bluuebunny/crossref_metadata_2025_split huggingface dataset:
Transport of cytoskeletal proteins in axons of hippocampal pyramidal cells
Authors: Watson Danny F. , Fittro Kenneth P. 
Published: May 2005

AbstractAxonal transport of cytoskeletal proteins has not yet been extensively studied in the brain proper, in contrast to the peripheral nerves and optic nerves. The authors have developed a means for the study of transport of cytoskeletal proteins in axons of hippocampal pyramidal cells. Proteins of intrinsic neurons of the dorsal hippocampus were labeled by microinjection of 35S methionine, and the subsequent transport of labeled proteins was characterized in the axons projecting into the fimbria‐fornix. A peak of labeled proteins was present in the fimbria‐fornix at 4–12 days after labeling, corresponding to transport rates 0.2–0.7 mm/day. The most abudant proteins at each time studied exhibited one‐dimensional electrophoretic mobilites of actin and tubulin; neurofilaments were less intensely labeled. The observed specializations of cytoskeletal transport, especially the paucity of tubulin transport at rates of 2–4 mm/day, may predispose hippocampal pyramidal cells to accumulate tubulin and microtubule‐associated proteins in their cell bodies in various disease states.
Pathway specificity of noradrenergic plasticity in the dentate gyrus
Authors: Pelletier Marc R. , Kirkby R. Duncan , Jones Sandra J. , Corcoran Michael E. 
Published: May 2005

AbstractPrevious experiments have described highly specific effects of noradrenergic agonists on synaptic transmission in the dentate gyrus (DG). For example, perfusion of hippocampal slices with the beta‐noradrenergic agonist isoproterenol induces a long‐lasting potentiation (LLP) of extracellularly recorded responses following stimulation of the medial perforant path (PP), and long‐lasting depression (LLD) of responses evoked by stimulation of the lateral PP (Dahl D, Sarvey JM, 1989, Proc Natl Acad Sci USA 86:4776–4780). To examine the possible interactions of LLP, LLD, and long‐term potentiation induced by tetanic stimulation (LTP), the authors recorded extracellular field potentials evoked in the DG by stimulation of the lateral or medial perforant path following LTP and LLP or LLD, invoked in different orders. After establishment of LLP or LLD by path application of isoproternol, subsequent tetanization of the respective afferents resulted in additional potentiation of the medial PP‐evoked response and return of the lateral PP‐evoked response to baseline levels. In other slices application of isoproterenol after establishment of LTP resulted in further potentiation of medial PP‐evoked responses but no change in the potentiated response evoked by lateral PP stimulation. Thus the pathway specificity was maintained irrespective of the history of previous potentiation or depression. Experiments using the specific beta1 antagonist metoprolol further confirmed pathway specificity. Perfusion with 20 μM of metoprolol appeared to reduce LTP evoked by stimulation of the medial but not lateral PP. In a subsequent experiment, metoprolol in the absence of tetanization produced LLD of the medial PP‐evoked response and LLP of the lateral PP‐evoked response, opposite to the effects of ISO. These results confirm the impressive extent of pathway specificity in the DG and reveal the persistent capacity for synaptic modification as exemplified by the processes of LLP, LLD, and LTP. © 1994 Wiley‐Liss, Inc.
Selective degeneration of CA1 pyramidal cells by chronic application of bismuth
Authors: Müller Michael , Rietschin Lotty , Grogg Franziska , Streit Peter , Gähwiler Beat H. 
Published: May 2005

