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PubMed1983

The indusium griseum and anterior hippocampal continuation in the rat.

The morphology and connections of the indusium griseum (IG) and anterior hippocampal continuation (AHC) suggest that this cortex contains analogues to several portions of the hippocampal formation. Whereas the outer neuronal layer of this cortex is made up of cells which are similar in structure to the neurons of the granule cell layer of the dentate gyrus, the three successively deeper layers contain morphological analogues to the neurons of the dentate hilus, Ammon's horn, and the subiculum, respectively. The neurons within each of these four layers of the AHC and IG have afferent and efferent connections which are quite similar to the connections of their hippocampal counterparts. Thus, the granule cells of the IG and AHC receive laminar inputs from the entorhinal cortex, the IG-AHC itself, and the supramammillary region. Each of these three classes of inputs ends at successively more proximal positions on the dendritic tree of these granule cells. Other inputs to this region include those from the septal nuclei and the olfactory bulb. The deeper layers of the IG and AHC receive several inputs, including those from the thalamic and septal nuclei and the entorhinal cortex. The efferent cell bodies of the IG and AHC are segregated in such a way that the granule cells appear to give rise to only short connections, while the hilar cells project to the granule cells, the intermediate pyramidal neurons project to other portions of the IG and AHC and to the olfactory bulb, and the deep pyramidal neurons project to the diencephalon. These results demonstrate that the IG-AHC is a continuation of the hippocampal formation.

Afferent Pathways↗
PubMed2006

Anticipatory brainstem activity predicts neural processing of pain in humans.

Previous neuroimaging studies have shown brain activity during not only the application of noxious stimuli, but also prior to stimulation. The functional significance of the anticipatory response, however, has yet to be explored. Two theoretical responses involve either a decrease or an increase in sensitivity of the nociceptive system. In a functional magnetic resonance imaging (fMRI) study, brainstem responses during anticipation and processing of thermal noxious stimuli were investigated. Twelve healthy subjects were warned prior to and then received noxious stimulation to their left hand. Behavioral data showed a positive correlation between the intensity of anticipation and pain. FMRI data revealed brainstem activation in the PAG during the anticipation period. When correlated with individual anticipation ratings, activation during anticipation included significant clusters within the entorhinal cortex and ventral tegmental area (VTA). During receipt, activation within the brainstem included the PAG, VTA, rostral ventromedial medulla (RVM), and the parabrachial nucleus (PB), all elements of descending pain pathways. Using a backward model approach, we explored the functional significance of the anticipatory neural response for subsequent pain processing. Results of this regression analysis revealed that insula activity during receipt was predicted by activity in both the entorhinal cortex and VTA during anticipation. We suggest that activation in both regions before and during pain may underlie anticipation and subsequent pain modulatory responses, possibly involving the appraisal and control of attention necessary for pain modulation. Together, the results suggest a possible role of brainstem areas in anticipatory mechanisms involved in the maintenance of chronic pain.

Adult↗
PubMed2001

Decreased hippocampal N-acetylaspartate in the absence of atrophy in posttraumatic stress disorder.

BACKGROUND: Previous magnetic resonance imaging studies of posttraumatic stress disorder reported hippocampal volume loss. The goals of this study were 1) to determine the relationship between hippocampal atrophy and posttraumatic stress disorder in the absence of alcohol abuse, and 2) to test if loss of N-acetylaspartate (a neuron marker) in the hippocampus of posttraumatic stress disorder occurs separate from atrophy. In addition, volume changes in the entorhinal cortex were also explored. METHODS: Eighteen male patients with combat-related posttraumatic stress disorder (mean age 51.2 +/- 2.5 years) and 19 male control subjects (mean age 51.8 +/- 3.2 years) were studied using magnetic resonance imaging and Proton magnetic resonance spectroscopic imaging. Both groups had no alcohol and drug abuse during the past 5 years. RESULTS: Posttraumatic stress disorder and control subjects had similar volumes of hippocampus and entorhinal cortex. In contrast to volume, N-acetylaspartate was significantly reduced by about 23% bilaterally in the hippocampus of posttraumatic stress disorder when compared with control subjects, and creatine-containing compounds were reduced by 26% in the right hippocampus of posttraumatic stress disorder. CONCLUSIONS: N-acetyl asparate and creatine reductions imply that there are hippocampal abnormalities in posttraumatic stress disorder. Furthermore, these metabolite changes seem to be better indicators of posttraumatic stress disorder pathology than volume losses.

