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At least 217 records · Page 12Linked to original sources
PubMed2000

Action of 4-aminopyridine on extracellular amino acids in hippocampus and entorhinal cortex: a dual microdialysis and electroencehalographic study in awake rats.

In order to study the role of amino acids in the hippocampus and the entorhinal cortex during the convulsive process induced by 4-aminopyridine (4-AP), we have used a device allowing the simultaneous microdialysis and the recording of their electrical activity of both regions in freely moving rats. We found that infusion of 4-AP into the entorhinal cortex resulted in a large increase in extracellular glutamate and glutamine and small increases in glycine and taurine levels. Likewise, infusion of 4-AP into the hippocampus resulted in a major increase in glutamate, as well as slight increases in taurine and glycine. In both infused regions the peak concentration of extracellular glutamate was observed 15 min after 4-AP administration. No significant changes were found in the non-infused hippocampus or entorhinal cortex of the same rats. Simultaneous electroencephalographic recordings showed intense epileptiform activity starting during 4-AP infusion and lasting for the rest of the experiment (1 h) in both the entorhinal cortex and the hippocampus. The discharges were characterized by poly-spikes and spike-wave complexes that propagated almost immediately to the other region studied. These findings suggest that increased glutamatergic synaptic function in the circuit that connects both regions is involved in the epileptic seizures induced by 4-AP.

4-Aminopyridine↗
PubMed2004

Entorhinal cortex lesioning promotes neurogenesis in the hippocampus of adult mice.

Hippocampal neurogenesis in adult mammals is influenced by many factors. Lesioning of the entorhinal cortex is a standard model used to study injury and repair in the hippocampus. Here we use bromodeoxyuridine (BrdU) labeling combined with immunohistochemical identification using cell type specific markers to follow the fate of neural progenitors in the hippocampus following entorhinal cortex lesioning in mice. We show that unilateral entorhinal cortex lesioning does not alter the rate of neural progenitor proliferation in the ipsilateral dentate gyrus during the first 3 days after lesioning. However it enhances cell survival at 42 days post-lesioning leading to an increased number of beta-III tubulin and calbindin-immunoreactive neurons being produced. By contrast, when BrdU was administered 21 days post-lesioning, the number of surviving cells 21 days later was similar on the lesioned and non-lesioned sides. Thus, acutely entorhinal cortex lesioning promotes neurogenesis by enhancing survival of either neural progenitors or their progeny. However, this stimulus to neurogenesis is not sustained into the recovery period.

Animals↗
PubMed1996

Functional activation of somatostatin- and neuropeptide Y-containing neurons in the entorhinal cortex of chronically epileptic rats.

The in vitro release of somatostatin and neuropeptide Y, their tissue concentration and immunocytochemical pattern were examined in the entorhinal cortex of chronically epileptic rats. A systemic administration of 12 mg/kg kainic acid causing generalized tonic-clonic seizures for at least 3 h after injection was used to induce, 60 days later, a chronically enhanced susceptibility to seizures in the rats. The release of both peptides under depolarizing conditions was significantly reduced by 15% on average from slices of the entorhinal cortex two days after kainic acid-induced status epilepticus. At 60 days, the spontaneous and 30 mM KCl-induced release of somatostatin was significantly enhanced by 30% on average. The release induced by 100 mM KCl was raised by 70%. The spontaneous, 30 mM and 100 mM KCl-induced release of neuropeptide Y from the same slices was increased, respectively, by 120%, 76% and 36%. The late changes were associated with an increased tissue concentration of neuropeptide Y but not of somatostatin. This was confirmed by immunocytochemical evidence showing that neuropeptide Y-, but not somatostatin-immunoreactive neurons were increased in the entorhinal cortex of kainic acid-treated rats. These results indicate that neurotransmission mediated by somatostatin and neuropeptide Y, two peptides previously shown to play a role in limbic epileptogenesis, is enhanced in the entorhinal cortex of chronically epileptic rats.

Animals↗
PubMed1997

GABA release and GAD67 mRNA expression in rat hippocampus following entorhinal cortex activation.

