Time-dependent blockade of STP and LTP in hippocampal slices following acute stress in mice

García, René; Musleh, Wael; Tocco, Georges; Thompson, Richard F.; Baudry, Michel

doi:10.1016/s0304-3940(97)00621-6

Cited by 78 publications

(47 citation statements)

References 23 publications

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“…Given that the stress paradigm employed in the present study also impairs LTP in the hippocampus (Foy et al 1987;Shors et al 1989;Kim et al 1996Kim et al , 2001, it is plausible that stress-induced LTP impairments in the hippocampus might contribute to impairments in recognition memory. Consistent with this notion, the duration of stress effects on recognition memory (which lasted <48 h poststress) corresponds to the duration of stress effects on hippocampal LTP (which also lasts Յ48 h poststress; Garcia et al 1997;Shors et al 1997).…”

Section: Baker and Kimsupporting

confidence: 54%

Effects of Stress and Hippocampal NMDA Receptor Antagonism on Recognition Memory in Rats

2002

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Exposures to uncontrollable stress have been shown to alter ensuing synaptic plasticity in the hippocampus and interfere with hippocampal-dependent spatial memory in rats. The present study examined whether stress, which impairs hippocampal long-term potentiation (LTP), also affects (nonspatial) hippocampal-dependent object-recognition memory, as tested on the visual paired comparison task (VPC) in rats. After undergoing an inescapable restraint-tailshock stress experience, rats exhibited markedly impaired recognition memory at the 3-h (long) familiarization-to-test phase delay but not at the 5-min (short) delay. In contrast, unstressed control animals showed robust recognition memory (i.e., they exhibited reliable preferences for novel over familiar objects) at both short-and long-delay periods. The impairing effect of stress on long-delay recognition memory was transient because 48 h after undergoing stress experience, animals performed normally at the long delay. Similar to stress, microinfusions of DL-2-amino-5-phosphonovaleric acid (APV), a competitive N-methyl-D-aspartate receptor (NMDAR) antagonist that blocks LTP, into the dorsal hippocampus selectively impaired object-recognition memory at the long-delay period. Together, these results suggest that stress and intrahippocampal administration of APV affect recognition memory by influencing synaptic plasticity in the hippocampus.[The following individuals kindly provided reagents, samples, or unpublished information as indicated in the paper H. Blair.]

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Section: Baker and Kimsupporting

confidence: 54%

Effects of Stress and Hippocampal NMDA Receptor Antagonism on Recognition Memory in Rats

2002

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“…1). Because previous studies have demonstrated that stress-induced LTP impairments last at least 48 h in rats (Shors et al, 1997) and 24 h in mice (Garcia et al, 1997), any potential differences in LTP magnitudes between prestress and poststress muscimol groups in experiment 2 can be attributed to whether the amygdala was inactivated during stress or immediately after stress (by comparing the experiment 1 MUSC-STRESS group with the experiment 2 STRESS-MUSC group) rather than to the temporal difference from muscimol infusions to hippocampal slice preparation (by comparing the STRESS-MUSC and MUSC-STRESS groups, both in experiment 2).…”

Section: Experiments 2: Prestress and Poststress Intra-amygdalar Muscimentioning

confidence: 99%

Amygdalar Inactivation Blocks Stress-Induced Impairments in Hippocampal Long-Term Potentiation and Spatial Memory

Kim¹,

Koo²,

Lee³

et al. 2005

J. Neurosci.

167

145

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Electrolytic lesions to the amygdala, a limbic structure implicated in stress-related behaviors and memory modulation, have been shown to prevent stress-induced impairments of hippocampal long-term potentiation (LTP) and spatial memory in rats. The present study investigated the role of intrinsic amygdalar neurons in mediating stress effects on the hippocampus by microinfusing the GABA A receptor agonist muscimol into the amygdala and examining stress effects on Schaffer collateral/commissural-CA1 LTP and spatial memory. The critical period of the amygdalar contribution to stress effects on hippocampal functions was determined by applying muscimol either before stress or immediately after stress. Our results indicate that intra-amygdalar muscimol infusions before uncontrollable restrainttailshock stress effectively blocked stress-induced physiological and behavioral effects. Specifically, hippocampal slices prepared from vehicle-infused stressed animals exhibited markedly impaired LTP, whereas slices obtained from muscimol-infused stressed animals demonstrated robust LTP comparable with that of unstressed animals. Correspondingly, vehicle-infused stressed animals displayed impaired spatial memory (on a hidden platform version of the Morris water maze task), whereas muscimol-infused stressed animals revealed unimpaired spatial memory. In contrast to prestress muscimol effects, however, immediate poststress infusions of muscimol into the amygdala failed to interfere with stress impairments of LTP and spatial memory. Together, these results suggest that the amygdalar neuronal activity during stress, but not shortly after stress, is essential for the emergence of stress-induced alterations in hippocampal LTP and memory.

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“…Numerous of studies, using a broad range of stressors (novelty, restraint, shock, predator exposure) have consistently shown that stress or elevated levels of corticosterone inhibit the induction of excitatory plasticity (LTP and PBP) and promote the induction of inhibitory plasticity (long-term depression; LTD) (27,29,30,(36)(37)(38)(39)(40)(41)(42)(43)(44)(45). Nevertheless, lower concentrations of corticosterone, such as those that occur naturally during the diurnal rise, enhance such plasticity (37,46,47).…”

Section: Stress and The Hippocampusmentioning

confidence: 99%

Amygdala-Hippocampus Dynamic Interaction in Relation to Memory

2000

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Time-dependent blockade of STP and LTP in hippocampal slices following acute stress in mice

Cited by 78 publications

References 23 publications

Effects of Stress and Hippocampal NMDA Receptor Antagonism on Recognition Memory in Rats

Effects of Stress and Hippocampal NMDA Receptor Antagonism on Recognition Memory in Rats

Amygdalar Inactivation Blocks Stress-Induced Impairments in Hippocampal Long-Term Potentiation and Spatial Memory

Amygdala-Hippocampus Dynamic Interaction in Relation to Memory

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