bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hippocampal theta rhythm in behaving rats following ibotenic acid lesion of the septum
Authors: Leung L. Stan , Martin Lee‐Anne , Stewart Dwight J. 
Published: May 2005

AbstractThe effects of ibotenic acid lesion of the septum were studied in rats implanted with chronically indwelling electrodes and septal cannula. Each rat served as its own control and the properties of the hippocampal theta rhythm were studied before and after ibotenic acid and control saline infusion into the medial septal area. Ibotenic acid preferentially killed neurons in the lateral septum, and significantly attenuated the hippocampal theta rhythm about 50% bilaterally, at both surface and deep electrodes. The coherence and the phase of the theta rhythm at the CA1 apical dendrites, with respect to a superficial electrode, also declined significantly after ibotenic acid lesion. Pilocarpine (25 mg/kg i. p.) induced a theta rhythm of 7–9 Hz during immobility in the lesioned rats that was significantly higher in frequency than that induced in intact rats (4–6 Hz). In lesioned rats, the theta rhythm during tail pinch under urethane anesthesia was largely abolished, and the theta during walking was attenuated by atropine sulfate (50 mg/kg i. p.). Phencyclidine (10 mg/kg i. p.) or parachlorophenylaline (PCPA) alone, which was inferred to abolish an atropine‐resistant theta input, did not affect the power of the walking theta rhythm in either the lesioned or the normal rat. It was concluded that the theta in the behaving rats after ibotenic acid lesion in the septum has a strong astropine‐sensitive component, and that it is not predominantly atropine‐resistant, as suggested previously. The lack of PCPA effect on the theta phase in intact and lesioned rats also suggested a different view of the atropine‐resistant theta in hippocampal region CA1. One possible mechanism of the atropine‐resistant theta at the distal dendrites of pyramidal cells may result from rhythmic inhibition by stratum lacunosum‐moleculare interneurons which may be activated by either serotonergic or cholinergic inputs. © 1994 Wiley‐Liss, Inc.
Somatostatin‐containing neurons in rat organotypic hippocampal slice cultures: Light and electron microscopic immunocytochemistry
Authors: Kunkel Dennis D. , Nguyen Loan B. , Harrigan Mark R. , Schwartzkroin Philip A. , Malouf Alfred T. 
Published: May 2005

AbstractLight and electron microscopic immunocytochemical techniques were used to study the interneuron population staining for somatostain (SRIF) in cultured slices of rat hippocampus. The SRIF immunoreactive somata were most dense in stratum oriens of areas CA1 and CA3, and in the dentate hilus. Somatostain immunoreactive cells in areas CA1 and CA3 were characteristically fusiform in shape, with dendrites that extended both parallel to and into the alveus. The axonal plexus in areas CA1 and CA3 was most dense in stratum lacunosum‐moleculare and in stratum pyramidale. Electron microscopic analysis of this area revealed that the largest number of symmetric synaptic contacts from SRIF immunoreactive axons were onto pyramidal cell somata and onto dendrites in stratum lacunosum‐moleculare. In the dentate gyrus, SRIF somata and dendrites were localized in the hilus. Hilar SRIF immunoreactive neurons were fusiform in shape and similar in size to those seen in CA1 and CA3. Axon collaterals coursed throughout the hilus, projected between the granule cells and into the outer molecular layer. The highest number of SRIF synaptic contacts in the dentate gyrus were seen on granule cell dendrites in the outer molecular layer. Synaptic contacts were also observed on hilar neurons and granule cell somata. SRIF synaptic profiles were seen on somata and dendrites of interneurons in all regions. The morphology and synaptic connectivity of SRIF neurons in hippocampal slice cultures appeared generally similar to intact hippocampus. © 1994 Wiley‐Liss, Inc.
Dopamine D2 receptor expression in hippocampus and parahippocampal cortex of rat, cat, and human in relation to tyrosine hydroxylase‐immunoreactive fibers
Authors: Goldsmith Sara K. , Joyce Jeffrey N. 
Published: May 2005