AbstractThe heavy metal bismuth induces a new type of selective neuronal degeneration that shares some common aspects with that seen following hypoxia and ischemia. Continuous application of 3 μm bismuth to organotypic cultures of rat hippocampus resulted after 2–3 weeks in selective degeneration of CA1 pyramidal cells, while CA3 pyramidal cells, dentate granule cells, and subicular neurons were resistant. With 10 μm MK‐801, a noncompetitive NMDA‐antagonist, during the entire culturing period failed to prevent neuronal degeneration induced by 3 μm bismuth. GABA‐immunoreactive interneurons were also affected by bismuth, but were generally less sensitive than CA1 pyramidal cells. Acute application of up to 100 μm bismuth did not change the electrophysiological properties of CA1 pyramidal cells. © 1994 Wiley‐Liss, Inc.
Postmortem changes in the levels and localization of microtubule‐associated proteins (tau, MAP2 and MAP1B) in the rat and human hippocampus
Authors: Schwab Claudia , Bondada Vimala , Sparks D. Larry , Cahan Leslie D. , Geddes James W. 
Published: May 2005

AbstractThe neuronal cytoskeleton is disrupted in neurodegenerative disorders such as Alzheimer's disease. Due to the lack of suitable animal models, studies examining the events involved in the neurodegeneration have relied on postmortem human brain tissue obtained from individuals with the disease and from normal controls. However, it is uncertain if the neuronal cytoskeleton is stable during the postmortem interval. Immunohistochemistry and immunoblots were used to examine the microtubule–associated proteins tau, MAP2, and MAP1B in the rat hippocampus at various times after death. Shortly after death, tau immunoreactivity was lost from axons and accumulated in somatodendritic compartments. MAP2 and MAP1B also accumulated in neuronal cell bodies prior to a loss of immunostaining in some regions, notably subiculum. Immunoblots confirmed a loss of MAP2 and MAP1B within a few hours after death. Tau levels remained constant during the 8–hour postmortem interval examined, although the electrophoretic mobility of some tau bands was altered. Human brain tissue obtained at autopsy and at surgery demonstrated similar cytoskeletal alterations in postmortem tissue. These results demonstrate that microtubules and associated proteins are not stable postmortem. © 1994 Wiley‐Liss, Inc.
Principal cells are the postsynaptic targets of supramammillary afferents in the hippocampus of the rat
Authors: Maglóczky Zsófia , Acsády László , Freund Tamás F. 
Published: May 2005

AbstractNeurons of the supramammillary nucleus are known to fire phase‐locked to hippocampal theta rhythm. Stimulation of this area induces theta activity in the hippocampus via the medial septum and facilitates perforant pathway stimulation‐evoked population spikes in the dentate gyrus even if the medial septum is inactivated. This latter effect was suggested to be due to a direct inhibitory input from the supramammilary nucleus to hippocampal nonpyramidal cells resulting in disinhibition. In the present study, using anterograde tracing with Phaseolus vulgaris leucoagglutinin, we aimed to identify the types of neurons innervated by the supramammillary projection in the dentate gyrus and Ammons horn, with particular attention to the presumed postsynaptic inhibitory neurons, which may mediate the proposed disinhibitory action. Double‐immunostaining for the tracer and different neuropeptides (somatostatin, cholecystokinin, neuropeptide Y) or calcium binding proteins (calretinin, parvalbumin, calbindin D28k) present in different subpopulations of interneurons revealed no multiple contacts between supramammillary afferents and labeled inhibitory cells at the light microscopic level. Furthermore, postembedding immunostaining of electron microscopic sections for GABA demonstrated that none of the 68 PHAL‐labeled supramammillary boutons examined and none of their postsynaptic targets were immunoreactive for the inhibitory neurotransmitter. We conclude, therefore, that most if not all postsynaptic targets of the supramammillary projection are principal cells both in the dentate gyrus and in the CA2‐CA3a subfields. This suggests that a mechanism other than disinhibition is responsible for the facilitatory effect of this pathway on hippocampal evoked activity. © 1994 Wiley‐Liss, Inc.
Spatial information content and reliability of hippocampal CA1 neurons: Effects of visual input
Authors: Markus Etan J. , Barnes Carol A. , McNaughton Bruce L. , Gladden Victoria L. , Skaggs William E. 
Published: May 2005