Aspartic Acid↗
PubMed1993

On the origin of Alzheimer's disease: a hypothesis.

There is no unifying hypothesis to account for the anatomical distribution of neuropathology, the involvement of beta-amyloid precursor protein (beta APP) and the role of increasing age in triggering the Alzheimer disease process. We report here that layer II pre-alpha neurones in transentorhinal and entorhinal cortex contain more beta APP immunoreactivity than other cortical neurones in normal individuals. This immunoreactivity increased in the early stages of Alzheimer's disease and was lost as the disease progressed. These neurones are known to undergo genetically programmed re-sprouting and synaptogenesis during the fifth and sixth decades of life. We hypothesize that these phenomena are related and that the Alzheimer's disease process originates in entorhinal cortex neurones due to the enhancement of their normally high content of beta APP during age-related resprouting.

Adult↗
PubMed1990

The connections of presubiculum and parasubiculum in the rat.

The present study describes the differences and similarities between the connections of the presubiculum and parasubiculum based on retrograde and anterograde tracing experiments. The results demonstrate that both areas have several similar afferent connections, particularly those from subcortical areas such as the claustrum, diagonal band of Broca, anterior thalamus, nucleus reuniens, locus coeruleus, and raphe nuclei. Both subicular areas also are innervated by axons originating in the ipsilateral and contralateral entorhinal cortex, presubiculum, and parasubiculum. In contrast to these similarities, most axons innervating the presubiculum originate in the lateral dorsal thalamic nucleus, the claustrum, and the contralateral presubiculum. Conversely, the parasubiculum is innervated primarily by axons that originate in area CA1 of the hippocampus, the basolateral nucleus of the amygdala, and the contralateral presubiculum and parasubiculum. The major efferent projection from the presubiculum and parasubiculum courses bilaterally to the medial entorhinal cortex; however, the results of the present study confirm previous suggestions that presubicular axons terminate almost exclusively in layers I and III, whereas parasubicular axons innervate layer II. The presubiculum also projects to the anteroventral and laterodorsal nuclei of the thalamus, and the lateral ventral portion of the medial mammillary nucleus, whereas the parasubiculum projects prominently to the anterodorsal nucleus of the thalamus, the contralateral presubiculum and parasubiculum, and the lateral dorsal segment of the medial mammillary nucleus. Thus despite some similarities, the major connections of presubiculum and parasubiculum are distinct from one another and distinct from the projections of the adjacent subiculum and postsubiculum. These results suggest that the subicular cortex is considerably more complex than previously envisioned and indicate that each segment may subserve a distinct role in the processing of information by the hippocampal formation.

Acetylcholinesterase↗
PubMed1997

Sequelae of parenteral domoic acid administration in rats: comparison of effects on different metabolic markers in brain.

Parenterally administered domoic acid, a structural analog of the excitatory amino acids glutamic acid and kainic acid, has specific effects on brain histology in rats, as measured using different anatomic markers. Domoic acid-induced convulsions affects limbic structures such as hippocampus and entorhinal cortex, and different anatomic markers can detect these neurotoxic effects to varying degrees. Here we report effects of domoic acid administration on quantitative indicators of brain metabolism and gliosis. Domoic acid, 2.25 mg/kg i.p., caused stereotyped behavior and convulsions in approximately 60% of rats which received it. Six to eight days after domoic acid or vehicle administration, the animals were processed to measure regional brain incorporation of the long-chain fatty acids [1-(14)C]arachidonic acid ([14C]AA) and [9,10-(3)H]palmitic acid ([3H]PA), or regional cerebral glucose utilization (rCMRglc) using 2-[1-(14)C]deoxy-D-glucose, by quantitative autoradiography. Others rats were processed to measure brain glial fibrillary acidic protein (GFAP) by enzyme-linked immunosorbent assay. Domoic acid increased GFAP in the anterior portion of cerebral cortex, the caudate putamen and thalamus compared with vehicle. However, in rats that convulsed after domoic acid GFAP was significantly increased throughout the cerebral cortex, as well as in the hippocampus, septum, caudate putamen, and thalamus. Domoic acid, in the absence of convulsions, decreased relative [14C]AA incorporation in the claustrum and pyramidal cell layer of the hippocampus compared with vehicle-injected controls. In the presence of convulsions, relative [14C]AA incorporation was decreased in hippocampus regions CA1 and CA2. Uptake of [3H]PA into brain was unaffected. Relative rCMRglc decreased in entorhinal cortex following domoic acid administration with or without convulsions. These results suggest that acute domoic acid exposure affects discrete brain circuits by inducing convulsions, and that domoic acid-induced convulsions cause chronic effects on brain function that are reflected in altered fatty acid metabolism and gliosis.

