Five subtypes have been molecularly and pharmacologically characterized. Using in situ hybridization with oligonucleotide probes selective for these five mGluRs, we have found that each has a unique pattern of expression in the hippocampus and entorhinal cortex. mGluR1 is expressed predominantly in the dentate gyrus and CA3. mGluR2 is enriched in the dentate gyrus and inner layer of the entorhinal cortex. mGluR3 is also expressed in these two structures, but unlike all the other mGluRs, is found in white matter areas as well. mGluR4 is present predominantly in CA2 while mGluR5 is concentrated in most regions of the hippocampus and entorhinal cortex. Comparative analysis of the distributions of these receptors with that of the components of their putative downstream signal transduction mechanisms suggests that mGluR5 may be the main subtype of mGluR which mediates the excitatory actions of glutamate in CA1 and could contribute to the elevation of calcium levels found in CA1 pyramidal neurons in long term potentiation and in ischemic/hypoxic injury. mGluR2 and mGluR3, the main subtypes contributing to the inhibitory actions of glutamate, are absent in CA1. Thus, the mGluR-mediated excitatory actions of glutamate can occur in all regions of the hippocampus whereas the mGluR-mediated inhibitory actions of glutamate may be restricted to the dentate gyrus and CA3.

Animals↗

PubMed1982

Topography between the entorhinal cortex and the dentate septotemporal axis in rats: I. Medial and intermediate entorhinal projecting cells.

Retrograde tracing experiments were performed to clarify the topographic projection from medial (area 28m) and intermediate (area 28i) divisions of the entorhinal cortex to the dentate gyrus. Pipets filled with horseradish peroxidase (HRP) were positioned by electrophysiologic guidance at one of several septotemporal (S-T) levels in the dentate molecular layer of anesthetized rats; the tracer was expelled iontrophoretically to minimize its spread. Retrograde labeling of neurons within areas 28m and 28i was analyzed in relation to cytoarchitectonic as well as spatial features of the region (obtained by histologic reconstruction). Regardless of the S-T level, ejections of HRP which were confined to the dentate gyrus labeled only layer II neurons of each area. Following septal pole ejections, labeled neurons were located in the posterolateral, extreme posterior, and posteromedial parts of both areas 28m and 28i. Mid S-T ejections produced not only a ventral, but also an anteromedial, shift in the location of entorhinal projection cells; no cells were labeled posterolaterally. After temporal dentate ejections labeled neurons occupied the most anteromedial part of these entorhinal areas. For both areas, but especially for area 28i, convergence of entorhinal efferents upon a single S-T level in the dentate gyrus occurred from neurons which lay in a dorsoventral (i.e., frontal), and to a lesser extent a rostrocaudal, plane. The efferent axes of both areas 28m and 28i thus appear to be curved and are therefore best described in three dimensions. The entorhinal axes begin in a posterodorsolateral location, wrap around the posterior cortical convexity, and end in an anteroventromedial position. The results provide a useful map for in situ exploration of entorhinodentate connections in the rat, emphasize the parallel innervation of the dentate gyrus by distinct entorhinal fiber systems, and reflect the importance of the S-T axis as a framework for interpreting hippocampal organization.

Animals↗

PubMed2002

Muscarinic activation of a cation current and associated current noise in entorhinal-cortex layer-II neurons.