AbstractThe effects of darkness on quantitative spatial firing characteristics of 235 hippocampal CA1 “complex spike” (CS) cells were studied in young and old Fischer‐344 rats during food‐motivated performance of a randomized, forced‐choice task on an eight‐arm radial maze. The room lights were turned on or off on alternate blocks of all eight arms.In the dark, a lower proportion of CS cells had “place fields,” and the fields were less specific and less reliable than in the light. A small number of cells had place fields unique to the dark condition. Like CS cells, Theta cells showed a reduction in spatially related firing in the dark. The specificity and reliability of the place fields under both light and dark conditions were similar for both age groups. Increasing the salience of the environment, by increasing the light level and the number of visual cues in the light condition, did not affect the specificity or reliability of the place fields.Even though all rats had substantial prior experience with the environment, and were placed on the maze center under normal illumination before the first dark trial, the correlation between the firing pattern in the light and dark increased after the rat first traversed the maze in the light. Thus, even after considerable experience with the environment over days, experiencing the illuminated environment from different locations on a given day was a significant factor affecting subsequent location and reliability of place fields in darkness.While the task was simple and errors rare, rats that made fewer errors (i.e., re‐entries into the previously visited arm) also had more reliable place cells, but no such correlation was found with place cell specificity. Thus, the reliability of spatial firing in the hippocampus may be more important for spatial navigation than the size of the place fields per se. Alternatively, both spatial memory and place field reliability may be modulated by a common variable, such as attention. © 1994 Wiley‐Liss, Inc.
Ipsilateral associational pathway in the dentate gyrus: An excitatory feedback system that supports N‐methyl‐D‐aspartate—dependent long‐term potentiation
Authors: Hetherington Phil A. , Austin Kevin B. , Shapiro Matthew L. 
Published: May 2005

AbstractAxons from granule cells in the dentate gyrus of the rat hippocampus project to cells in the hilar region, including mossy cells, which project along the longitudinal axis of the hippocampus and synapse in the inner (proximal) one‐third of the molecular layer of the dentate gyrus. To study this feedback system, multiple recording electrodes were located along the longitudinal (septo‐temporal) axis in the dorsal leaf of the dentate gyrus in urethane‐anesthetized rats. Single pulse electrical stimuli delivered to the hilar region evoked negative‐going, monosynaptic field potentials that were largest in the inner one‐third of the molecular layer (commissural zone). These evoked field potentials (EFPs) were recorded simultaneously at three to five locations. The latency to onset and peak amplitude of the EFP varied linearly with distance from point of stimulation, and EFPs were elicited in both directions along the longitudinal axis. The transmission speed was estimated to be 1.4 m/s. Tetanic stimulation of the hilar region potentiated the EFP slopes (mean= 26%). Potentiation lasted at least 2 hours and was specific to responses from the tetanized stimulating electrode; the responses to other stimulating electrodes in the hilus and the angular bundle of the perforant path changed less than 4%. Combined stimulation of the hilus and the medial perforant path increased the magnitude of recorded field potentials and population spikes, demonstrating that both pathways are excitatory. NMDA antagonist NPC‐17742 blocked potentiation of EFP slopes in both the medial perforant path and hilus pathways. The results suggest that the ipsilateral associational system of the dentate gyrus is excitatory and capable of supporting long‐lasting, NMDA‐dependent, synapse‐specific plasticity. © 1994 Wiley‐Liss, Inc.
Differential NPY mRNA expression in granule cells and interneurons of the rat dentate gyrus after kainic acid injection
Authors: Gruber Bernhard , Greber Susanne , Rupp Elke , Sperk Günther 
Published: May 2005