AbstractA detailed study comparing the distribution of D2 receptors and tyrosine hydroxylase‐immunoreactive fibers in the hippocampus and parahippocampal cortices of the rat, cat, and human was conducted. The distribution of [125I]epidepride binding to D2 receptors along the transverse and longitudinal axes of the hippocampus and parahippocampus differed among the species. In rat hippocampus, the number of sites was highest in septal portions of lacunosum‐moleculare of CA1 and stratum moleculare of the subiculum. Virtually no binding to D2 receptors existed in the temporal hippocamps. For the cat hippocampus, the highest binding existed in the inner one‐third of the molecular layer of the dentate gyrus (DG). There were also significant numbers of D2 receptors in strata radiatum and oriens of the CA subfields, with almost undetectable levels in lacunosum moleculare and subiculum. The number of sites was higher in the septal than temporal hippocampus. In the human hippocampus, highest binding was observed in the molecular layer of DG and the subiculum, with lower levels in strata oriens and lacunosum‐moleculare of CA3, and very low binding in CA1. The histochemical demonstration of the pattern of mossy fibers revealed an organization complementary to that of D2 receptors in cat and human. In none of the species was there significant expression of D2 receptors in the entorhinal cortex, except in the caudal extreme of this region in the rat. In that region a trilaminar pattern was exhibited that continued into the perirhinal cortex. A trilaminar pattern of D2 receptor expression was observed in the perirhinal cortex of all species, with the highest values in the external and deep laminae and low expression in the middle laminae. The organization of dopamine fibers was assessed by comparing the distribution of tyrosine hydroxylase‐positive and dopamine β‐hydroxylase‐immunoreactive fibers in these same regions. It revealed consistent mismatches between the pattern of D2 receptor expression and dopaminergic innervation in all three species. The implications for this mismatch are discussed. It is hypothesized that the distribution of D2 receptors, and not of dopamine fibers, determines what neural systems dopamine influences in the hippocampal complex. © 1994 Wiley‐Liss, Inc.
Maturation of long‐term potentiation in the hippocampal dentate gyrus of the freely moving rat
Authors: Bronzino Joseph D. , Abu‐Hasaballah Khamis , Austin‐LaFrance Robert J. , Morgane Peter J. 
Published: May 2005

AbstractThe ability of the perforant path/dentate granule cell synapse of the hippocampal formation to establish and maintain enhanced levels of synaptic transmission in response to tetanization (long‐term potentiation, LTP) was investigated in freely moving rats at 15, 30, and 90 days of age. Measures of (1) the slope of the population excitatory postsynaptic potential (EPSP), and (2) the population spike amplitude (PSA) obtained before, and at several times following tetanization, were used to evaluate the magnitude and duration of LTP as a function of age. Significant enhancement of both EPSP slope and PSA measures was obtained from animals of all three ages in response to perforant path tetanization. The initial degree of enhancement was essentially the same across the age groups, ranging from +27% to +38% of pretetanization levels for EPSP slope measures and +60% to +75% of pretetanization levels for PSA measures, obtained 15 min after tetanization. The duration of this enhancement obtained from animals of the preweaning group was significantly longer than that obtained from either 30‐ or 90‐day‐old animals. Enhanced measures of both EPSP slope and PSA decayed to baseline levels in these older animals 18 to 24 h after tetanization, while animals tetanized at 15 days of age maintained potentiated levels of both measures for a period of 5 days following tetanization. Tetanization of 15‐day‐old animals resulted in a significant reduction in the latency to EPSP onset without affecting the time‐based relationships among the other measured parameters, which included latency of the population spike onset, population spike minimum, and population spike offset. Tetanization had no effect on the latency measure of any of these parameters in either of the two older age groups. The primarily postnatal development of the dentate granule cell population suggests that both functionally immature GABAergic modulation of granule cell activity and the differential development of components of the N‐methyl‐D‐aspartate receptor complex may be involved in the age‐related differences in the induction and expression of the LTP phenomenon. This study represents the first developmental characterization of LTP in the perforant path/dentate granule cell synapse in freely moving rats during early development. The results indicate that LTP can be reliably established and maintained in behaving rats as young as 15 days of age. Whereas the degree of potentiation at this age is equivalent to that obtained from juveniles and young adults, the duration of the effect significantly outlasts that obtained from older animals in which development of the dentate gyrus is more functionally mature. © 1994 Wiley‐Liss, Inc.
Localization of mRNAs encoding two forms of glutamic acid decarboxylase in the rat hippocampal formation
Authors: Houser Carolyn R. , Esclapez Monique 
Published: May 2005