The effects of muscarinic stimulation on the membrane potential and current of in situ rat entorhinal-cortex layer-II principal neurons were analyzed using the whole cell, patch-clamp technique. In current-clamp experiments, application of carbachol (CCh) induced a slowly developing, prolonged depolarization initially accompanied by a slight decrease or no significant change in input resistance. By contrast, in a later phase of the depolarization input resistance appeared consistently increased. To elucidate the ionic bases of these effects, voltage-clamp experiments were then carried out. In recordings performed in nearly physiological ionic conditions at the holding potential of -60 mV, CCh application promoted the slow development of an inward current deflection consistently associated with a prominent increase in current noise. Similarly to voltage responses to CCh, this inward-current induction was abolished by the muscarinic antagonist, atropine. Current-voltage relationships derived by applying ramp voltage protocols during the different phases of the CCh-induced inward-current deflection revealed the early induction of an inward current that manifested a linear current/voltage relationship in the subthreshold range and the longer-lasting block of an outward K(+) current. The latter current could be blocked by 1 mM extracellular Ba(2+), which allowed us to study the CCh-induced inward current (I(CCh)) in isolation. The extrapolated reversal potential of the isolated I(CCh) was approximately 0 mV and was not modified by complete substitution of intrapipette K(+) with Cs(+). Moreover, the extrapolated I(CCh) reversal shifted to approximately -20 mV on removal of 50% extracellular Na(+). These results are consistent with I(CCh) being a nonspecific cation current. Finally, noise analysis of I(CCh) returned an estimated conductance of the underlying channels of approximately 13.5 pS. We conclude that the depolarizing effect of muscarinic stimuli on entorhinal-cortex layer-II principal neurons depends on both the block of a K(+) conductance and the activation of a "noisy" nonspecific cation current. We suggest that the membrane current fluctuations brought about by I(CCh) channel noise may facilitate the "theta" oscillatory dynamics of these neurons and enhance firing reliability and synchronization.

Animals↗

PubMed1992

Antibody to NGF inhibits collateral sprouting of septohippocampal fibers following entorhinal cortex lesion in adult rats.

We have used an antiserum raised against mouse 2.5S NGF to examine the involvement of endogenous neurotrophins in the collateral sprouting of septohippocampal fibers in the adult rat brain. The antiserum was administered intraventricularly. Immunocytochemical techniques indicated that the injected antibodies penetrated into brain tissue that included the basal forebrain, cortex, striatum, corpus callosum, and hippocampus. Unilateral lesioning of the entorhinal cortex was done to evoke the sprouting of the cholinergic septohippocampal fibers. At 8 days postlesion, the sprouting was much advanced, as evidenced by an increase in density of the acetylcholinesterase (AChE) staining in the outer molecular layer (OML) of the dentate gyrus and by the associated increase in the absolute number of AChE-positive fibers in the OML. As well, there was a widening of the inner molecular layer (IML), interpreted as being due to sprouting of noncholinergic axons in that region. In rats injected daily with anti-NGF or anti-NGF Fab fragments, no increase in AChE density, or in the population of AChE-positive fibers, was observed in the OML. In contrast, the widening of the IML seemed to be unaffected by the anti-NGF treatment. No changes were observed in the AChE related parameters in the dentate gyrus of nonlesioned animals treated similarly for 8 days with anti-NGF; there was, however, a decrease of choline acetyltransferase (ChAT) immunostaining in the ChAT-positive cells of the basal forebrain. Our findings and the confirmation that our polyclonal anti-NGF also recognizes other members of the NGF neurotrophin family, specifically brain-derived neurotrophic factor and neurotrophin-3, indicate that at least one of these neurotrophins plays a key role in the collateral sprouting of the cholinergic septohippocampal fibers (but not that presumed to occur within the IML) following an entorhinal cortex lesion.

Acetylcholinesterase↗

PubMed1995

Classification of theta-related cells in the entorhinal cortex: cell discharges are controlled by the ascending brainstem synchronizing pathway in parallel with hippocampal theta-related cells.

