Dorsal hippocampal kindling selectively impairs spatial learning/short‐term memory

Hannesson, Darren K.; Mohapel, Paul; Corcoran, Michael E.

doi:10.1002/hipo.1042

Cited by 37 publications

(22 citation statements)

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“…Kindled rats' performance was comparable with controls' on both measures of object recognition in the open field object exploration task. This is consistent with our previous finding that full dHPC kindling spares object associative memory (Hannesson et al, 2001) and suggests that object-related memory in general is unaffected by dHPC kindling. Thus, the type of information processing required by a task (e.g., spatial versus object related) is a critical determinant of the susceptibility of a task to disruption by dHPC kindling.…”

Section: Discussionsupporting

confidence: 82%

“…Increased activity-exploration is generally consistent with the pattern of effects of hippocampal lesions on open field behavior (O' Keefe and Nadel, 1978) and thus could indicate a disruption of hippocampal function. This interpretation is consistent with the hypothesis that hippocampal dysfunction also underlies impaired spatial task performance after kindling (Lopes Da Silva et al, 1986;Leung and Shen, 1991;Leung et al, 1990Leung et al, , 1994Leung et al, , 1996Sutherland et al, 1997;Hannesson et al, 2001) and presents a possible explanation for the effects of dHPC kindling on brightness discrimination task performance (Becker et al, 1997). Because the task is sensitive to the effects of hippocampal lesions (Munoz and Grossman, 1981;McLamb et al, 1988), the effect of kindling may also be a result of a direct alteration of hippocampal function.…”

Section: Discussionsupporting

confidence: 74%

“…Kindling disrupts performance in both the radial arm maze (Lopes Da Silva et al, 1986;Leung et al, 1990Leung et al, , 1996 and the Morris water maze (MWM) (Gilbert et al, 1996;Sutherland et al, 1997;Hannesson et al, 2001). Moreover, in the MWM, this effect is preferentially induced by kindling in the dorsal hippocampus (dHPC), by full rather than partial kindling, and is manifest in a disruption of learning and/or short-term memory-but not longterm memory-dependant performance (Hannesson and Corcoran, 2000;Hannesson et al, 2001). The interpretation of these effects, however, is complicated because kindling also produces changes in non-mnemonic functions that might impact spatial task performance.…”

Section: Abstract: Activity; Anxiety; Ca1; Dmtp; Elevated Plus Maze;mentioning

confidence: 99%

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Dorsal Hippocampal Kindling Produces a Selective and Enduring Disruption of Hippocampally Mediated Behavior

et al. 2001

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Kindling produces enduring neural changes that are subsequently manifest in enhanced susceptibility to seizure-evoking stimuli and alterations in some types of behavior. The present study investigated the effects of dorsal hippocampal (dHPC) kindling on a variety of behaviors to clarify the nature of previously reported effects on spatial task performance. Rats were kindled twice daily with dHPC stimulation until three fully generalized seizures were evoked. Beginning 7 d later and on successive days, rats were tested in an elevated plus maze, a large circular open field, an open field object exploration task, and a delayed-match-to-place (DMTP) task in a water maze to assess anxiety-related and activity-related behavior (tasks 1 and 2), object recognition memory (task 3), and spatial cognition (task 4). Kindling disrupted performance on the DMTP task in a manner that was not delay dependent and produced a mild enhancement of activity-related behaviors in the open field task but not the elevated plus maze. All other aspects of testing were spared. These findings indicate that dHPC kindling produces enduring and selective effects on behavior that are consistent with a restricted disruption of hippocampally mediated functions. Possible bases for these effects are changes in local NMDA receptor function and/or changes in local inhibition, which might alter the optimal conditions for experiencedependent induction of intrahippocampal plasticity. This preparation may be useful for studying the mechanisms of mnemonic dysfunction associated with temporal lobe epilepsy and may offer unique insights into the mechanisms underlying normal hippocampal function.

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Section: Discussionsupporting

confidence: 82%

Section: Discussionsupporting

confidence: 74%

Section: Abstract: Activity; Anxiety; Ca1; Dmtp; Elevated Plus Maze;mentioning

confidence: 99%

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Dorsal Hippocampal Kindling Produces a Selective and Enduring Disruption of Hippocampally Mediated Behavior

et al. 2001

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“…Partial kindling refers to the repeated delivery of afterdischarges (ADs) or electrical seizures without motor convulsions. Kindling of the hippocampus induced spatial memory deficits, as tested on the radial arm maze (RAM) (Lopes da Silva et al 1986;Leung et al 1990Leung et al , 1993Leung et al , 1996Leung and Shen 1991;Robinson et al 1993;Feasey-Truger et al 1993;Sutula et al 1995) or water maze (Gilbert et al 1996;Sutherland et al 1997;Hannesson and Corcoran 2000;Hannesson et al 2001).…”

