摘要:

AbstractSutherland and Rudy ([1989] Psychobiology 17:129–144) proposed that the hippocampal system is critical to normal learning and memory because of its function as the central part of aconfigural association system. This system constructs a unique representation of the joint occurrence of the independent elements of a compund. There is evidence consistent with the theory's predictions, however, there also are data that unambiguously demonstrate that, under some conditions, animals lacking an intact hippocampal system acquire configural associations. Thus, Sutherland and Rudy's fundamental assumption cannot be correct. To integrate the supporting and contradictory data, we propose two simple modifications of our position: (1) The critical neural system for configural associations is in cortical circuitry outside the hippocampus, and (2) the output from the hippocampal formation contributes to configural processing by selectively enhancing, thereby making more salient, cortical units representing stimulus conjunctions. This enhancement has two important effects: (1) It decreases the similarity between the configural units representing the co‐occurrence of cues and the units representing the cues, and (2) it increases the rate at which the configural units can acquire associative strength. The modified theory explains why damage to the hippocampal formation only impairs learning on a subset of nonlinear discrimination problems. It also integrates recent data on the effects of hippocampal formation damage on conditioning involving context cues and makes novel predictions about performance on nonlinear discrimination problems and place learning. © 1995 Wiley‐Lis

ISSN:1050-9631    

DOI:10.1002/hipo.450050502

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

ISSN:1050-9631    

DOI:10.1002/hipo.450050503

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractRecordings were made from single neurons in the hippocampus and parahippocampal gyrus while macaques were moved on a platform mounted on a free‐moving robot or on wheels in a cue‐controlled 2 m × 2 m × 2 m environment, in order to investigate the representation of space and of spatial memory in the primate hippocampus. The test conditions allowed factors that might account for spatial firing of the cells, including the spatial location where the monkey looked, the place were the monkey was, and the head direction of the monkey, to be identified. The responses of some (“view”) neurons depended on where the monkey was looking in the enviornment, but not on the place of the monkey in the environment. The responses of one other neuron depended on a combination of where the monkey was facing and his place in the test chamber. The response of view‐dependent neurons was affected by occlusion of the visual field. It was possible to show for one neuron that its “view” response rotated with rotation of the test chamber. Some neurons responded to a combination of whole‐body motion and view or place, and one neuron responded in relation to whole‐body movement to a particular place. One neuron responded depending on the place where the monkey was in the environment and relatively independently of view.The representations of space provided by hippocampal view‐responsive neurons may be useful in forming memories of spatial environments (for example, of where an object has been seen and of where the monkey is as defined by seen views) and, together with whole‐body motion cells, in remembering trajectories through environments, which is of use, for example, in short range spatial navigation.

ISSN:1050-9631    

DOI:10.1002/hipo.450050504

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractCultured hippocampal slices retain many in vivo features with regard to circuitry, synaptic plasticity, and pathological responsiveness, while remaining accessible to a variety of experimental manipulations. The present study used ligand binding, immunostaining, and in situ hybridization assays to determine the stability of AMPA‐ and NMDA‐type glutamate receptors and other synaptic proteins in slice cultures obtained from 11 day postnatal rats and maintained in culture for at least 4 weeks. Binding of the glutamate receptor ligands [3H]AMPA and [3H]MK‐801 exhibited a small and transient decrease immediately after slice preparation, but the binding levels recovered by culture day (CD) 5–10 and remained stable for at least 30 days in culture. Autoradiographic analyses with both ligands revealed labeling of dendritic fields similar to adult tissue. In addition, slices at CD 10–20 expressed a low to high affinity [3H]AMPA binding ratio that was comparable with that in the adult hippocampus (10:1). AMPA receptor subunits GluR1 and GluR2/3 and an NMDA receptor subunit (NMDAR1) exhibited similar postcutting decreases as that exhibited by the ligand binding levels, followed by stable recovery. The GluR4 AMPA receptor subunit was not evident during the first 10 CDs but slowly reached detectable levels thereafter in some slices. Immunocytochemistry and in situ hybridization techniques revealed adult‐like labeling of subunit proteins in dendritic processes and their mRNAs in neuronal cell body layers. Long‐term maintenance was evident for other synapse‐related proteins, including synaptophysin, neural cell adhesion molecule isoforms (NCAMs), and an AMPA receptor related antigen (GR53), as well as for certain structural and cytoskeletal components (e. g., myelin basic protein, spectrin, microtubule‐associated proteins). In summary, following an initial and brief depression, many synaptic components were expressed at steady‐state levels in long‐term hippocampal slices, thus allowing the use of such a culture system for investigations into mechanisms of brain synapses.