Single-unit discharge patterns of entorhinal cortex (EC) cells were characterized in relation to simultaneously recorded hippocampal (HPC) field activity according to criteria used previously to classify cells in the hippocampal formation, medial septum, cingulate cortex, and caudal diencephalon. EC cells related to HPC theta field activity were classified as 1) phasic theta-on, if they discharged rhythmically, and in phase, with ongoing HPC theta, but nonrhythmically during large, irregular hippocampal field activity (LIA); 2) tonic theta-on, if they discharged nonrhythmically and increased their discharge rates during HPC theta relative to LIA; 3) phasic theta-off, if they discharged rhythmically, and in phase, with ongoing HPC theta, but increased their discharge rates during LIA; and 4) tonic theta-off, if they discharged nonrhythmically and decreased their discharge rates during HPC theta relative to LIA. Cells not meeting any of these criteria were classified as nonrelated. A total of 168 EC cells were recorded, and of these 56 (33%) were classified as theta related, with the remaining 112 (67%) classified as nonrelated. Of the 56 theta-related cells, 41 (73%) had significantly higher discharge rates during HPC theta than during LIA and were classified as theta-on cells (15 phasic theta-on cells and 26 tonic theta-on cells). Nine of the 26 tonic theta-on cells showed a phase relation of their arrhythmic discharges to simultaneously recorded HPC theta field activity. EC phasic theta-on cells did not discharge preferentially on any portion of the HPC theta field recorded from the region of the stratum moleculare of the dentate gyrus. In general, cells classified as phasic revealed a wide distribution of phase preferences. The remaining 15 (26.7%) cells were classified as theta-off cells and discharged at higher rates during HPC LIA than during HPC theta field activity (3 phasic theta-off cells and 12 tonic theta-off cells). Systemic administration of physostigmine significantly increased the discharge rate of tonic and phasic theta-on cells relative to LIA. Electrical stimulation in the posterior hypothalamic region (PH) significantly increased the discharge rate of EC theta-on cells and significantly decreased the discharge rate of EC theta-off cells relative to HPC LIA. The discharge rates of nonrelated EC cells were not influenced by electrical stimulation of the PH. Procaine microinfusion into the medical septum (MS) abolished spontaneously occurring HPC theta and theta induced with PH stimulation. In addition, 5 min after MS procaine, the ability of PH stimulation to modulate EC theta-on cell discharge was abolished. The modulation of cellular discharges produced by PH stimulation recovered by 60 min post-procaine infusion into the MS. The findings support two main conclusions: 1) theta-related cells in the EC are comprised of two main populations of cells, theta-on and theta-off, similar to other regions of limbic cortex and nuclei of the ascending brainstem synchronizing pathway; 2) the ascending brainstem synchronizing pathway exerts both similar and parallel effects on theta-related cells in entorhinal cortex and hippocampus.

Anesthetics, Local↗

PubMed1993

Entorhinal cortex lesions transiently alter glucocorticoid but not mineralocorticoid receptor gene expression in the rat hippocampus.

Entorhinal cortex lesions destroy an important hippocampal input and lead to axonal sprouting in the dentate gyrus. Glucocorticoids are known to inhibit this reinnervation process. In the present study, we examined changes in hippocampal glucocorticoid receptor (GR) and mineralocorticoid receptor (MR) mRNA expression using in situ hybridization following unilateral entorhinal cortex lesioning (ECL) in the rat. As early as 1 day postlesioning, a 33% bilateral decrease in GR mRNA expression was observed in the dentate gyrus. By contrast, a 36% bilateral increase in GR mRNA expression was detected in the CA1 cell field. GR mRNA levels in both regions returned to those of control animals 2 days postlesioning, indicating that these effects were transient. Adjacent sections hybridized with probes to MR mRNA revealed no changes in hippocampal MR gene expression as a result of ECL. The selective decrease in GR mRNA expression observed in the dentate gyrus following ECL is specific to the hippocampal subregion targeted for reactive synaptogenesis and thus may serve to attenuate the inhibitory actions of circulating glucocorticoids.

Animals↗

PubMed1996

Branched connections to the septum and to the entorhinal cortex from the hippocampus, amygdala, and diencephalon in the rat.

Neuronal cell populations giving origin to bifurcating projections to the septum and the entorhinal cortex were studied in the rat by means of double retrograde labeling using the fluorescent tracers Fast Blue and Diamidino Yellow. Double labeled pyramidal neurons were consistently detected in the temporal level of the CA1 area and subiculum of the hippocampal formation, where they represented at least 50% of the cells retrogradely labeled from the entorhinal injections. Double labeled neurons were also detected in the amygdala, where they prevailed in the basal complex. Scattered double labeled neurons were observed in a number of hypothalamic nuclei, with a slight predominance in the preoptic region. Finally, a few double labeled cells were detected in the midline thalamus, and especially in the thalamic paraventricular nucleus. In all these structures, double labeled neurons were located ispilaterally to the injection sites. The present data indicate that the septum and entorhinal cortex are tightly interconnected by axonal bifurcations deriving from a variety of telencephalic and diencephalic sources.

Amygdala↗

PubMed1997

Ionic mechanisms of muscarinic depolarization in entorhinal cortex layer II neurons.