Animals↗
PubMed1983

Denervation-induced decrease in mitochondrial calcium transport in rat hippocampus.

Calcium accumulation by mitochondria and the activity and in vitro phosphorylation of pyruvate dehydrogenase were measured in control and partially denervated hippocampus. Calcium uptake was measured with a calcium-sensitive electrode and 45Ca2+ accumulation; both methods indicated that lesions of the entorhinal cortex produced a sizable reduction of calcium transport when mitochondria were fueled with pyruvate while much smaller changes were observed using succinate or ATP as energy sources. The decrease in calcium transport was evident by 24 hr after the lesion and was still present 6 months later. Synaptic and nonsynaptic mitochondria were similarly affected by the lesions. The activity and in vitro phosphorylation of pyruvate dehydrogenase were also significantly reduced following lesions of the entorhinal cortex, suggesting that denervation altered the endogenous state of phosphorylation of the mitochondrial enzyme. Commissural lesions but not septal lesions also resulted in a decrease in mitochondrial calcium transport when mitochondria were fueled with pyruvate. These findings suggest that denervation disturbs mitochondrial regulation of free calcium via an action on enzymes which regulate pyruvate dehydrogenase phosphorylation and activity. The potential relationship of this effect to degenerative changes associated with deafferentation and certain disease states is discussed.

Adenosine Triphosphate↗
PubMed1996

The neuropathological changes associated with normal brain aging.

Neurofibrillary tangles and senile plaques are common neuropathological features in both normal brain aging and Alzheimer's disease. In order to examine the patterns of lesion distribution in cerebral aging, we review the clinicopathological analysis of 1144 nondemented cases comparing their neuropathologic features to that reported in cases with mild cognitive impairment and cases with Alzheimer's disease. Regardless of cognitive status, layer II of the entorhinal cortex is involved with neurofibrillary tangle formation in all of the cases, while the CA1 field of the hippocampus and the subiculum are less consistently affected. Neocortical area 20 is particularly prone to develop neurofibrillary tangles in intellectually preserved elders, whereas other neocortical areas are relatively spared. Substantial senile plaque formation is seen in the neocortex of non-demented cases. Quantitatively, mild cognitive impairment is correlated with neurofibrillary tangle densities in layer II of the entorhinal cortex, and clinically overt Alzheimer's disease with neurofibrillary tangle densities in area 20. In non-demented centenarians, there is an early development of neurofibrillary tangles in areas usually spared in the course of the degenerative process in younger individuals. These observations demonstrate that mesial and inferior temporal lobe structures are affected more frequently than originally thought in normal brain aging. In this respect, neurofibrillary tangle formation in area 20 may represent a crucial step of the degenerative process, because it may precede the emergence of the neuropsychological deficits characteristic of Alzheimer's disease. In addition, this study reveals age-related heterogeneity in the regional vulnerability of the cerebral cortex during normal brain aging.

Aged↗
PubMed1996

Distribution of alpha 1A, alpha 1B and alpha 1E voltage-dependent calcium channel subunits in the human hippocampus and parahippocampal gyrus.