ISSN:1050-9631    

DOI:10.1002/hipo.450050505

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractThe pattern of impulse transfer along the entorhinal‐hippocampal‐entorhinal loop has been analyzed in the guinea pig by field potential analysis. The loop was driven by impulse volleys conducted by presubicular commissural fibers, directly stimulated in the dorsal psalterium, which monosynaptically activated perforant path neurons in the medial entorhinal cortex. Perforant path volleys activated in sequence the dentate gyrus, field CA3, field CA1, subiculum, and entorhinal cortex. Input‐output curves were reconstructed from responses simultaneously recorded from different stations along the loop.The entorhinal response to the presubicular volley was found to increase gradually with respect to its input. The population excitatory postsynaptic potential (EPSP) of the dentate gyrus granule cells had a similar behavior. By contrast, the input‐output relation between the granule cell population spike and population EPSP was described by a very steep sigmoid curve. The population spike of CA3 and CA1 pyramidal neurons as well as the response evoked in the entorhinal cortex by the hippocampal output had slightly higher threshold than the granule cell population spike and, like the latter, abruptly reached maximum amplitude.These findings show that the entorhinal‐hippocampal‐entorhinal loop transforms a linear input in a non‐linear, almost all‐or‐none output and that the dentate gyrus is the critical site where the transformation occurs. Beyond the dentate gyrus, the loop appears very permeant to impulse traffic. © 19

ISSN:1050-9631    

DOI:10.1002/hipo.450050506

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractIn the present report, we describe a morphological and quantitative analysis of subicular synapses in layer V of the lateral entorhinal cortex (LEA) of the rat. Projections from the dorsal subiculum were labeled anterogradely, and areas in LEA showing high terminal density were randomly selected for ultrathin sectioning. More than 400 terminals in LEA were photographed in the electron microscope, and synapse types and postsynaptic targets were identified and, subsequently, quantified with the unbiased disector method. Most subicular terminals appeared to form asymmetrical synapses. A majority of asymmetrical synapses terminated on spines (67.5%), whereas a smaller fraction of asymmetrical synapses (23.5%) terminated on dendritic shafts. A small fraction of the terminals (7%) had symmetrical features. These symmetrical synapses had an almost equal percentage of spines and dendritic shafts as postsynaptic elements. Labeled synapses on somata or axons were never observed. The findings of this study in conjunction with relevant electrophysiological observations (Jones [1987] Neurosci Lett 81:209–214) leads to the conclusion that the subiculo‐entorhinal pathway comprises a large excitatory and a smaller inhibitory projection, both making synaptic contacts with presumed principal neurons and interneurons in the entorhinal cortex. © 1995 Wiley‐Lis

