bluuebunny/crossref_metadata_2025_split huggingface dataset:
Hippocampal mediation of stimulus representation: A computational theory
Authors: Gluck Mark A. , Myers Catherine E. 
Published: May 2005

AbstractThe authors propose a computational theory of the hippocampal region's function in mediating stimulus representations. The theory assumes that the hippocampal region develops new stimulus representations that enhance the discriminability of differentially predictive cues while compressing the representation of redundant cues. Other brain regions, including cerebral and cerebellar cortices, are presumed to use these hippocampal representations to recode their own stimulus representations. In the absence of an intact hippocmpal region, the theory implies that other brain regions will attempt to learn associations using previously established fixed representations. Instantiated as a connectionist network model, the theory provides a simple and unified interpretation of the functional role of the hippocampal region in a wide range of conditioning paradigms, including stimulus discrimination, reversal learning, stimulus generalization, latent inhibition, sensory preconditioning, and contextual sensitivity. The theory makes novel predictions regarding the effects of hippocampal lesions on easy‐hard transfer and compound preexposure. Several prior qualitative characterizations of hippocampal function–including stimulus selection, chunking, cue configuration, and cotextual coding–are identified as task‐specific special cases derivable from this more general theory. The theory suggests that a profitable direction for future empirical and theoretical research will be the study of learning tasks in which both intact and lesioned animals exhibit similar initial learning behaviors but differ on subsequent transfer and generalization tasks.
Flip side of synaptic plasticity: Long‐term depression mechanisms in the hippocampus
Authors: Christie Brian R. , Kerr D. Steven , Abraham Wickliffe C. 
Published: May 2005

AbstractThere is growing interest in the phenomenon of long‐term depression (LTD) of synaptic efficacy that, together with long‐term potentiation (LTP), is a putative information storage mechanism in mammalian brain. In neural network models, multiple learning rules have been used for LTD induction. Similarly, in neurophysiological studies of hippocampal synaptic plasticity, a variety of activity patterns have been effective at inducing LTD, although experimental paradigms are still being optimized. In this review the authors summarize the major experimental paradigms and compare what is known about the mechanisms of LTD induction. Although all paradigms appear to initiate a cascade of events leading to an elevated level of Ca2+ postsynaptically, the extent to which these paradigms involve common expression mechanisms has not yet been tested. The authors discuss several critical experiments that would address this latter issue. Numerous questions about the properties and mechanisms of LTD(s) in the hippocampus remain to be answered, but it is clear that LTD has finally arrived, and will soon be attracting attention equal to its flip side, LTP. © 1994 Wiley‐Liss, Inc.
Dissociation between long‐term potentiation and associated changes in field epsp waveform in the hippocampal CA1 region: An in vitro study in guinea pig brain slices
Authors: Asztely F. , Gustafsson B. 
Published: May 2005

AbstractThe present study examines changes in field excitatory postsynaptic potential (EPSP) waveform in association with long‐term potentiation (LTP) in the CA1 region of the hippocampal slice preparation. Experiments were performed in the presence of the GABAA‐antagonist picrotoxin. With test field EPSP about one‐third the size of that evoking spike activity (measured in the cell body layer along the same somatodendritic axis as the dendritic recording) a decreased decay time constant (approximately 8%) was seen in association with LTP. This change in field EPSP waveform was not associated with any apparent spike activity in the cell body recording. Nevertheless, several findings suggest that increased spike activity explains the change in the decay time constant of the field EPSP during LTP. First, when reducing the stimulation strength after the induction of LTP to obtain a field EPSP of the same magnitude as the pretetanus one, the change of the decay time constant was reduced to only 2.8%. Second, when using small test field EPSP (about one‐fourth the size of that evoking spike activity) the decay time constant was not significantly affected in association with LTP. Third, when cutting the slice in such a manner that spike activity originating from somatic regions closer to the stimulating electrode was removed, the EPSPs decay time constant was not significantly affected in association with LTP. It is concluded that LTP is not associated with a change in the shape of the field EPSP. © 1994 Wiley‐Liss, Inc.
Somatostatin‐immunoreactivity in the hippocampus of mouse, rat, guinea pig, and rabbit
Authors: Buckmaster Paul S. , Kunkel Dennis D. , Robbins Richard J. , Schwartzkroin Philip A. 
Published: May 2005