mentioning

confidence: 99%

“…We and others have studied the spatial memory and performance after repeated seizures in the hippocampus using the kindling model (Lopes da Silva et al 1986;Hannesson and Corcoran 2000;Leung et al 2000;Hannesson et al 2001). Kindling refers to the delivery of spaced, repeated (electrical or chemical) stimulations to the brain that result in a progression of clinical signs of epilepsy, culminating in motor and spontaneous seizures (Goddard et al 1969).…”

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confidence: 99%

Hippocampal CA1 kindling but not long-term potentiation disrupts spatial memory performance

Leung¹,

Shen²

2006

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Long-term synaptic enhancement in the hippocampus has been suggested to cause deficits in spatial performance. Synaptic enhancement has been reported after hippocampal kindling that induced repeated electrographic seizures or afterdischarges (ADs) and after long-term potentiation (LTP) defined as synaptic enhancement without ADs. We studied whether repeated stimulations that gave LTP or ADs resulted in spatial performance deficits on the radial arm maze (RAM) and investigated the minimal number of ADs required for such deficits. Three experimental groups were run as follows: (1) 5 hippocampal ADs in 1 d (5-AD group), (2) 10 hippocampal ADs in 2 d (10-AD group), and (3) 12 θ-frequency primed-burst stimulations (PBSs) in 2 d in order to induce LTP without ADs (LTP group). Each experimental group was run together with a control group during the same time period. Rats were first trained in a spatial task on a radial arm maze with four of the eight arms baited, then given control or experimental treatment, and maze performance was tested in the first week (1-4 d) and fourth week (22-25 d) after treatment. Basal dendritic population excitatory postsynaptic potentials (pEPSPs) and medial perforant path (MPP)-evoked dentate gyrus population spike and polysynaptic CA1 excitation were recorded before and after experimental and control treatment. Spatial memory errors, in particular reference memory errors, were significantly higher in the 10-AD kindled group than any other group on the first and fourth week after treatment. Spatial memory errors were not significantly different in the 5-AD and LTP groups as compared with any control groups at any time. Basal dendritic pEPSP in CA1 was enhanced for about 1 wk after 12 PBSs, 10 ADs, or 5 ADs, while the dentate gyrus population spike and CA1 polysynaptic excitation evoked by MPP was increased for up to 4 wk after 10 ADs, but not 12 PBSs. Thus, distributed alteration of multiple synaptic transmission in the entorhinal-hippocampal circuit, but not LTP at the basal dendritic synapses in CA1, may disrupt spatial performance after 10 hippocampal ADs.

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A companion to the preclinical common data elements for pharmacologic studies in animal models of seizures and epilepsy. A Report of the TASK3 Pharmacology Working Group of the ILAE/AES Joint Translational Task Force

et al. 2018

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SummaryPreclinical pharmacology studies in animal models of seizures and epilepsy have provided a platform to identify more than 20 antiseizure drugs in recent decades. To minimize variability in lab‐to‐lab studies and to harmonize approaches to data collection and reporting methodology in pharmacologic evaluations of the next generation of therapies, we present common data elements (CDEs), case report forms (CRFs), and this companion manuscript to help with the implementation of methods for studies in established preclinical seizure and epilepsy models in adult rodents. The development of and advocacy for CDEs in preclinical research has been encouraged previously by both clinical and preclinical groups. It is anticipated that adoption and implementation of these CDEs in preclinical studies may help standardize approaches to minimize variability and increase the reproducibility of preclinical studies. Moreover, they may provide a methodologic framework for pharmacology studies in atypical animal models or models in development, which may ultimately promote novel therapy development. In the present document, we refer selectively to animal models that have a long history of preclinical use, and in some cases, are clinically validated.

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Dorsal hippocampal kindling selectively impairs spatial learning/short‐term memory

Cited by 37 publications

References 41 publications

Dorsal Hippocampal Kindling Produces a Selective and Enduring Disruption of Hippocampally Mediated Behavior

Dorsal Hippocampal Kindling Produces a Selective and Enduring Disruption of Hippocampally Mediated Behavior

Hippocampal CA1 kindling but not long-term potentiation disrupts spatial memory performance

A companion to the preclinical common data elements for pharmacologic studies in animal models of seizures and epilepsy. A Report of the TASK3 Pharmacology Working Group of the ILAE/AES Joint Translational Task Force

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