The distribution of voltage-dependent calcium channel subunits in the central nervous system may provide information about the function of these channels. The present study examined the distribution of three alpha-1 subunits, alpha 1A, alpha 1B and alpha 1E, in the normal human hippocampal formation and parahippocampal gyrus using the techniques of in situ hybridization and immunocytochemistry. All three subunit mRNAs appeared to be similarly localized, with high levels of expression in the dentate granule and CA pyramidal layer. At the protein level, alpha 1A, alpha 1B and alpha 1E subunits were differentially localized. In general, alpha 1A-immunoreactivity was most intense in cell bodies and dendritic processes, including dentate granule cells, CA3 pyramidal cells and entorhinal cortex pre-alpha and pri-alpha cells. The alpha 1B antibody exhibited relatively weak staining of cell bodies but stronger staining of neuropil, especially in certain regions of high synaptic density such as the polymorphic layer of the dentate gyrus and the stratum lucidum and radiatum of the CA regions. The alpha 1E staining pattern shared features in common with both alpha 1A and alpha 1B, with strong immunoreactivity in dentate granule, CA3 pyramidal and entorhinal cortex pri-alpha cells, as well as staining of the CA3 stratum lucidum. These findings suggest regions in which particular subunits may be involved in synaptic communication. For example, comparison of alpha 1B and alpha 1E staining in the CA3 stratum lucidum with calbindin-immuno-reactivity suggested that these two calcium channels subunits may be localized presynaptically in mossy fibre terminals and therefore may be involved in neurotransmitter release from these terminals.

Aged↗
PubMed2001

Serotonin 5-HT(1A) receptor mRNA expression in dorsal hippocampus and raphe nuclei after gonadal hormone manipulation in female rats.

Female ovarian steroids influence mood and cognition, an effect presumably mediated by the serotonergic system. A key receptor in this interplay may be the 5-HT(1A) receptor subtype. We gave adult ovariectomized female rats subcutaneous pellets containing different dosages of 17 beta-estradiol alone or in combination with progesterone, or placebo pellets, for 2 weeks. 5-HT(1A) receptor mRNA levels were analyzed by in situ hybridization in the dorsal hippocampus, dorsal and median raphe nuclei, and entorhinal cortex. Estradiol treatment alone reduced 5-HT(1A) gene expression in the dentate gyrus and the CA2 region (17 and 19% decrease, respectively). Estradiol combined with progesterone supplementation increased 5-HT(1A) gene expression versus placebo in the CA1 and CA2 subregions of the dorsal hippocampus (16 and 30% increase, respectively). Concomitantly, 5-HT(1A) mRNA expression was decreased by 13% in the ventrolateral part of the dorsal raphe nuclei, while no changes were found in the median raphe nucleus and entorhinal cortex. Chronic effects of ovarian hormones on 5-HT(1A) receptor mRNA expression appear tissue-specific and involve hippocampal subregions and the raphe nuclei. Modulation of 5-HT(1A) receptor gene expression may be of importance for gonadal steroid effects on mood and cognition.

Animals↗
PubMed2006

Path integration and the neural basis of the 'cognitive map'.

The hippocampal formation can encode relative spatial location, without reference to external cues, by the integration of linear and angular self-motion (path integration). Theoretical studies, in conjunction with recent empirical discoveries, suggest that the medial entorhinal cortex (MEC) might perform some of the essential underlying computations by means of a unique, periodic synaptic matrix that could be self-organized in early development through a simple, symmetry-breaking operation. The scale at which space is represented increases systematically along the dorsoventral axis in both the hippocampus and the MEC, apparently because of systematic variation in the gain of a movement-speed signal. Convergence of spatially periodic input at multiple scales, from so-called grid cells in the entorhinal cortex, might result in non-periodic spatial firing patterns (place fields) in the hippocampus.

Animals↗
PubMed1996

Glutamate release correlates with brain-derived neurotrophic factor and trkB mRNA expression in the CA1 region of rat hippocampus.

Synthesis of the neurotrophic factor brain-derived neurotrophic factor (BDNF) and its receptor TrkB in the hippocampus have been proposed to be influenced by endogenous glutamate. To test this hypothesis we have investigated if increases in BDNF and trkB mRNAs are associated with changes in the synaptic release of glutamate in the dorsal hippocampus in the conscious rat by combining the technique of in vivo microdialysis with in situ hybridization histochemistry. A 35% and 66% increase in extracellular levels of glutamate in the dorsal CA1 region was detected following injection into the lateral entorhinal cortex of 2.4 and 9.6 microg of the non-NMDA glutamate receptor agonist quisqualate, respectively. The increase in glutamate was attenuated by local administration of tetrodotoxin (TTX) indicating neuronal origin. Levels of BDNF and trkB mRNAs were increased in the hippocampus in a dose-dependent fashion following the stimulations. The extracellular levels of glutamate in individual animals correlated to the levels of BDNF and trkB mRNAs in the dorsal CA1 region of the hippocampus. This study provides for the first time evidence of an entorhinal cortex influenced concentration-dependent relationship between the release of endogenous glutamate in vivo and neuronal expression of mRNAs for BDNF and its receptor trkB in the hippocampus.