AbstractUsing in situ hybridization histochemistry neuropeptide Y (NPY) mRNA expression was investigated after intraperitoneal injection of kainic acid (KA) and after local application of KA or quinolinic acid into the dentate gyrus of the rat. Enhanced concentrations of NPY mRNA were observed in interneurons of the hilus, including presumptive fusiform neurons and pyramidal‐shaped basket cells already 4 hours after initiation of limbic seizures by KA (10 mg/kg, i.p.). IncreaseD NPY expression persisted in neurons resistant to seizure‐induced cell death (6–48 h after i.p. KA). Exceptionally high hybridization signals were found in interneurons of the hilus and the CA1 and CA3 sectors 8 months after KA‐induced limbic seizures. In the granule cell layer only a transient but pronounced increase in NPY mRNA was observed 12–24 h after injection. Only moderate changes were observed in this cell layer at later intervals. Anticonvulsant treatment with thiopental, after a brief period of generalized seizures, prevented the increase in NPY mRNA in granule cells but not in interneurons. No change in NPY message was found also in granule cells of rats which responded with mild “wet dog shake” behvior but not with motor seizures to KA injection.Local injections of low doses of KA (0.05–0.2 nmol) or quinolinic acid (6.5–100 nmol) into the dentate gyrus of the hippocampus under deep thiopental anesthesia, after 24 h, resulted in increased concentrations of NPY message in interneurons of the ipsilateral, but not of the contralateral hilus and not in granule cells. Higher doses of the excitatory amino acid analogs caused partial neurodegeneration at the injection site, but enhanced NPY expression in interneurons of the contralateral dentate. Only the highest dose of quinolinic acid (100 nmol), resulting in general neuronal cell loss at the injection area, induced enhanced NPY mRNA expression also in granule cells of the contralateral dentate gyrus.The experiments suggest different mechanisms for NPY mRNA expression in interneurons and in granule cells of the dentate gyrus. Whereas in the stratum granulosum NPY mRNA expression was only observed after generalized limbic seizures, in hilar interneurons it was augmented by only moderate neuronal stimulation or directly by KA. © 1994 Wiley‐Liss, Inc.
Severity of memory impairment in monkeys as a function of locus and extent of damage within the medial temporal lobe memory system
Authors: Zola‐Morgan Stuart , Squire Larry R. , Ramus Seth J. 
Published: May 2005

AbstractDuring the past decade, work with monkeys has helped identify the structures in the medial temporal lobe that are important for memory: the hippocampal region (including the hippocampus proper, the dentate gyrus, and the subicular complex) and adjacent cortical areas that are anatomically linked to the hippocampus, i.e., the entorhinal, perirhinal, and parahippocampal cortices. One idea that has emerged from this work is that the severity of memory impairment might increase as more components of the medial temporal lobe are damaged. We have evaluated this idea directly by examining behavioral data from 30 monkeys (ten normal monkeys and 20 monkeys with bilateral lesions involving structures within the medial temporal lobe) that have completed testing on our standard memory battery during the last 10 years. The main finding was that the severity of memory impairment depended on the locus and extent of damage to the medial temporal lobe. Specifically, damage limited to the hippocampal region produced a mild memory impairment. More severe memory impairment was produced when the damage was increased to include the adjacent entorhinal and parahippocampal cortices (the H+ lesion). Finally, memory impairment was even more severe when the H+ lesion was extended forward to include the anterior entorhinal cortex and the perirhinal cortex (H++ lesion). Taken together, these findings suggest that, whereas damage to the hippocampal region produces measurable memory impairment, a substantial part of the severe memory impairment produced by large medial temporal lobe lesions in humans and monkeys can be attributed to damage to entorhinal, perirhinal, and parahippocampal cortices adjacent to the hippocampal region. © 1994 Wiley‐Liss, Inc.
Sprouting of central noradrenergic fibers in the dentate gyrus following combined lesions of its entorhinal and septal afferents
Authors: Peterson Gray M. 
Published: May 2005