The mechanisms underlying direct muscarinic depolarizing responses in the stellate cells (SCs) and non-SCs of medial entorhinal cortex layer II were investigated in tissue slices by intracellular recording and pressure-pulse applications of carbachol (CCh). Subthreshold CCh depolarizations were largely potentiated in amplitude and duration when paired with a short DC depolarization that triggered cell firing. During Na+ conductance block, CCh depolarizations were also potentiated by a brief DC depolarization that allowed Ca2+ influx and the potentiation was more robust in non-SCs than in SCs. Also, in non-SCs, CCh depolarizations could be accompanied by spikelike voltage oscillations at a slow frequency. In both SCs and non-SCs, the voltage-current (V-I) relations were similarly affected by CCh, which caused a shift to the left of the steady-state V-I relations over the entire voltage range and an increase in apparent slope input resistance at potentials positive to about -70 mV. CCh responses potentiated by Ca2+ influx demonstrated a selective increase in slope input resistance at potentials positive to about -75 mV in relation to the nonpotentiated responses. K+ conductance block with intracellular injection of Cs+ (3 M) and extracellular Ba2+ (1 mM) neither abolished CCh depolarizations nor resulted in any qualitatively distinct effect of CCh on the V-I relations. CCh depolarizations were also undiminished by block of the time-dependent inward rectifier Ih, with extracellular Cs . However, CCh depolarizations were abolished during Ca2+ conductance block with low-Ca2+ (0.5 mM) solutions containing Cd2+, Co2+, or Mn2+, as well as by intracellular Ca2+ chelation with bis-(o-aminophenoxy)-N,N,N',N'-tetraacetic acid. Inhibition of the Na+-K+ ATPase with strophanthidin resulted in larger CCh depolarizations. On the other hand, when NaCl was replaced by N-methyl-D-glucamine, CCh depolarizations were largely diminished. CCh responses were blocked by 0.8 microM pirenzepine, whereas hexahydro-sila-difenidolhydrochloride,p-fluoroanalog (p-F-HHSiD) and himbacine were only effective antagonists at 5- to 10-fold larger concentrations. Our data are consistent with CCh depolarizations being mediated in both SCs and non-SCs by m1 receptor activation of a Ca2+-dependent cationic conductance largely permeable to Na+. Activation of this conductance is potentiated in a voltage-dependent manner by activity triggering Ca2+ influx. This property implements a Hebbian-like mechanism whereby muscarinic receptor activation may only be translated into substantial membrane depolarization if coupled to postsynaptic cell activity. Such a mechanism could be highly significant in light of the role of the entorhinal cortex in learning and memory as well as in pathologies such as temporal lobe epilepsy.

Animals↗

PubMed1983

Functional anatomy of limbic seizures: focal discharges from medial entorhinal cortex in rat.

Focal seizure discharges were induced in the ventral aspect of the medial entorhinal cortex of awake, freely moving rats, either with cannula injections of penicillin or picrotoxin (0.02 microliters every 10-15 min) or by repetitive tetanic electrical stimulation. [14C]Deoxyglucose autoradiography (DG) was performed when animals were in a 'steady-state' with respect to electrographic discharges and/or behavioral changes. During simple interictal spikes behavior remained normal and DG labeling was increased only in the entorhinal focus and stratum moleculare of the ventral dentate gyrus. With complex spikes and short seizures animals exhibited staring, decreased responsiveness, and occasional wet dog shakes. DG labeling was increased in all layers of the dentate gyrus, Ammon's horn (ipsilateral greater than contralateral) and, to a lesser degree, in ipsilateral amygdala, and the accumbens-ventral pallidum area. During strong seizures, rearing and forelimb clonus occurred and metabolism was strongly activated bilaterally in the hippocampal formation, amygdala, accumbens, substantia nigra, and the anterior and periventricular thalamic nuclei. These studies indicate that the dentate gyrus initially restricts the entry of seizures from entorhinal cortex into the rest of hippocampus. As this is overcome there is rapid bilateral spread through the hippocampal formation with passive interruption of normal behavior. With prolonged seizure discharges there is further capture of amygdala and subcortical extrapyramidal and thalamic nuclei associated with behavioral convulsions.

Animals↗