Animals↗
PubMed1999

Perirhinal cortex input to the hippocampus in the rat: evidence for parallel pathways, both direct and indirect. A combined physiological and anatomical study.

The possibility of a direct projection from the perirhinal cortex (PER) to areas CA1 and subiculum (SUB) in the hippocampus has been suggested on the basis of tracer studies, but this projection has not unequivocally been supported by physiological studies. The demonstration of such a functional pathway might be important to understand the functioning of the hippocampal memory system. Here we present physiological and further anatomical evidence for such a connection between PER and the hippocampus. Electrical stimulation of PER in vivo evoked field potentials (EFPs) at the border area of CA1/SUB, consisting of a short latency and a longer latency component. Current source density analysis revealed that the sink of the short latency component was situated in the molecular layer of area CA1/SUB, while the longer latency component had its sink in the outer molecular layer of the dentate gyrus (DG). Anterograde tracer injections in PER showed labelled fibres in the border area of CA1/SUB, but anatomical evidence for a projection of PER to DG was not found. When synaptic transmission in the entorhinal cortex was partly blocked, the amplitude of the longer latency component of the recorded EFPs in the hippocampus was decreased while the short latency component was not affected, which suggests that the indirect pathway originating in PER is mediated through a synaptic relay in the entorhinal cortex. From the present results we conclude that information originating in PER reaches area CA1/SUB by parallel, direct and indirect, routes. The existence of this parallel organization appears to form an essential feature for the proper function of the medial temporal lobe memory system.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1991

A case of progressive supranuclear palsy with widespread senile plaques.

A case of progressive supranuclear palsy (PSP) with frontal lobe atrophy is reported, in which many senile plaques were widely distributed in the neocortex, the entorhinal cortex, the amygdala, and, to a lesser extent, the cerebellar cortex, but not in the hippocampus. Most of the plaques were of the diffuse and primitive types. They were well visualized by beta-protein immunostaining, modified Bielschowsky staining and methenamine silver staining, but were not seen by Bodian staining. The widespread distribution of senile plaques in the cerebral and cerebellar cortices was far beyond that seen in normal aging, and was reminiscent of concomitant Alzheimer's disease (AD). Unlike AD, however, this case had neither senile changes in the hippocampus nor neurofibrillary tangles in the amygdala and entorhinal cortex. It seems that many senile plaques may appear widely in the cerebral cortex and even, to a lesser extent, in the cerebellar cortex of some patients with PSP. Additional case studies using sensitive silver and amyloid antibody preparations are required to elucidate the presence of senile plaques in the cerebral cortex of PSP.

Aged↗
PubMed1999

Two peptidergic drugs increase the synaptophysin immunoreactivity in brains of 24-month-old rats.

The brain-derived peptidergic drug Cerebrolysin has been found to support the survival of neurones in vitro and in vivo. Positive effects on learning and memory have been demonstrated in various animal models and also in clinical trails. In the present study, the effects of Cerebrolysin and its peptide preparation E021 on the synapse density in the hippocampus, the dentate gyrus and in the entorhinal cortex of 24-month-old rats were investigated. Rats received the drugs or saline for control for 19 consecutive days (2.5 ml/kg per day). Slices of the brains were immunohistochemically stained with anti-synaptophysin, which is a specific marker of presynaptic terminals. Quantification of the synapse density was done by using light microscopy and a computerised image analysing system. Our results clearly showed that the rats benefit from the administration of both drugs, showing an enhancement in the number of synaptophysin-immunostained presynaptic terminals in the entorhinal cortex, the dentate gyrus, and also in the hippocampal subfields CA1, CA2, CA3 stratum lucidum and CA3 stratum radiatum. It can be assumed that these effects are the reason for improved cognitive performances of rats treated with Cerebrolysin and E021.