AbstractThe hippocampi of species commonly used for in vitro physiologic studies were examined to determine if there were species‐specific and regional differences in somatostatin immunoreactivity. The distributions of somatostatin‐immunoreactive somata and fiber plexuses were determined, and the concentration of somatostatin along the septotemporal axis of the hippocampus was measured using a radioimmunoassay. There are many similarities in the patterns of somatostatin immunoreactivity in the hippocampi of mice, rats, guinea pigs, and rabbits. All species had a relatively even distribution of somatostatin‐positive perikarya across three fields of the hippocampus (dentate gyrus, CA3, and CA1‐2), a similar distribution of somatostatin‐immunoreactive perikarya across the strata of the CA1‐2 field and the dentate gyrus; and more somatostatin‐positive cells in temporal than in septal hippocampus. However, there are species‐specific differences in the distribution of somatostatin‐immunoreactive perikarya across the strata of CA3. In addition, unlike the other species examined, mice appeared not to have a somatostatin‐immunoreactive fiber plexus in the molecular layer of the dentate gyrus. The functional significance of these differences remains to be determined. © 1994 Wiley‐Liss, Inc.
Glutamatergic hippocampal formation projections to prefrontal cortex in the rat are regulated by GABAergic inhibition and show convergence with glutamatergic projections from the limbic thalamus
Authors: Gigg John , Tan Aiko M. , Finch David M. 
Published: May 2005

AbstractAnatomic and physiologic studies in the rat have shown projections from the hippocampal formation (HF) and mediodorsal (MD) thalamic nucleus to the medial prefrontal cortex (mPFC). The authors used multi‐barrel iontophoresis to: confirm the neurotransmitter used in the projection from HF to mPFC; investigate the role of GABAergic inhibition in the regulation of this projection; and examine the functional convergence of projections from HF and MD onto single mPFC neurons. During HF stimulation, nine cells (6%) showed excitation followed by prolonged inhibition, 39 cells (26%) showed prolonged inhibition alone and 100 cells (68%) showed no clear response. In a further 12 cells that showed no predrug excitation to HF stimulation (representing 16% of the cells in this category), iontophoresis of the GABAA antagonist bicuculline methiodide (BMI) revealed excitatory responses. A total of six mPFC cells (38% of the cells showing excitatory responses to HF stimulation) showed convergent excitation to HF and MD thalamic (or adjacent paratenial nucleus) stimulation. Five out of eight (63%) of the predrug or BMI‐revealed excitatory responses of mPFC neurons to HF stimulation were selectively decreased after AMPA antagonist iontophoresis (either CNQX or DNQX). These data confirm that the HF projection to prefrontal cortex is, at least in part, glutamatergic; suggest that the responses of mPFC neurons to activity in this HF pathway are regulated by GABAergic inhibition; and indicate that projections from HF and MD converge onto single mPFC neurons. © 1994 Wiley‐Liss, Inc.
Hippocampal sympathetic ingrowth and cholinergic denervation alter hippocampal muscarinic cholinergic receptors
Authors: Harrell Lindy E. , Ayyagari Viswaprabhu , Peagler Andrea , Parsons Dee S. 
Published: May 2005

AbstractCholinergic denervation of the hippocampus by medial septal (MS) lesions results in the ingrowth of peripheral sympathetic fibers, originating from the superior cervical ganglia, into the hippocampus. To determine the effect of hippocampal sympathetic ingrowth (HSI) [3H]‐QNB (L‐quinuclidinyl [benzilic‐4, 4(n)] benzilate) binding was assessed in the dorsal and ventral hippocampus four weeks after MS lesions. In dorsal hippocampus, HSI was found to signignificantly increase the number (Bmax) of [3H]‐QNB binding sites and to normalize the decrease in affinity found in animals with MS lesions plus ganglionectomy (i. e., no ingrowth). In ventral hippocampus, HSI was found to normalize the increased number of binding sites and decreased affinity found in animals with MS lesions without ingrowth. No effect on either Kd or Bmax was found in animals that had undergone ganglionectomy with sham MS lesions. These results suggest that HSI can induce changes in hippocampal muscarinic cholinergic receptors. © 1994 Wiley‐Liss, Inc.
Alterations of inhibitory synaptic responses in the dentate gyrus of temporal lobe epileptic patients
Authors: Uruno Katsuhisa , O'Connor Michael J. , Masukawa Leona M. 
Published: May 2005