AbstractThe mRNAs for two forms of glutamic acid decarboxylase (GAD65 and GAD67) were localized in the rat hippocampal formation by nonradioactive in situ hybridization methods with digoxigeninlabeled cRNA probes. Some neurons in all layers of the hippocampus and dentate gyrus were readily labeled for each GAD mRNA, and the patterns of labeling for GAD65 and GAD67 mRNAs were very similar. All major groups of previously described GAD‐and GABA‐containing neurons appeared to be labeled for each GAD mRNA. Such findings suggest that most GABA neurons in the hippocampal formation contain both GAD mRNAs. When the labeling of neurons in the hippocampal formation and cerebral cortex was compared in the same sections, the intensity of neuronal labeling for GAD67 mRNA was generally similar in the two regions. However, the intensity of labeling for GAD65 mRNA was generally stronger for many neurons in the hippocampal formation than for most neurons in the cerebral cortex. Neurons in the hilus of the dentate gyrus were particularly well labeled for GAD65.The nonradioactive labeling for the GAD mRNAs was confined to the cytoplasm of neuronal cell bodies, and this allowed a clear visualization of the relative number and location of labeled neurons. Several distinct patterns of GAD mRNA‐containing neurons were observed among different regions of the hippocampal formation. In the hilus of the dentate gyrus, GAD mRNA‐containing neurons were numerous in the regions deep to the granule cell layer as well as in more central parts of the hilus. Within CA3, the densities (quantities) of labeled neurons varied among the regions. In the inner or hilar segment of CA3, the density of labeled neurons was often lower than that in the outer part of CA3 where numerous labeled neurons were distributed throughout all layers. In CA1, GAD mRNA‐labeled neurons were distributed in a relatively laminar pattern with the highest density in stratum pyramidale and moderate densities in stratum oriens and at the interface between strata radiatum and lacunosum‐moleculare. Lower densities were found within the latter two layers.The prominent localization of the two GAD mRNAs in the hippocampal formation suggests that dual system for GABA synthesis is necessary for normal GABAergic function in this brain region. Most putative GABA neurons contain relatively high levels of GAD67 mRNA as might be expected if this GAD form is responsible for the synthesis of GABA for metabolic and baseline synaptic function. The relatively high levels of GAD65 mRNA in many hippocampal neurons, particularly those of the dentate hilus, may indicate that these neurons have a well‐developed reserve system for GAD and GABA synthesis. © 1994 Wiley‐Liss, Inc.
Ultrastructural identification of entorhinal cortical synapses in CA1 stratum lacunosum‐moleculare of the rat
Authors: Desmond Nancy L. , Scott Carol A. , Jane John A. , Levy William B. 
Published: May 2005

AbstractThe goal of the present study was to identify and characterize, at the electron microscopic level, the synapses formed by entorhinal cortical (EC) axons in the hippocampal CA1 stratum lacunosummoleculare of the adult rat. Phaseolus vulgaris leucoagglutinin was ionotophoresed at various loci throughout the mediolateral and dorsoventral extent of the EC to label EC‐CA1 synapses. Virtually all labeled synapses were asymmetric and axospinous. EC axons did not preferentially synapse with any particular type of dendritic spine; rather, EC axons formed synapses with the range of dendritic spine morphologies observed in CA1 s. lacunosum‐moleculare. Spines with either perforated or nonperforated postsynaptic densities were contacted by EC axons. Occasionally both a labeled and an unlabeled axon synapsed on a single dendritic spine head. The data are discussed in relation to the morphology of other afferent systems synapsing in s. lacunosum‐moleculare and to the physiology of the EC‐CA1 system. © 1994 Wiley‐Liss, Inc.
Ultrastructural plasticity of the dentate gyrus granule cells following recurrent limbic seizures: I. Increase in somatic spines
Authors: Bundman Marsha C. , Pico Richard M. , Gall Christine M. 
Published: May 2005

