bluuebunny/crossref_metadata_2025_split huggingface dataset:
Monkey hippocampal neuron responses to complex sensory stimulation during object discrimination
Authors: Tamura Ryoi , Ono Taketoshi , Fukuda Masaji , Nishijo Hisao 
Published: May 2005

AbstractThe purpose of this study was to investigate, during the performance of an object discrimination task, responses of neurons in the monkey hippocampal formation to the sight of several objects that have biological meaning, and compare these responses with those of amygdalar neurons studies previously using the same task. Neuronal activity in the hippocampal formation of conscious monkeys was recorded during performance of a task that led to presentation of familiar rewarding, familiar aversive, or unfamiliar objects. Of 864 neurons recorded in the hippocampal formation and adjacent cortices, 160 (18.5%) responded to the sight of a certain object(s). Responses to the sight of different kinds of objects were analyzed in detail. Nondifferential neurons (n = 73) responded to different objects with no significant difference in response magnitudes, and differential neurons (n = 87) responded to different objects with different response magnitudes. Of the differential neurons, 23 responded more strongly to rewarding objects than to other objects (rewarding‐object‐dominant neurons), but the magnitude of responses to objects did not necessarily correlate with the order of preference to the objects as determined from observation of animal behavior. Aversive‐object‐dominant neurons (n = 13) responded more to aversive objects than to other objects. Unfamiliar‐object‐dominant neuron (n = 7) responded more to unfamiliar objects than to familiar objects. Selective neurons (n = 10) responded selectively to only one object or one category of objects. Fourteen of the rewarding‐ or aversive‐object‐dominant neurons were tested in extinction or reversal trials. In 12 of 14 neurons, responses to a rewarding or aversive object did not change, or slightly weakened, in extinction or reversal trials. The results suggest the following. (1) Responses of rewarding‐or aversive‐object‐dominant neurons may be involved in object‐reward or object‐aversion association. However, responses of many of these neurons might reflect past inputs related to reinforcement rather than extant emotional processing. (2) Responses of unfamiliar‐object‐dominant neurons may be involved in recognition of objects based on their familiar or unfamiliar aspects. These results are further discussed and compared with responsiveness of amygdalar neurons.
Amygdala kindling‐induced seizures selectively impair spatial memory. 1. Behavioral characteristics and effects on hippocampal neuronal protein kinase C isoforms
Authors: Beldhuis Hans J. A. , Everts Henk G. J. , Van der Zee Eddy A. , Luiten Paul G. M. , Bohus Béla 
Published: May 2005

AbstractProtein kinase C (PKC) comprises a family of kinases consisting of nine subspecies that are differentially distributed in the central nervous system. This implies distinct functions. Its involvement is suggested in cellular and molecular mechanisms by which the hippocampus exerts influence on information processing. In this study, it was questioned whether abnormal activity in the neuronal substrate, particularly the hippocampal formation, induced by amygdala kindling indeed impairs spatial memory performance and correlated α, βI/II, and γ PKC subspecies expression. Rats were trained in a spatial discrimination task (SDT) and simultaneously kindled in the amygdala to induce abnormal, epileptiform activity. Control rats were only trained in the holeboard, a “free choice” maze, in which working (WM) and reference memory (RM) were simultaneously examined. Halfway through and at the end of the experiments the influence of kindling and SDT training on the immunoreactivity for PKC subspecies α, βI/II, and γ was evaluated in the hippocampal formation. Kindling resulted in a gradual increase in afterdischarge duration and motor seizure (MS) severity. Repeated SDT training ultimately resulted in an asymptotic level of WM and RM performance. As soon as generalized MSs developed, kindled rats failed to improve RM, whereas WM was not influenced. Compared to untrained rats, in trained controls PKCγ but not PKCαβI/II immunoreactivity was elevated in CA1 pyramidal and dentate gyrus granular cells. Generalized but not partial MSs abolished these alterations in PKCγ immunoreactivity. The present data indicate that repeated training in a SDT affects the expression of PKC subspecies γ but not of α or β in the rat hippocampus. Generalized epileptiform activity impair both acquisition of new spatial RM information and PKCγ expression. It is argued that PKCγ plays a role in cellular mechanisms through which pathological brain activity impairs certain aspects of spatial memory.
Inverted‐U relationship between the level of peripheral corticosterone and the magnitude of hippocampal primed burst potentiation
Authors: Diamond David M. , Bennett M. Catherine , Fleshner Monika , Rose Gregory M. 
Published: May 2005