AbstractThe number of orthodromically evoked population spikes was used to classify brain slice tissue from the dentate gyrus of temporal lobe epileptic patients as “more excitable” (multiple population spikes) or “less excitable” (a single population spike). During orthodromic stimulation, “more excitable” tissue exhibited less paired‐pulse depression in comparison to “less excitable” tissue. During antidromic stimulaltion, both multiple population spikes and paired‐pulse depression were observed in “more excitable” tissue. “Less excitable” tissue exhibited a single antidromic spike and often on antidromically evoked paired‐pulse depression. The strength of antidromic paired‐pulse depression was correlated positively with the number of antidromic spikes and was correlated negatively with orthodromic paired‐pulse depression. Although orthodromic and antidromic paired‐pulse depression were correlated to the number of orthodromically evoked populaltion spikes, this correlation was not as strong as that between orthodromic paired‐pulse depression, antidromic paired‐pulse depression, and number of antidromically evoked population spikes.The antidromic paired‐pulse depression observed in tissue exhibiting antidromically evoked multiple population spikes was enhanced rather than blocked by bicuculline. In addition, the blockade of the antidromic paired‐pulse depression by CNQX indicated that this inhibition is mediated by an AMPA‐type glutamatergic synapse. We suggest that alterations in circuitry occur in the dentate gyrus of some temporal lobe epileptic patients and were manifested by both a loss of inhibitory input as well as an increase of inhibition, which was dependent on the pathway of stimulaltion. The results of pairing antidromic and orthodromic stimuli were consistent with these conclusions. © 1994 Wiley‐Liss, Inc.
Multideterminant role of calcium in hippocampal synaptic plasticity
Authors: Teyler Timothy J. , Cavus I. , Coussens C. , Discenna P. , Grover L. , Lee Y. P. , Little Z. 
Published: May 2005

AbstractHippocampal CA1 cells possess several varieties of long‐lasting synaptic plasticity: two different forms of long‐term potentiation (LTP) and at least one form of long‐term depression (LTD). All forms of synaptic plasticity are induced by afferent activation, all involve Ca2+ influx, all can be blocked by Ca2+ chelators, and all activate Ca2+‐dependent mechanisms. The question arises as how different physiological responses can be initiated by activation of the same second messenger. We consider two hypotheses which could account for these phenomena: voltage‐dependent differences in cytosolic Ca2+ concentration acting upon Ca2+ substrates of differing Ca2+ affinities and compartmentalization of the Ca2+ and its substrates. © 1994 Wiley‐Liss, Inc.
Spontaneous and synaptic input from granule cells and the perforant path to dentate basket cells in the rat hippocampus
Authors: Kneisler Tracy B. , Dingledine Raymond 
Published: May 2005

AbstractTo characterize excitatory inputs to dentate basket cells from dentate granule cells and the perforant path, the whole‐cell recording technique was used in neonatal rat hippocampal slices. Spontaneous excitatory input to basket cells was also examined and compared to that of other interneurons in the dentate gyrus. Basket cells were separable from other neurons in the dentate gyrus based on morphology and location, as determined by biocytin staining following recording, and by resting membrane potential, propensity to fire action potentials spontaneously, and miniature excitatory postsynaptic current (EPSC) characteristics. Minimal electrical stimulation of the granule cell layer evoked in basket cells short latency EPSCs that were composed of both N‐methyl‐D‐aspartate (NMDA) and α‐amino‐3‐hydroxy‐5‐methyl‐4‐isoxazole‐propionate (AMPA) components as judged by their time course, voltage dependence, and blockade by selective antagonists. Perforant path EPSCs exhibited slower kinetics than EPSCs evoked by granule cell stimulation. Like granule cell evoked EPSCs, however, perforant path EPSCs were composed of both NMDA and AMPA components. Minimal electrical stimulation of the granule cell layer and perforant path evoked monosynaptic EPSCs in only 67% and 62% of the trials, respectively, suggesting that these inputs are as unreliable as previously determined inputs from CA3 pyramidal cells (48%).Tetrodotoxin‐insensitive spontaneous miniature EPSCs were frequent in basket cells and non‐basket interneurons residing either at the border between the granule cell layer and the hilus or deep within the hilus. Miniature EPSCs recorded from all cells held at −70 mV were blocked completely by 3 μSM 6‐cyano‐7‐nitro‐quinoxaline‐2,3‐dione (CNQX). Though a component of the miniature EPSCs recorded from border and deep hilar interneurons at +40 mV was blocked by the NMDA receptor antagonist D‐2‐amino‐phosphonovaleric acid (D‐APV), miniature EPSCs in basket cells were insensitive to D‐APV.We conclude that input from granule cells and the perforant path results in activation of basket cells via glutamatergic synapses that employ both NMDA and AMPA receptors. These inputs to basket cells likely contribute to feedback and feedforward inhibition of granule cells. The absence of an NMDA receptor component in spontaneous miniature EPSCs of dentate basket cells implies a difference in organization of excitatory synapses made onto basket cells compared with other hilar interneurons. © 1995 Wiley‐Liss, Inc.
Changes in exploratory activity following stimulation of hippocampal 5‐HT1A and 5‐HT1B receptors in the rat
Authors: Buhot Marie‐Christine , Naili Said 
Published: May 2005