AbstractVarious paradigms have been used to assess the capacity of the adult brain to undergo activity‐dependent morphological plasticity. In this report we have employed recurrent limbic seizures as a means of studying the effects of this form of enhanced neuronal activity on cellular morphology and, in particular, on the incidence of somatic spines on the dentate gyrus granule cells. Seizure activity was induced by the placement of focal, unilateral electrolytic lesions in the dentate gyrus hilus of adult rats. At various intervals postlesion, rats with behaviorally verified seizures were sacrificed, and the hippocampi contralateral, to the lesions were removed and prepared for electron microscopy. Quantitative analysis showed that as early as 5 hours postlesion there was a dramatic increase in the density and morphological complexity of spines on the perikarya of the granule cells in rats that received seizure‐producing hilus lesions when compared to granule cells from control rats. Many of the somatic spines received asymmetric synapses. The increase in somatic spines was dependent on seizure activity and persisted for at least 1 month following a single recurrent seizure episode. CA1 pyramidal neurons, which exhibit changes in gene expression in response to hilus lesion‐induced seizures but do not normally possess somatic spines, did not exhibit an activity‐dependent elaboration of somatic spines. Thus, the seizure‐induced elaboration of somatic spines represents an amplification of an existing feature of the granule cells and not an effect occurring throughout hippocampus. These data provide evidence for very rapid and long‐lasting structural plasticity in response to brief episodes of seizure activity in the adult brain. © 1994 Wiley‐Liss, Inc.
Effects of perforant path procaine on hippocampal type 2 rhythmical slow‐wave activity (theta) in the urethane‐anesthetized rat
Authors: Heynen Arnold J. , Bilkey David K. 
Published: May 2005

AbstractPrevious research has suggested that the entorhinal cortex plays a major role in the production of type 1 rhythmical slow‐wave activity (RSA) recorded in the hippocampus of the freely moving preparation. In the present experiment we investigated the contribution of the entorhinal cortex to the type 2 fields recorded under urethane anesthesia. Rats had stimulating electrodes and cannulae filled with procaine positioned in the perforant pathway of one or both hemispheres. Recording electrodes were positioned in the dorsal hippocampus of each hemisphere to record perforant path and commissural/associational evoked potentials and RSA fields. Following unilateral procaine blockade, a decrease in RSA amplitude was observed in the stratum oriens and fissure regions of both hemispheres. Concomitant with this change in RSA, there was a loss of perforant path evoked responses, although commissural/associational control potentials remained unaltered. A greater reduction in RSA amplitude was observed following bilateral procaine microinfusion. RSA phase reversal also occurred more dorsally in microelectrode depth profiles conducted through the hippocampus during perforant path inactivation. In current source density analyses performed under baseline conditions, large rhythmic sinks were observed in stratum oriens, in stratum radiatum, and in strata adjacent to the hippocampal fissure. A rhythmic source was often observed in stratum pyramidale. Following perforant path inactivation decreases in the magnitude of the phasic sinks located near the fissure and stratum radiatum were observed. In contrast to the reduction in RSA amplitude observed in the stratum oriens region, the sink in this region and the source in stratum pyramidale remained relatively unaltered. These results demonstrate that the entorhinal region contributes to the production of RSA observed under urethane anesthesia. Furthermore, the CSD and amplitude changes following perforant path inactivation suggest that a substantial portion of RSA recorded in stratum oriens may result from ventrally located RSA dipoles. © 1994 Wiley‐Liss, Inc.
Interhippocampal synthesis of lateralized place navigation engrams
Authors: Fenton André A. , Arolfo Maria P. , Nerad Ludek , Bures Jan 
Published: May 2005

AbstractRats were trained in a water maze in a dark room with the extramaze cues restricted to only dimly back‐lit shapes. We used lidocaine to reversibly lesion the dorsal hippocampus and this controlledcue room in order to examine interhippocampal synthesis of lateralized place engrams. Experiment 1 showed that lidocaine injected into both hippocampi effectively abolished place navigation for up to 25 min but not at 45 min. In experiment 2, each day under lidocaine blockade of one hippocampus, pretrained rats were trained in the water maze to locate the target according to two cues (e. g., AB). Two hours later, the contralateral hippocampus was inactivated and the rats were trained to the same location with two other cues (CD). On day 5, intact brain retrieval was tested in one of three conditions: ACQ (e. g., AB), one of the pairs of cues used in acquisition training; SYNTH (e. g., AC), one cue from each of the pairs used in acquisition; CONT (e. g., AE), one cue that was used in acquisition training and a novel cue. The results show that the hippocampi learned the two tasks independently and similarly [latency (L) at the asymptote = 7 s]. Retrieval performance was at the asymptote for ACQ (AB) and SYNTH (AC) (L = 6 and 7, respectively) but was disrupted for CONT (L = 12). In experiment 3 as in experiment 2, the rats were trained, under unilateral blockade, to a new place for 4 days. On day 5, retrieval with the trained hippocampus blocked was worse (L = 11) than with the untrained side blocked (L = 5). We conclude that interhippocampal synthesis of lateralized place engrams is automatic and highly efficient. © 1995 Wiley‐Liss, Inc.
Simultaneous blockade of non‐NMDA ionotropic receptors and NMDA receptor‐associated ionophore partially protects hippocampal slices from protein synthesis impairment due to simulated ischemia
Authors: Virgili Marco , Contestabile Antonio , Barnabei Ottavio 
Published: May 2005