This study investigate the effect of stimulation of glutamatergic afferents originating in the entorhinal cortex on possible changes of GABAergic transmission in the CA1 subregion of the hippocampus. Microdialysis was used to monitor extracellular GABA and in situ hybridization to measure levels of glutamic acid decarboxylase67 (GAD67) mRNA. A dose-dependent increase in extracellular levels of GABA in the dorsal CA1 subregion was detected following injection of 2.4 and 9.6 micrograms quisqualate into the lateral entorhinal cortex whereas 0.24 microgram had no effect. The GABA increase was attenuated by local administration of tetrodotoxin (TTX), indicating neuronal origin. A 60% decrease and a 160% increase were seen in levels of GAD67 mRNA in the CA1 following injection of 0.24 and 9.6 micrograms quisqualate, respectively. This study provides evidence of an entorhinal cortex influenced stimulatory effect on GABAergic activity in the CA1. However, no direct relationship was found between stimulated GABA release and subsequently measured GAD67 mRNA levels. The increased GABA release and the apparent adaptive increase in GAD67 mRNA levels by the strongest stimulation may be due to an endogenous inhibitory neuroprotective response to an excitotoxic influence.

Animals↗
PubMed2002

A volumetric MRI study of the entorhinal cortex in first episode neuroleptic-naive schizophrenia.

BACKGROUND: Imaging studies have frequently reported volume loss of limbic structures in schizophrenia, yet there appears to be no quantitative data on entorhinal cortex volumes in patients with neuroleptic naive first-episode schizophrenia. METHODS: The volume of the entorhinal cortices of 22 control subjects and 18 patients with neuroleptic-naïve first-episode schizophrenia were measured from magnetic resonance images (MRI) scans using recently designed anatomic criteria for MRI anatomy of the entorhinal cortex. RESULTS: Smaller entorhinal volumes were found bilaterally in the schizophrenic patients. This volume loss did not correlate with items on the Positive and Negative Syndrome Scale. CONCLUSIONS: These data suggest early involvement of the entorhinal cortex in schizophrenia.

Adult↗
PubMed2006

Conjunctive representation of position, direction, and velocity in entorhinal cortex.

Grid cells in the medial entorhinal cortex (MEC) are part of an environment-independent spatial coordinate system. To determine how information about location, direction, and distance is integrated in the grid-cell network, we recorded from each principal cell layer of MEC in rats that explored two-dimensional environments. Whereas layer II was predominated by grid cells, grid cells colocalized with head-direction cells and conjunctive grid x head-direction cells in the deeper layers. All cell types were modulated by running speed. The conjunction of positional, directional, and translational information in a single MEC cell type may enable grid coordinates to be updated during self-motion-based navigation.

Animals↗
PubMed1997

Sequential role of hippocampus and amygdala, entorhinal cortex and parietal cortex in formation and retrieval of memory for inhibitory avoidance in rats.

The hippocampus and amygdala, the entorhinal cortex and the parietal cortex participate, in that sequence, both in the formation and in the expression of memory for a step-down inhibitory avoidance task in rats. Bilateral infusion of AP5 or muscimol caused retrograde amnesia when given 0 min after training into both hippocampus and amygdala, when given or 180 min after training into the entorhinal cortex, or when given 180 min after training into the parietal cortex. Therefore, memory formation requires the sequential and integrated activity of all these areas mediated by glutamate NMDA receptors in each case. Pre-test administration of CNQX 1 day after training into hippocampus and amygdala, 1 or 31 days after training in entorhinal cortex, or 1, 31 or 60 days after training in the parietal cortex temporarily blocked retention test performance. Therefore, 1 day after training, all these brain structures are necessary for retrieval; 1 month later, the hippocampus and amygdala are no longer necessary for retrieval but the entorhinal and parietal cortex still are; and 60 days after training only the parietal cortex is needed. In all cases the mechanisms of retrieval require intact glutamate AMPA receptors.

2-Amino-5-phosphonovalerate↗
PubMed1999

Carbachol-induced changes in excitability and [Ca2+]i signalling in projection cells of medial entorhinal cortex layers II and III.