ISSN:1050-9631    

DOI:10.1002/hipo.450050507

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractThe neuroprotective effects of enhancing neuronal inhibition with a γ‐aminobutyric acid (GABA) uptake inhibitor were studied in gerbil hippocampus following transient ischemia. We used in vivo microdialysis to determine a suitable dosing regimen for tiagabine (NNC 328) to elevate extracellular levels of GABA within the hippocampus. In anesthetized (normothermic) gerbils, tiagabine (45 mg/kg, i. p.) selectively elevated extracellular GABA levels 450% in area CA1 of the hippocampus. In gerbils subjected to cerebral ischemia via 5‐min bilateral carotid occlusion, extracellular GABA levels increased 13‐fold in area CA1, returning to baseline within 30–45 min. When tiagabine was injected 10 min following onset of reperfusion, GABA levels remained elevated (200–470%) for 90 min. In addition, tiagabine significantly reduced the ischemic‐induced elevation of glutamate levels in area CA1 during the postischemic period when GABA levels were elevated. There was no effect of postischemic tiagabine on aspartate or six other amino acids. Using the same dosing regimen, we evaluated the degree of neuroprotection in the hippocampus of gerbils 4 and 21 days after ischemia. Tiagabine decreased body temperature a maximum of 2.7°C beginning 30 min into reperfusion and lasting 90 min. In untreated gerbils sacrificed 4 and 21 days after ischemia, there was severe necrosis (99%) of the pyramidal cell layer in area CA1. Whereas tiagabine significantly protected the CA1 pyramidal cell layer in ischemic gerbils at 4 days (overt necrosis confined to about 17% of area CA1), the protection diminished significantly 21 days postischemia. When normothermia was maintained both during and after ischemia in a separate group of tiagabine‐treated animals, approximately 77% of the CA1 pyramidal cell layer was necrotic at 4 days. Based on these findings, we suggest that (1) tiagabine slows the development of hippocampal degeneration following ischemia, and (2) that mild, postischemic hypothermia is responsible, in large part, for the neuroprotective actions of this drug. We conclude that the histological outcome after administration of cerebral neuroprotectants should be assessed following long‐term survival. © 19

ISSN:1050-9631    

DOI:10.1002/hipo.450050508

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

摘要:

AbstractImmunocytochemical techniques were employed in order to examine the distribution and relative intensity of the AMPA receptor subunits GluR1 and GluR2/3 within the hippocampal formation of normal controls and Alzheimer's disease (AD) cases. Throughout our investigation we examined cases exhibiting a wide range of pathologic severity, thus allowing us to correlate our immunohistochemical data with the extent of pathology. Specifically, we investigated the distribution of these receptor subunits in hippocampal sectors that are particularly vulnerable to AD pathology (i. e., CA1 and subiculum) and compared these findings with those obtained following examination of sectors that are generally resistant to pathologic change (i. e., CA2/3, dentate gyrus). Within vulnerable sectors we observed a variable loss of GluR1 and GluR2/3 immunolabeling. The degree to which these proteins were reduced appeared to correlate with the extent of neurofibrillary pathology and cell loss. Despite the loss of labeled cells, the intensity of immunolabeling within the remaining neurons was comparable with, and in many instances even greater than, that observed in control cases. Within resistant sectors, the distribution of immunoreactive elements was comparable in both case groups yet the intensity of immunolabeling was markedly increased in AD cases, particularly in the molecular layer of the dentate gyrus and in the stratum lucidum of CA3 (i. e., the termination zones of perforant pathway and mossy fibers). In addition, within AD cases dramatic increases were observed within the supragranular and polymorphic layer of the dentate gyrus (i. e., the terminal zones of sprouting mossy fiber collaterals). The increase in GluR1 and GluR2/3 immunolabeling is hypothesized to occur in response to the deafferentation of selected glutamatergic pathways. Moreover, our data support that hippocampal plasticity is preserved, even in severe AD cases, and suggest a critical role for AMPA receptor subunits in this plasticity and in maintaining hippocampal functioning. © 1995 Wiley‐Liss, I

ISSN:1050-9631    

DOI:10.1002/hipo.450050509

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY

ISSN:1050-9631    

DOI:10.1002/hipo.450050501

出版商:Wiley Subscription Services, Inc., A Wiley Company    

年代:1995

数据来源: WILEY