AbstractStudies have shown that peripheral levels of corticosterone correlate with the magnitudes of two well‐described physiological models of memory, long‐term potentiation (LTP) and primed burst (PB) potentiation. In the present experiments, the authors investigated the effects of experimenter‐controlled manipulations of the levels of corticosterone on the magnitude of hippocampal PB potentiation in urethane‐anesthetized rats. Primed burst potentiation is a long‐lasting (at least 30 minutes) increase in the amplitude of the CA1 population spike and EPSP slope in response to physiologically patterned stimulation of the hippocampal commissure. The levels of serum corticosterone were controlled by implanting corticosterone pellets in adrenalectomized rats (ADX/PELLET). In the first experiment, a significant negative linear correlation between elevated (stress) levels of serum corticosterone (greater than 20 μm/dL) and the magnitude of PB potentiation in ADX/PELLET subjects (r = 0.60, P <.05) was found. In the second experiment, the shape of the corticosterone‐PB potentiation function was different at low and intermediate levels of corticosterone than it was at high levels of corticosterone: There was a positive correlation at low levels (0–10 μm/dL), a peak response at intermediate levels (11–20 μm/dL), and a negative correlation at high levels (21–93 μm/dL) of corticosterone. Thus, the overall relationship between corticosterone and PB potentiation is an inverted‐U function. These findings provide strong support for the hypothesis that corticosterone exerts a concentration‐dependent biphasic influence on the expression of hippocampal plasticity.
Phenytoin prevents stress‐ and corticosterone‐induced atrophy of CA3 pyramidal neurons
Authors: Watanabe Yoshifumi , Gould Elizabeth , Cameron Heather A. , Daniels Deborah C. , McEwen Bruce S. 
Published: May 2005

AbstractRepeated daily restraint stress and daily corticosterone administration to adult male Sprague‐Dawley rats leads to decreases in the number of branch points and length of dendrites of CA3 pyramidal neurons of the hippocampal formation. This decrease is prevented by daily administration of the antiepileptic drug phenytoin (Dilantin), which is known to interfere with excitatory amino acid release and actions. Phenytoin had no obvious effect on behavior during and after stress and failed to prevent stress‐induced reduction of body weight gain and stress‐induced increases of adrenal weight relative to body weight; it also failed to attenuate glucocorticoid‐induced diminution of the size of the thymus gland, indicating that it does not directly antagonize glucocorticoid actions. Stress‐ and corticosterone‐induced effects on dendritic length and branch point number are more pronounced on the apical, as opposed to the basal, CA3 dendrites that receive the largest mossy fiber input from the dentate gyrus. Because phenytoin is also known to prevent ischemic damage, these results are consistent with a model in which stress‐ and corticosterone‐induced CA3 dendritic atrophy is produced by excitatory amino acids released from the mossy fibers.
Age‐related loss of axospinous synapses formed by two afferent systems in the rat dentate gyrus as revealed by the unbiased stereological dissector technique
Authors: Geinisman Yuri , de Toledo‐Morrell Leyla , Morrell Frank , Persina Inna S. , Rossi Marvin 
Published: May 2005