The entorhinal cortex (EC) is a major gateway for sensory information into the hippocampus and receives a cholinergic input from the forebrain. Therefore, we studied muscarinic effects on excitability and intracellular Ca2+ signalling in layer II stellate and layer III pyramidal projection neurons of the EC. In both classes of neurons, local pressure-pulse application of carbachol (1 mM) caused small, atropine-sensitive membrane depolarizations that were not accompanied by any detectable changes in [Ca2+]i. At a higher concentration (10 mM), carbachol induced a larger membrane depolarization associated with synaptic oscillations and epileptiform activity in both classes of neurons. In contrast to the intrinsic theta rhythm in stellate cells with one dominant peak frequency at approximately 7 Hz, the synaptically mediated oscillation induced by carbachol showed three characteristic peaks in the theta and gamma frequency range at approximately 11, 23 and 40 Hz. Although carbachol-induced epileptiform activity was associated with increases in intracellular free Ca2+ in both layer II and III cells, the observed [Ca2+]i accumulation was significantly larger in layer III than in layer II cells. Responses to intracellular current injections showed differences in Ca2+ accumulation in layer II and III cells at the same membrane potentials, suggesting a dominant expression of low- and high-voltage-activated Ca2+ channels in these layer II and III cells, respectively. In conclusion, we present evidence for significant differences in the [Ca2+]i regulation between layer II stellate and layer III pyramidal cells of the medial EC.

2-Amino-5-phosphonovalerate↗
PubMed1998

Serotonin reduces polysynaptic inhibition via 5-HT1A receptors in the superficial entorhinal cortex.

The superficial cells of the entorhinal cortex (EC), main input to the hippocampus, receive a serotonergic input from the raphe nuclei and express 5-hydroxytryptamine creatine sulfate complex (5-HT) receptors at high density. With the use of intracellular recordings, we investigated the effects of serotonin on synaptic inhibition of layer II and III neurons of the EC. Serotonin reduced both polysynaptic fast and slow inhibitory postsynaptic potentials (IPSPs) in projection neurons of the superficial EC. Polysynaptic fast and slow IPSPs were depressed by serotonin in a dose-dependent manner (0.1-100 microM). Serotonin in a concentration of 1 microM reduced the amplitudes of polysynaptic fast and slow IPSPs by approximately 40 and 50%, respectively. To identify the subtype of the 5-HT-receptor mediating the effects on polysynaptic IPSPs, we applied various 5-HT-receptor agonists and antagonists. Although the serotonin agonists for the 5-HT1B,2C,3 receptors were ineffective, the effects were mimicked by the 5-HT1A-receptor agonists (8-OH-DPAT, 5-CT) and prevented by the 5-HT1A-receptor antagonist NAN-190. To look at the direct effects of 5-HT on inhibitory interneurons, we elicited monosynaptic IPSPs in the absence of excitatory synaptic transmission. In contrast to the polysynaptic IPSPs, monosynaptic IPSPs were not significantly affected by serotonin. Recordings from putative inhibitory interneurons revealed that their excitatory postsynaptic potentials (EPSPs) were reversibly reduced by serotonin. We conclude that serotonin suppresses polysynaptic inhibition in projection neurons of layers II and III of the EC by depression of EPSPs on inhibitory interneurons via 5-HT1A receptors.

2-Amino-5-phosphonovalerate↗
PubMed1996

The role of postlesion seizures and spreading depression in the upregulation of glial fibrillary acidic protein mRNA after entorhinal cortex lesions.

Unilateral lesions of the entorhinal cortex have been shown to lead to dramatic increases in GFAP mRNA levels in denervated zones in the hippocampus and dentate gyrus and sometimes (but not always) in nondenervated zones in the contralateral hippocampus and dentate gyrus. The variable distribution of the increases in GFAP mRNA expression suggests that the events which trigger changes in GFAP mRNA levels occur to a variable extent in individual animals. The companion paper characterizes two candidate triggering events: spreading depression (SD) that occurs to a variable extent at the time of the lesion and recurrent seizures that occur during the early postlesion interval. The goal of the present study was to evaluate whether individual differences in the extent or spatial distribution of lesion-induced increases in GFAP mRNA are related to the occurrence of either SD or seizures. We quantified the increases in GFAP mRNA levels in individual animals that had been monitored physiologically to define the incidence of SD and postlesion seizures. The results revealed that the quantitative extent of the increases in GFAP mRNA in denervated zones and was not related to either SD or postlesion seizures. The increases in GFAP mRNA in nondenervated zones also were not related to episodes of spreading depression that occurred at the time of lesion production but were related to the spontaneous seizures that developed during the first 24 h postlesion after the animals had recovered from the surgical anesthesia. Taken together, these data indicate that physiological events that occur during the early postlesion interval can play an important role in determining the pattern and extent of altered cellular gene expression in response to an injury.

Animals↗
PubMed2001

A comparison of the firing properties of putative excitatory and inhibitory neurons from CA1 and the entorhinal cortex.