AbstractThe object exploration task allows the measure of changes in locomotor and exploratory activities, habituation, and reaction to a spatial change and to novelty. The effects of intrahippocampal (dorsal CA1 field) microinjections of serotonin 1 receptor (5‐HT1) agonists on these behavioral components were evaluated in the rat. 8‐Hydroxy‐2‐(din‐propylamino)‐tetralin (8‐OH‐DPAT,5 μg/μl) was used as a 5‐HT1A agonist, 3‐(1,2,5,6‐tetrahydropyrid‐4‐yl) pyrrolo[3,2‐b] pyrid‐5‐one (CP 93,129, 16 μg/μl) as a 5‐HT1B agonist, and scopolamine (10 μg/μl) as a muscarinic cholinergic antagonist. Scopolamine induced a long‐lasting increase in locomotor activity and a lack of reaction to spatial change; both these results are in agreement with the known crucial influence of the septo‐hippocampal cholinergic system in hippocampal functioning. Stimulation of 5‐HT1A and 5‐HT1B receptors induced a decrease in object exploration and habituation without affecting the retrieval of spatial information. But stimulation of hippocampal 5‐HT1B receptors induced a selective change in the animal's emotional state, i.e., an initial decrease in locomotor activity and a neophobic reaction in response to a new object; such effects did not occur following stimulation of 5HT1A receptors. These results have to be considered in the light of the anxiogenic propety of 5‐HT1B agonists. On the whole, they support the hypothesis of the involvement of the serotonergic system, via 5HT1A and 5‐HT1B receptors, in the modulation of hippocampal functions. © 1995 Wiley‐Liss, Inc.
Electrophysiological diversity of pyramidal‐shaped neurons at the granule cell layer/hilus border of the rat dentate gyrus recorded in vitro
Authors: Scharfman Helen E. 
Published: May 2005

AbstractIn the rat dentate gyrus, pyramidal‐shaped cells located on the border of the granule cell layer and the hilus are one of the most common types of γ‐aminobutyric acid (GABA)‐immunoreactive neurons. This study describes their electrophysiological characteristics. Membrane properties, patterns of discharge, and synaptic responses were recorded intracellularly from these cells in hippocampal slices. Each cell was identified as pyramidal‐shaped by injecting the marker Neurobiotin intracellularly (n =17).In several respects the membrane properties of the sampled cells were similar to “fast‐spiking” cells (putative inhibitory interneurons) that have been described in other areas of the hippocampus. For example, input resistance was high (mean 91.3 megohms), the membrane time constant was short (mean 7.7 ms), and there was a large afterhyperpolarization following a single action potential (mean 10.5 mV at resting potential). However, the action potentials of most pyramidal‐shaped cells were not as brief (mean 1.2 ms total duration) as those of most previously described fast‐spiking cells. Many pyramidal‐shaped neurons had strong spike frequency adaptation relative to other fast‐spiking cells. Although these latter two characteristics were apparent in the majority of the sampled cells, there were exceptional pyramidal‐shaped neurons with fast action potentials and weak adaptation, demonstrating the electrophysiological variability of pyramidal‐shaped cells.Responses to outer molecular layer stimulation were composed primarily of excitatory postsynaptic potentials (EPSPs) rather than inhibitory postsynaptic potentials (IPSPs), and were usually small (EPSPs evoked at threshold were often less than 2 mV), and brief (less than 30 ms). There was variability, because in a few cells EPSPs evoked at threshold were much larger. However, regardless of EPSP amplitude, suprathreshold stimulation (up to 4 times the threshold stimulus strength) rarely evoked more than one action potential in any cell. The results suggest that stimulation of perforant path axons produces limited excitatory synaptic responses in pyramidal‐shaped neurons. This may be one of the reasons why they are relatively resistant to prolonged perforant path stimulation.The pyramidal‐shaped neurons located at the base of the granule cell layer have been associated historically with a basket plexus around granule cell somata, and have been called pyramidal “basket” cells. However, basket‐like endings were rare and axon collaterals outside the granule cell layer were common. Many axon collaterals were as far from the granule cell layer as the outer molecular layer and the central hilus, and antidromic action potentials could be recorded in some cells in response to weak stimulation of these areas. Taken together with the electrophysiological variability, the results indicate that these cells are physiologically heterogeneous. © 1995 Wiley‐Liss, Inc.
Co‐localization of somatostatin mRNA and parvalbumin in the dorsal rat hippocampus after cerebral ischemia
Authors: Bering Robert , Diemer Nils Henrik , Draguhn Andreas , Johansen Flemming Fryd 
Published: May 2005