AbstractA large body of evidence exists to demonstrate that excitatory amino acids (EAA) and their receptors are involved in the pathophysiological mechanisms linking several acute brain insults, such as cerebral ischemia, to neuronal degeneration and death. Accordingly, the use of EAA receptor antagonists can be beneficial in attenuating or preventing the neuronal irreversible damage subsequent to various neuropathological syndromes. We have investigated the effect of 15 min of simulated ischemic conditions, i. e., oxygen/glucose deprivation, on hippocampal slices preparation measuring, as neurotoxicity indexes, both the amino acids efflux in the incubation medium, detected by HPLC, and the inhibition of protein synthesis, evaluated as 3H‐Leucine incorporation into proteins. Accumulation of neurotransmitter amino acids was measured in the medium during the “ischemic” period. Glutamate increased 30‐fold over the basal level while aspartate was sevenfold and GABA 12‐fold higher than in normal conditions. After a reoxygenation period of 30 min, the rate of protein synthesis of hippocampal slices subjected to “ischemia” was reduced to 35–50% of controls. The non‐competitive NMDA antagonist MK‐801 (100 μM) and the competitive NMDA antagonist CGP 39551 (100–250 μM) as well as the non‐NMDA receptor antagonist NBQX (100 μM) and AP3 (300 μM) were unable to counteract the metabolic impairment when they were present alone in the incubation fluid during simulated “ischemia.” An incomplete, but highly significant (p < 0.001), protection from protein synthesis impairment was achieved in the presence of an equimolar concentration (100 μM) of MK‐801 and NBQX. A similar protective effect could be reproduced using 100 μM NBQX in concomitance with a high Mg++ (20 μM) voltage‐dependent block of the NMDA receptor‐associated channel but not exposing the slices to a NBQX (100 μM) and CGP 39551 (100–250 μM) mixture. The recovery of protein synthesis in the presence of the MK‐801/NBQX effective combination was not paralleled by a detectable decrease in the amount of amino acids released in the incubation medium during the “ischemic” period. Taken together, the present data allow new insights into neurotoxicity‐mediating mechanisms, suggesting that multiple additive processes are involved and that antagonists acting at different sites on excitatory amino acid receptor subtype can show different neuroprotective potency. © 1995 Wiley‐Liss, Inc.
Effects of hippocampal lesions on spatial delayed responses in dog
Authors: Kowalska Danuta M. 
Published: May 2005

AbstractThirteen dogs were trained to perform spatial delayed responses to auditory cues in a three‐choice Nencki testing apparatus with a delay of 0 s and then 10 s with a criterion of 90% correct responses in 90 consecutive trials. Then six dogs received bilateral surgical removal of the hippocampus via the cortex of the suprasylvian gyrus (without additional injury to the entorhinal and parahippocampal cortex). Three dogs received control surgical ablation of the suprasylvian gyrus, which was damaged in ablation of the hippocampus, and four dogs served as intact controls. After the surgery or rest period, the dogs were tested for their retention (10‐s delay), and then they were given additional tests with extended delays (30, 60, and 120 s) and with distractions during the 60‐s delay period. In comparison with both control groups, dogs with hippocampal ablations had moderately impaired postoperative retention, as evidenced by the elevated numbers of errors on criterion. In subsequent stages of testing with extended delays, the impairment was greater and was significantly correlated with the extent of injury to the hippocampus. These data, together with an analysis of the animals' responses to the three‐choice situation, indicate that in dogs lesions of the hippocampus impair spatial memory. © 1995 Wiley‐Liss, Inc.