The superficial layers of the entorhinal cortex (EC) provide the majority of the neocortical input to the hippocampus, and the deep layers of the EC receive the majority of neocortically bound hippocampal outputs. To characterize information transmission through the hippocampal and EC circuitry, we recorded simultaneously from neurons in the superficial EC, the CA1 region of hippocampus, and the deep EC while rodents ran for food reward in two environments. Spike waveform analysis allowed us to classify units as fast-spiking (FS) putative inhibitory cells or putative excitatory (PE) cells. PE and FS units' firing were often strongly correlated at short time scales, suggesting the presence a monosynaptic connection from the PE to FS units. EC PE units, unlike those found in CA1, showed little or no tendency to fire in bursts. We also found that the firing of FS and PE units from all regions was modulated by the approximately 8 Hz theta rhythm, although the firing of deep EC FS units tended to be less strongly modulated than that of the other types of units. When we examined the spatial specificity of FS units, we determined that FS units in all three regions showed low specificity. At the same time, retrospective coding, in which firing rates were related to past position, was present in FS units from all three regions and deep EC FS units often fired in a "path equivalent" manner in that they were active in physically different, but behaviorally related positions both within and across environments. Our results suggest that while the firing of FS units from CA1 and the EC show similarly low levels of position specificity, FS units from each region differ from one another in that they mirrored the associated PE units in terms of their tendency to show more complex positional firing properties like retrospective coding and path equivalence.

Action Potentials↗
PubMed1998

Noise from voltage-gated ion channels may influence neuronal dynamics in the entorhinal cortex.

Neurons of the superficial medial entorhinal cortex (MEC), which deliver neocortical input to the hippocampus, exhibit intrinsic, subthreshold oscillations with slow dynamics. These intrinsic oscillations, driven by a persistent Na+ current and a slow outward current, may help to generate the theta rhythm, a slow rhythm that plays an important role in spatial and declarative learning. Here we show that the number of persistent Na+ channels underlying subthreshold oscillations is relatively small (<10(4)) and use a physiologically based stochastic model to argue that the random behavior of these channels may contribute crucially to cellular-level responses. In acutely isolated MEC neurons under voltage clamp, the mean and variance of the persistent Na+ current were used to estimate the single channel conductance and voltage-dependent probability of opening. A hybrid stochastic-deterministic model was built by using voltage-clamp descriptions of the persistent and fast-inactivating Na+ conductances, along with the fast and slow K+ conductances. All voltage-dependent conductances were represented with nonlinear ordinary differential equations, with the exception of the persistent Na+ conductance, which was represented as a population of stochastic ion channels. The model predicts that the probabilistic nature of Na+ channels increases the cell's repertoire of qualitative behaviors; although deterministic models at a particular point in parameter space can generate either subthreshold oscillations or phase-locked spikes (but rarely both), models with an appropriate level of channel noise can replicate physiological behavior by generating both patterns of electrical activity for a single set of parameters. Channel noise may contribute to higher order interspike interval statistics seen in vitro with DC current stimulation. Models with channel noise show evidence of spike clustering seen in brain slice experiments, although the effect is apparently not as prominent as seen in experimental results. Channel noise may contribute to cellular responses in vivo as well; the stochastic system has enhanced sensitivity to small periodic stimuli in a form of stochastic resonance that is novel (in that the relevant noise source is intrinsic and voltage-dependent) and potentially physiologically relevant. Although based on a simple model that does not include all known membrane mechanisms of MEC stellate cells, these results nevertheless imply that the stochastic nature of small collections of molecules may have important effects at the cellular and network levels.

Animals↗
PubMedDate not supplied

[Quantitative volumetric analysis of the hippocampus, amygdala and entorhinal cortex: normative database for the adult Portuguese population].