Amino Acids↗
PubMed1981

Facilitation and antagonism of kindled seizure development in the limbic system of the rat.

To study the relative contribution of positive and negative transfer during the kindling of motor seizures, we electrically stimulated the septal area and entorhinal cortex in rats according to two different stimulation paradigms. The first consisted of the usual transfer paradigm in which one site was consecutively stimulated until generalized convulsion were elicited and then the other, secondary site was consecutively stimulated ('transfer kindling'). The second paradigm differed only in that both sites were kindled concurrently by alternating stimulation--one site on one trial, the other on the next trial, etc. ('alternate kindling'). In agreement with results from other laboratories, transfer kindling produced positive transfer of seizure susceptibility in either direction between the septum and entorhinal cortex: primary kindling of one site facilitated secondary site kindling of the other. In marked contrast, alternate kindling was characterized by a striking antagonism of seizure development. Thirteen of 14 animals exhibited generalized convulsions from one site only. Motor seizure development at the alternately stimulated site was suppressed despite electrographic and behavioral evidence of limbic activation and despite stimulation for a number of trials more than sufficient for primary kindling. Which site became dominant during kindling appeared to be random and variable degrees of suppression were observed. Besides antagonizing motor seizure development at the suppressed site, alternate kindling facilitated dominant site kindling, particularly during the pre-motor phases. These results suggest that transsynaptic neural reorganization induced by kindling involves positive and negative effects upon seizure susceptibility. Positive effects are expressed as facilitation of inter-limbic connections whereas negative effects are expressed as antagonism of limbic motor connections which lead to motor convulsive behaviors.

Animals↗
PubMed1980

Accelerated rates of synaptogenesis by "sprouting" afferents in the immature hippocampal formation.

Light and electron microscopic methods were used to study the rate with which undamaged afferents sprout into and form synapses within denervated dendritic zones in the immature rat brain. The middle and outer molecular layers of the dentate gyrus were deafferented by ablation of the ipsilateral entorhinal cortex in 14-day-old rats, and the extension of the commissural projections, which are normally restricted to the inner molecular layer, into the denervated territory was studied by light microscopic autoradiographic tracing methods. Collateral growth was noted as early as 13 hours after the lesion and was found to reach throughout the middle and outer molecular layers by 48 hours postlesion. Quantitative analyses (grain counts) revealed that the addition of commissural fibers and terminals to the denervated zones proceeded extremely rapidly up to 72 hours after the removal of the entorhinal cortex, but slowed markedly thereafter. Electron microscopic procedures were used to assess the rate at which synapses formed during this period and yielded the following information: 1) The density of intact synapses fell to below 20% of normal values within 20 hours of the lesion, 2) reinnervation began before 30 hours postlesion, and 3) the rate at which synapses were added to deafferented middle molecular layer was much more rapid from 20-96 hours postlesion than is observed in this zone during normal development. Furthermore, the sprouting of the inner molecular layer afferents into the middle molecular layer did not retard the pace of synaptogenesis in their normal target region. These results suggest that intrinsic limitations in the capacity of axons and dendrites are not responsible for determining the rate of synaptogenesis in the developing hippocampus. It is proposed instead that existing synapses (or terminals and spines) tend to suppress the formation of new contacts such that the local density of connections regulates the speed with which further innervation occurs.

Animals↗
PubMed2001

Basolateral amygdala lesions disrupt latent inhibitionin rats.

Latent inhibition (LI) refers to the retardation of acquisition of conditioned responding produced by repeated non-reinforced preexposure to the conditioned stimulus (CS) prior to its pairing with the unconditioned stimulus (US) during conditioning. LI has recently been shown to depend upon the integrity of temporal lobe structures, including regions of the hippocampal formation such as the entorhinal cortex. The present study investigated the effects of excitotoxic lesions of another temporal lobe structure, the basolateral nucleus of the amygdala (BLA), on LI. LI was studied in a within-subjects appetitive conditioning preparation in which an auditory CS was paired with food US. In this procedure, preexposure to the CS results in slower acquisition of magazine approach behaviour. Lesions of the BLA reduced the effect of preexposure, disrupting LI. This result suggests that the BLA can play a crucial role in LI. The possible involvement of interactions between BLA and entorhinal cortex in LI is discussed.

Amygdala↗