AbstractVirtually all of the afferents to the hippocampal formation undergo collateral sprouting after removal of adjacent afferent systems. However, the central noradrenergic (NA) afferents, which demonstrate a remarkable propensity for regeneration and sprouting in other regions of the brain, have not been found to sprout in the denervated hippocampal formation. The present study was designed to determine if the pattern of innervation by NA fibers in the dentate gyrus of adult rats can be altered by interruption of the other major afferents. The innervation pattern of NA fibers was examined in the dentate gyrus 4 weeks after removal of the ipsilateral and/or contralateral entorhinal afferents and/or transection of the fimbria‐fornix and supracallosal stria. The noradrenergic identity of the fibers was indicated by immunoreactivity for dopamine beta hydroxylase (DBH) and peripheral sympathetic fibers were demonstrated by immunoreactivity for nerve growth factor receptor (NGFr), which did not stain cholinergic fibers in this application. In control brains, the noradrenergic innervation of the dentate molecular layer was light and uniform across the width of the layer. Transection of the perforant path (ipsilateral entorhinal afferents) or ventral hippocampal commissure (contralateral entorhinal afferents) resultd in a significant increase in innervation density in the outer half of the molecular layer, and the combination of these two lesions produced the greatest increase. In those brains with transection of the ipsilateral and contralateral entorhinal afferents, the denervated dentate gyrus had a nearly twofold increase in density of DBH‐immunoreactive fibers within the outer half of the molecular layer. These fibers tended to course parallel to the pial surface rather that perpendicular as in control sections. Transection of the fimbria‐fornix alone had no affect on the innervation pattern of DBH‐ir fibers in the molecular layer. When the fimbria‐fornix was transected in combination with both of the other lesions, an overall increase in innervation density occurred, but there was no further increase in the difference between the inner and outer halves of the molecular layer. No NGFr‐immunoreactive fibers were observed in the molecular layer in any of the brains, indicating that the DBH‐immunoreactive fibers in this region were not of peripheral origin. It is concluded that removal of the ipsi‐ and contralateral entorhinal afferents to the dentate gyrus results in the sprouting of central NA fibers in the outer half of the molecular layer. © 1994 Wiley‐Liss, Inc.
Extrinsic modulation of medial septal cell discharges by the ascending brainstem hippocampal synchronizing pathway
Authors: Bland Brain H. , Oddie Scott D. , Colom Luis V. , Vertes Robert P. 
Published: May 2005

AbstractSingle cells or simultaneously recorded cell pairs in the medial septum (MS) vertical limb of the diagonal band of Broca (vDBB) in the urethane‐anesthetized rat were initially classified as either theta‐on or non‐related according to the system of Colom and Bland (1987, Brain Res 422:277–286). Subgroups of these cells were then studied under various test conditions that included electrical stimulation of the nucleus pontis oralis (PO) or posterior hypothalamus (PH), microinfusion of carbachol into the PO or PH, and the microinfusion of atropine sulfate or procaine hydrochloride into the PH. Electrical stimulation of either the PO or PH induced theta (θ) activity in the hippocampal formation (HPC), and electrical stimulation of the PO resulted in a simultaneous increase in the discharge rate of all MS/vDBB θ‐on cells tested, compared to the rates recorded during HPC large‐amplitude irregular activity (LIA). Five of the MS/vDBB θ‐on cells were tested consecutively with electrical stimulation of the PO and PH, and were shown to be activated in a similar manner in either condition. Microinfusion of carbachol into either the PO or PH resulted in the induction of HPC θ field activity and the simultaneous intense activation of all MS/vDBB θ‐on cells tested. Following the microinfusion of either atropine sulfate or procaine into the PH, electrical stimulation of the PO failed to induce HPC θ field activity or the concomitant rhythmic discharges of all MS/vDBB phasic θ‐on cells tested. Microinfusing procaine into the PH also abolished the coupling between all MS/vDBB cell pairs during HPC θ field activity including that between two cell pairs that were coupled during HPC LIA. The data support the following conclusions: (1) The brainstem HPC synchronizing pathway originating in the pons region ascends to the medial septum via the midline posterior hypothalamic region; (2) the present results taken together with previous work suggest that a major component of the ascending synchronizing pathway, up to and including the hippocampal formation, is cholinergic, cholinoceptive, or both, and the receptors involved are primarily muscarinic; (3) the midline posterior hypothalamic region is an important source of inputs to the medial septum and their major contribution is to provide frequency‐coded inputs to the MS/vDBB for relay into the hippocampal formation. © 1994 Wiley‐Liss, Inc.