AbstractPrevious attempts to elucidate whether a loss of hippocampal synapses occurs during aging provided conflicting results, possibly due to the unavailability, at the time, of unbiased methods for synapse quantitation. This study was designed to reexamine the issue by means of modern technical procedures that provide unbiased estimates of synaptic numbers. Groups of 14 young adult (5 months old) and 14 aged (28 months old) male Fischer‐344 rats were compared. Synapses were examined in the middle (MML) and inner (IML) molecular layer of the hippocampal dentate gyrus, where synaptic contacts are predominantly formed by different systems of afferents, the entorhinal and commissural‐associational fibers, respectively. The number of synapses per neuron was estimated with the aid of the stereological dissector technique. The results showed that the total number of synaptic contacts per neuron was significantly diminished in the MML (by 23.6%) and IML (by 22.7%) of aged rats relative to young adults. This age‐related synaptic loss involved axospinous, but not axodendritic, junctions of the MML (−24.4%) and IML (−24.0%). Both perforated and nonperforated axospinous synapses (distinguished by a discontinuous or continuous postsynaptic density, respectively) exhibited an age‐dependent decrease in numbers, though this decrease did not reach statistical significance in the case of perforated junctions of the IML. The observed age‐related loss of axospinous synapses may underlie the reduction in the amplitude of excitatory postsynaptic potentials and the decline in functional synaptic plasticity detected in the dentate gyrus of senescent rats.
Spiny neurons of area CA3c in rat hippocampal slices have similar electrophysiological characteristics and synaptic responses despite morphological variation
Authors: Scharfman Helen E. 
Published: May 2005

AbstractArea CA3c is an area of morphologically diverse neurons. In addition to the presence of interneurons and pyramidal cells that are similar to those found in other subfields of area CA3, many neurons of area CA3c are different. They do not resemble interneurons, since they bear numerous spines, yet they also differ substantially from pyramidal cells in their morphology. To determine if the variants of area CA3c spiny cells are distinct physiologically as well as morphologically, intracellular recordings were made to record the electrophysiological properties of area CA3c cells in rat hippocampal slices, and each cell was identified morphologically following intracellular dye injection. The results show that the spiny cells, regardless of their often extensive morphological variation, have relatively uniform, pyramidal‐like electrophysiological properties. The aspiny cells are quite different from the spiny cells morphologically (i. e., in their paucity or complete lack of spines), and are also extremely different electrophysiologically, exhibiting features of “fast‐spiking” cells. Thus, spiny cells in area CA3c correspond to cells with pyramidal‐like electrophysiology, and the aspiny cells in area CA3c correspond to cells with interneuronal physiological properties. This correlation between structure and function appears to be a rule that pertains to each of the subfields of the hippocampus.
Modification of the responses of hippocampal neurons in the monkey during the learning of a conditional spatial response task
Authors: Cahusac Peter M. B. , Rolls Edmund T. , Miyashita Yasushi , Niki Hiroaki 
Published: May 2005

AbstractIn order to analyze the function of the hippocampus in learning, the activity of single neurons was recorded while monkeys learned a task of the type known to be impaired by damage to the hippocampus. In the conditional response task, the monkey had to learn to make one response when one stimulus was shown, and a different response when a different stimulus was shown. It had previously been shown that there are neurons in the hippocampal formation that respond in this task, to, for example, a combination of a particular visual stimulus that had been associated in previous learning with a particular behavioral response. In the present study, it was found that during such conditional response learning, the activity of 22% of the neurons in the hippocampus and parahippocampal gyrus with activity specifically related to the task altered their responses so that their activity, which was initially equal to the two new stimuli, became progressively differential to the two stimuli when the monkey learned to make different responses to the two stimuli. These changes occurred for different neurons just before, at, or just after the time when the monkey learned the correct response to make to the stimuli. In addition to these neurons, which had differential responses that were sustained for as long as the recordings continued, another population of neurons (45% of those with activity specifically related to the task) developed differential activity to the two new stimuli, yet showed such differential responses transiently for only a small number of trials at about the time when the monkey learned. These findings are consistent with the hypothesis that some synapses on hippocampal neurons modify during this type of learning so that some neurons come to respond to particular stimulus‐response associations that are being learned. Further, the finding that many hippocampal neurons started to reflect the new learning, but then stopped responding differentially (the transient neurons), is consistent with the hypothesis that the hippocampal neurons with large sustained changes in their activity inhibited the transient neurons, which then underwent reverse learning, thus providing a competitive mechanism by which not all neurons are allocated to any one learned association or event.
Changes in protein kinase C isozymes in the rat hippocampal formation following hippocampal lesion
Authors: Shimohama Shun , Saitoh Tsunao , Gage Fred H. 
Published: May 2005