INTRODUCTION: Atrophy of the hippocampus, amygdala and entorhinal cortex can be found in neurodegenerative diseases, head trauma and epilepsy and are expressed by means of volume reductions. The ability to detect these changes quantitatively depends on accurate comparisons with normative databases. AIM: To present standard magnetic resonance imaging (MRI) volumes of the mesio-temporal lobe structures and an objective statistical methodology for contrasting pathological states. SUBJECTS AND METHODS: Volumes of the right and left hippocampi, amygdalae and entorhinal cortex were measured from MRI in 34 right-handed healthy volunteers, aged 19-52 years. Data were normalized for the individual variation in total intracranial volume. Reproducibility was confirmed by intra/inter-observer tests. The statistical analyses included asymmetry comparisons, correlations between volumes and tests to assess the influence of age, gender and general morphometry (body mass index and height). For each volume, we further defined a normative interval by means of 99% confidence ellipses, accordingly to Hotteling's method. RESULTS: Right-left asymmetry in the volumes of the hippocampus and entorhinal cortex was a normal finding. Structures located in the right hemisphere were larger than the left by a small but statistically significant amount. No asymmetry was found in the amygdala. There was no correlation in-between these volumes. Gender differences were exclusively noted in the absolute amygdala volumes (male > female) but were eliminated by the normalization procedure. No effect of age or morphometry was seen in the absolute or normalized volumes (except for a milder correlation between hippocampal volumes and height). Confidence ellipses were built for every structure and provided a precise reading of the data. Particularly, it allowed for a clear distinction of pathological asymmetries and bilateral cases. CONCLUSION: These normative volumes serve as a reference for the assessment of pathologic groups within similar age-range. The use of a single graphic representation simplifies the clinical interpretation and enhances the precision of the results.

Adult↗
PubMed2003

Bilateral lesions of the entorhinal cortex differentially modify haloperidol- and olanzapine-induced c-fos mRNA expression in the rat forebrain.

Lesions of the entorhinal cortex are now an accepted model for mimicking some of the neuropathological aspects of schizophrenia, since evidence has accumulated for the presence of cytoarchitectonic abnormalities within this cortex in schizophrenic patients. The present study was undertaken to address the functional consequences of bilateral entorhinal cortex lesions on antipsychotic-induced c-fos expression. After a 15-day recovery period, the effect of a typical antipsychotic, haloperidol (1 mg/kg), on c-fos mRNA expression was compared with that of an atypical one, olanzapine (10 mg/kg), in both sham-lesioned and entorhinal cortex-lesioned rats. In sham-lesioned rats, both haloperidol and olanzapine induced c-fos expression in the caudal cingulate cortex, dorsomedial and dorsolateral caudate-putamen, nucleus accumbens core and shell and lateral septum. In addition, olanzapine, but not haloperidol, increased c-fos expression within the central amygdala. In entorhinal cortex-lesioned rats, haloperidol-induced c-fos expression was markedly reduced in most areas. In contrast, the olanzapine-induced c-fos expression was not altered in the nucleus accumbens shell and lateral septum of the lesioned rats. These findings reveal that entorhinal cortex lesions affect c-fos expression in a compound- and regional-dependent manner. Our results further emphasize the importance of the exploration of the mechanisms of action of antipsychotic drugs in the context of an associated cortical pathology.

Animals↗
PubMed1995

Reduction of AMPA-selective glutamate receptor subunits in the entorhinal cortex of patients with Alzheimer's disease pathology: a biochemical study.

Using biochemical techniques we determined concentrations of the AMPA-selective glutamate receptor subunits GluR1 and GluR2/3 in the entorhinal cortex of patients with Alzheimer's disease pathology and age-matched controls. Tangle density was also determined in anatomically matched samples and correlated with GluR1 and GluR2/3 receptor concentration. In Alzheimer's disease brain, Western blot analysis revealed average reductions of 43% and 38% for GluR1 and GluR2/3, respectively. Based on previous immunohistochemical studies, we infer that the majority of protein reduction was due to decreases in GluR1 and GluR2/3 immunolabeled elements in the more superficial layers of the entorhinal cortex (layers II and III). These layers of the entorhinal cortex contained numerous neurofibrillary tangles in Alzheimer's disease, but neither GluR1 nor GluR2/3 protein concentration correlated significantly with tangle density. We hypothesize that the decrease in specific glutamate receptor subunits, particularly GluR2/3, may contribute to the vulnerability of neurons in the entorhinal cortex via mechanisms involving calcium conductance through AMPA-selective channels.

Aged↗
PubMedDate not supplied

Neurons in the ventral subiculum, amygdala and entorhinal cortex which project to the nucleus accumbens: their input from somatostatin-immunoreactive boutons.