AbstractFollowing transient global ischemia most of the neurons containing somatostatin in the fascia dentata of the dorsal hippocampal formation die, while somatostatinergic neurons in the CA1 region survive. These neurons react to ischemia with a transiently reduced expression of somatostatin mRNA and peptide. We have tested the hypothesis that this selective vulnerability is solely related to those somatostatinergic neurons which do not express the calcium‐binding protein parvalbumin. Postischemic changes were studied in rat dorsal hippocampus at 2 and 16 days after 10 min of global cerebral ischemia using a four‐vessel occlusion model. We performed a double‐staining visualizing the mRNA coding for somatostatin by non‐radioactive in situ hybridization and parvalbumin protein by immunocytochemistry. Only 5% of the somatostatinergic cells in the fascia dentata contained parvalbumin. The number of somatostatinergic cells was permanently reduced following ischemia. Among surviving neurons we found cells with and without parvalbumin expression. Thus, expression of parvalbumin is not predictive for survival of somatostatinergic cells in the fascia dentata. In contrast, in CA1, 37% of the somatostatinergic cells contained parvalbumin. These cells were unaffected by the transient ischemic period. The somatostatinergic cells lacking parvalbumin showed transiently reduced mRNA levels at day 2, but recovered to control values at the 16th postischemic day. Thus, expression of the calcium‐buffering protein parvalbumin coincides with resistance of somatostatinergic neurons in CA1 to transient effects of ischemia.We conclude that the calcium‐buffering capacity of parvalbumin may partially contribute to the protection of somatostatinergic neurons from ischemia in the dorsal hippocampus. However, the survival of somatostatinergic cells without parvalbumin indicates the importance of other factors as well. © 1995 Wiley‐Liss, Inc.
Does electroconvulsive shock therapy work through opioid mechanisms?
Authors: Jackson Helen C. , Nutt David J. 
Published: May 2005

AbstractIt is now well‐established that electroconvulsive shock (ECS) is the most effective treatment for severe depression. Over the past two decades a great deal of new information has been obtained regarding its neuropharmacological basis. The present review examines evidence that the behavioural and mood‐elevating actions of ECS are mediated through changes in the function of opioid receptors or their endogenous transmitters. The recent discovery of stable, non‐peptide ligands for the δK‐ and δ‐receptor subtypes are detailed, and the prospects for a new phase of research in this area are expounded.
Creating equivalent word lists for the Buschke Selective Reminding Test
Authors: Coen R. F. , Kinsella A. , Lambe R. , Kenny M. , Darragh A. 
Published: May 2005

AbstractDuring investigation of DUP 996, a novel compound with potential memory‐enhancing properties, nine parallel forms of the Buschke Selective Reminding Test were required. Nine word lists were created using a previously published methodology and word pool. In order to assess the equivalence of these word lists, data on each of the nine test forms were obtained from 21 subjects who received a single placebo dose in closely controlled clinical trial conditions. Analysis of variance revealed between‐subject effect, confirming the large inter‐individual differences in performance which had been observed during testing. The subjects were categorized as poor or good performers, and in a subsequent analysis the test forms were not found to differ significantly within the groups, confirming the utility of the methodology and word pool for the creation of unmatched word lists of similar difficulty.