AbstractThe cellular and regional distribution of the four protein kinase C (PKC) isoforms in the rat hippocampal formation and the response of PKC to lesions were determined by employing immunohistochemical and immunochemical techniques with antibodies specific to PKC (α), ‐(β I), ‐(β II), and ‐(γ). PKC (α) intensely stained the periphery of the pyramidal cell in the stratum pyramidale. The granule cells, glial cells, and mossy fibers were anti‐PKC (α) negative. The cytoplasm, axons, and dendrites of basket cells and interneurons in the hilus were labeled with anti‐PKC (α). Anti‐PKC (β I) immunoreactivity was localized on the periphery of pyramidal cells and interneurons of the hilus, as well as the oriens, radiatum, and molecular layers of the CA regions. Anti‐PKC (β II) immunoreactivity was mainly cytoplasmic, extending into the dendrites in the hippocampal pyramidal cells and the dentate granule cells, and also in some glial cells. In the stratum radiatum of the CA1, anti‐PKC (γ) immunoreactivity localized to the pyramidal cell cytoplasm, extending into the dendrites. Following fimbria‐fornix (FF) lesions, the anti‐PKC (α) and ‐(β I) staining of the pyramidal cell periphery was markedly reduced. The anti‐PKC (γ) staining of the pyramidal and granular cells of the dentate gyrus was reduced whereas the interneuron staining in the hilus was increased. In the FF‐lesioned hippocampus, anti‐PKC (α) and antiαPKC (β II) labeled reactive glial cells, whereas anti‐PKC (β I) and ‐(γ) did not. Quantitative Western blot analysis revealed a dramatic increase in the particulate/total PKC for all isozyme forms, although the total levels of PKC, except PKC (γ), did not change following FF lesions. The PKC (γ) concentration doubled after FF lesions. Perforant path lesions resulted in a marked alteration in the neuronal staining in dentate gyrus with anti‐PKC (α) and ‐(β I) and in increased numbers of anti‐PKC (α)‐ and anti‐PKC (β II)‐positive glial cells. Anti‐PKC (γ) staining did not change noticeably. The total PKC concentration did not change for isozymes α, β I, and γ, but PKC (βII) concentration increased by 48% following perforant path lesions as detected by Western blot analysis. The particulate/total PKC decreased for all four isozymes although the reduction in PKC (β I) concentration was not statistically significant. This change in PKC compartmentalization is in marked contrast to an increased level of particulate PKC following FF lesions. Thus, the effects of deefferentation and deafferentation for each PKC isoform were different.
Quantal analysis of modulating action of adenosine on the mossy fiber synapse in hippocampal slices
Authors: Yamamoto Chosaburo , Sawada Satsuki , Ohno‐Shosaku Takako 
Published: May 2005

AbstractAlthough adenosine has been considered to depress release of neurotransmitter in central synapses, evidence for this notion is circumstantial. To obtain more direct and quantitative evidence, the suppressing action of adenosine on transmission through the mossy fiber synapse was examined by a quantal analysis in thin transverse sections of the guinea pig hippocampus. Adenosine suppressed excitatory postsynaptic potentials (EPSPs) induced in CA3 neurons by activation of single mossy fibers to 57 ± 19% at 10 μM (6 neurons). The input resistance of the postsynaptic neurons was reduced to 84 ± 5%. The suppression of the unitary EPSPs was accompanied by a reduction of the mean quantal content (m) to 51 = 13% with no significant decrease in mean quantal amplitude (q). These findings indicate that adenosine at 10 μM suppresses transmission through mossy fiber synapses mainly by depressing release of transmitter. This study provides direct evidence for the presynaptic action of adenosine on central synapses for the first time.
Hippocampal circuitry complicates analysis of long‐term potentiation in mossy fiber synapses
Authors: Claiborne Brenda J. , Xiang Zixiu , Brown Thomas H. 
Published: May 2005