Neurons in the hippocampus, amygdala and entorhinal cortex which project to the nucleus accumbens were labelled retrogradely following injection of horseradish peroxidase. The injections were targetted on the medial part of the nucleus accumbens, but some injection sites included the whole nucleus. Projection neurons in all three areas were found to be spiny, and from the entorhinal cortex and ventral subiculum of the hippocampus they were pyramidal neurons. Somatostatin (S28(1-12)-immunoreactive neurons were found in all parts of the three limbic areas examined. They were found to have various morphologies, but in the electron microscope all had the ultrastructural characteristics of interneurons. In the hippocampus the stratum lacunosum was found to contain the most immunoreactive fibres while most cells lay in the stratum oriens. In the amygdala the densest staining for both cells and fibres was in the central nucleus. In the entorhinal cortex somatostatin-immunoreactive fibres and cells seemed to have no preferential distribution. Examination of somatostatin-immunoreactive profiles in the electron microscope revealed that the majority of synaptic contacts were made with dendrites, many of which were spine-bearing. In the light microscope somatostatin-immunoreactive fibres could be seen to lie near the somata and proximal dendrites of neurons that projected to the nucleus accumbens. In the electron microscope it was found that somatostatin-immunoreactive boutons were in symmetrical synaptic contact with the somata and proximal dendrites of neurons in the ventral subiculum, entorhinal cortex and amygdala which project to the nucleus accumbens.

Amygdala↗
PubMed1990

Synchronous discharges in the rat entorhinal cortex in vitro: site of initiation and the role of excitatory amino acid receptors.

A slice preparation was used to study the spread of epileptiform activity in the rat entorhinal cortex. Interictal-like discharges were induced in the medial entorhinal cortex by blocking synaptic inhibition mediated via GABAA-receptors. Recorded intracellularly, these discharges consisted of an initial paroxysmal depolarizing shift followed by a variable number of afterdischarges. There was no apparent difference between these events whether they were recorded in isolated cortical slices or in slices where the hippocampus and subicular complex remained attached. The events were also unaffected by droplets of a xylocaine solution applied to sites in the hippocampus, subicular complex or superficial layers of the entorhinal cortex but applications to layer IV/V, lateral or medial to the recording site could reduce the number of afterdischarges without affecting the initial paroxysmal shift. Simultaneous intracellular recordings from neurons in layer IV/V and layer II of the medial entorhinal cortex showed that the paroxysmal depolarizing shift and all afterdischarges in the deeper layer always preceded those recorded in the superficial layer, and these events invariably occurred on a one-to-one basis. This was true whether the events were evoked or occurred spontaneously. The delay varied between 2 and 11 ms but was consistent for a given cell pair. A similar relationship existed between discharges recorded simultaneously in layer IV/V neurons and layer VI neurons, events in the layer IV/V cells preceding those in the deeper layer. Discharges recorded simultaneously in pairs of layer IV/V neurons showed more complex relationships. Paroxysmal depolarizing shifts were always recorded in both cells and the discharge could occur at the more medial site before the more lateral, or vice versa. For a given pair the temporal relationship was invariable. It was often the case, however, that the temporal relationship between afterdischarges was reversed with respect to the initial paroxysmal shift. This relationship was also invariable in a given pair of cells. Interictal-like discharges in layers II or IV/V neurons could be abolished by perfusion with 6-cyano-7-nitro-quinoxaline-2,3-dione which is an antagonist for the non-N-methyl-D-aspartate (i.e. quisqualate/kainate) subtype of excitatory amino acid receptor. The afterdischarges associated with the events were abolished in an all-or-none fashion whereas the blockade of the paroxysmal depolarizing shift was progressive. Antagonists of N-methyl-D-aspartate receptors also abolished afterdischarges but only reduced the initial paroxysmal shift. It is concluded that the interictal-like discharges arise intrinsically within the cortex and are not influenced by input from hippocampal or subicular structures.(ABSTRACT TRUNCATED AT 400 WORDS)

Action Potentials↗
PubMed1994

Autoradiographic characterization of 125I-neurotensin binding sites in human entorhinal cortex.

The laminar and rostro-caudal distribution of 125I-neurotensin binding sites is described in human entorhinal cortex using quantitative autoradiography. Specific binding was most prominent over the cell clusters of layer II of the entorhinal cortex throughout its rostro-caudal extent. Dense binding was also observed in the adjacent presubiculum and cortical amygdaloid transition area, whereas minimal binding was detected in the hippocampus and dentate gyrus. 125I-Neurotensin may serve as a selective probe for neurotensin receptor alterations and layer II-specific cytoarchitectural disturbances in the entorhinal cortex in neuropsychiatric diseases associated with abnormalities of the mesial temporal lobe.

Adult↗