AbstractMuch of the current interest in the hippocampus concerns a rapid and persistent form of synaptic plasticity, called long‐term potentiation (LTP), that is a candidate substrate for some of the mnemonic functions of this structure. There are at least two kinds of LTP in the hippocampus. One form is found at the synapse between the mossy fibers of the granule cells and the pyramidal neurons of the CA3 region. Attempts to examine the mechanism underlying this form of LTP have yielded contradictory conclusions. The authors show how the complex circuitry of the dentate gyrus and adjacent hippocampus may have caused the contradictions. To overcome problems introduced by the circuitry, a specific set of procedures and criteria for evoking and identifying mossy fiber responses is proposed. Use of these or similar procedures and criteria will improve the design and interpretation of experiments on mossy fiber LTP and allow more informative comparisons among species and brain regions and across laboratories.
Hippocampal synaptic enhancement and spatial learning in the morris swim task
Authors: Korol Donna L. , Abel Ty W. , Church Lloyd T. , Barnes Carol A. , McNaughton Bruce L. 
Published: May 2005

AbstractThe authors attempted to replicate the study of Castro, Silbert, McNaughton, and Barnes (1989) in which it was concluded that bilateral saturation of hippocampal synaptic enhancement produced a deficit in acquisition of a spatial navigation problem in the Morris swim task. The original protocol was followed as closely as possible, but no effect of long‐term enhancement (LTE) saturation on spatial performance in this task was found. This negative result suggests either that the previous finding using the swim task reflected statistical error or that some as yet undetermined variable is of critical importance in this phenomenon. The present negative finding also raises a question concerning the reproducibility of the earlier results of McNaughton, Barnes, Rao, Baldwin, and Rasmussen (1986) in which LTE saturation apparently led to a prolonged deficit on a different spatial task. Although negative results in such experiments do not constitute grounds for rejecting the underlying hypothesis, the present lack of a positive effect renders uncertain, for the time being, one of the lines of experimental support for the theory that LTE at hippocampal synapses reflects a mechanism for the associative, distributed storage of new spatial information.
An examination of the relations between hippocampal long‐term potentiation, kindling, afterdischarge, and place learning in the water maze
Authors: Cain Donald P. , Hargreaves Eric L. , Boon Francis , Dennison Zoe 
Published: May 2005

AbstractTwo approaches were used to study the relations between the acquisition of place learning in the Morris water maze and long‐term potentiation (LTP), kindling, and afterdischarge (AD). In the first, the possibility of behavioral LTP in the dentate gyrus field potential evoked by stimulation of the perforant path was evaluated in rats that showed robust place learning in the water maze. There was no effect of place learning on the field potential, and field potential measures did not correlate with place learning acquisition measures. In the second approach, the effect of bilateral saturation of LTP on subsequent place learning in the water maze task, begun within 5 minutes of the last LTP session, was evaluated. The effect of kindled seizures evoked bilaterally from the perforant path, or of a single unilateral AD, on acquisition of the water maze task (begun within 10 minutes) were also evaluated. Bilateral LTP saturation did not affect place learning, and the bilateral LTP group learned as readily as controls. In contrast, the kindled and AD groups were severely impaired in their performance of the place learning task. A second day of training in the water maze without any further electrical stimulation indicated that these groups had acquired considerable information on the first day of maze training and were not distinguishable from controls on the second day of training. This indicated that the deficit in these groups on the first day of training was temporary and likely resulted from a temporary perturbation of normal brain function due to the seizures. The results indicate that bilateral saturation of LTP in the dentate gyrus does not affect place learning in the water maze. They also indicate that recent hippocampal seizures, but not kindling, disrupt place learning in this task.