The DOI matches its Crossref record; 42 of the 43 references it cites were found in a registry or an index.
Exposure to Acute Stress Blocks the Induction of Long-Term Potentiation of the Amygdala–Prefrontal Cortex Pathway In Vivo
Open accessAbstract
In recent years, attention has been given to the interaction between the emotional state of the animal and its ability to learn and remember. Studies into the neural mechanisms underlying these interactions have focused on stress-induced synaptic plasticity impairments in the hippocampus. However, other brain areas, including the amygdala and the prefrontal cortex (PFC), have been implicated in relation to stress-mediated effects on memory. The present study examined whether stress, which impairs hippocampal long-term potentiation (LTP), also affects LTP of the basolateral amygdala (BLA)–PFC pathway in vivo. We first confirmed that the stress protocol we used, i.e., the elevated platform stress, was effective in blocking LTP in the CA1 area of the hippocampus. We then characterized activity and established the ability to induce LTP at the BLA–PFC pathway. Finally, we examined the effects of an exposure to the elevated platform stress on the ability to induce LTP in this pathway. The results indicate that, at the same time when LTP is blocked in the hippocampus, it is also inhibited in the BLA–medial PFC pathway. These results call for a shift from a focused attention on the effects of stress on plasticity in the hippocampus to a system level approach that emphasizes the possible modification of interactions between relevant brain areas after an exposure to a stressful experience.
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“Maroun and Richter-Levin [401] showed that electrical stimulation of the amygdala produced LTP in the PFC.”
From The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law (2007) · cites this paper as Maroun and Richter-Levin [401]
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“These researchers demonstrated that the same stress that blocked LTP in CA1 (placement of rats on an elevated platform) also blocked LTP in the PFC.”
From The Temporal Dynamics Model of Emotional Memory Processing: A Synthesis on the Neurobiological Basis of Stress-Induced Amnesia, Flashbulb and Traumatic Memories, and the Yerkes-Dodson Law (2007) · cites this paper as Maroun and Richter-Levin [401]
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“as well as modulate the nature of interactions among brain regions.123,124”
From Preferential loss of dorsal-hippocampus synapses underlies memory impairments provoked by short, multimodal stress (2014) · cites this paper as [124]
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“Animal studies demonstrated stress-induced deficits in a variety of hippocampal-dependent cognitive tasks, including water maze (Bodnoff et al., 1995; de Quervain et al., 1998), radial maze (Luine et al., 1994), and object recognition tasks (Baker and Kim, 2002).”
BackgroundSelective activation of the mesocortical DA system by stress
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Cited by
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Stress and the brain: from adaptation to disease
de Kloet, E. R., Joëls, M., & Holsboer, F. (2005) · Nature Reviews Neuroscience · doi:10.1038/nrn1683 · Cited by 4,621
Stress, Depression, and Neuroplasticity: A Convergence of Mechanisms
Pittenger, C., & Duman, R. S. (2008) · Neuropsychopharmacology · doi:10.1038/sj.npp.1301574 · Cited by 1,795
The stressed synapse: the impact of stress and glucocorticoids on glutamate transmission
Popoli, M., Yan, Z., McEwen, B. S., & Sanacora, G. (2012) · Nature Reviews Neuroscience · doi:10.1038/nrn3138 · Cited by 1,393
Diamond, D. M., Campbell, A. M., Park, C. R., Halonen, J., & Zoladz, P. R. (2007) · Neural Plasticity · doi:10.1155/2007/60803 · Cited by 762
“Our findings are consistent with recent work from other laboratories indicating that acute stress or corticosterone administration blocks hippocampal LTP (Shors et al. [141]; Shors and Thompson [142]; Pavlides et al. [143]; Pavlides et al. [144]; Pavlides et al. [145]; Garcia et al. [146]; Pavlides and McEwen [147]; Ak…”
BackgroundInfluentialPrefrontal mechanisms in extinction of conditioned fear
Quirk, G. J., Garcia, R., & González-Lima, F. (2006) · Biological Psychiatry · doi:10.1016/j.biopsych.2006.03.010 · Cited by 682
Metadata
- Authors
- Maroun, M., & Richter-Levin, G.
- Affiliations
- University of Haifa (IL)
- ORCID
- Maroun, Mouna
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 2003-06-01
- Volume
- 23
- Issue
- 11
- Pages
- 4406-4409
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6740777
- OpenAlex
- W1784991500
- Cited by
- 293
- References
- 43
- Citations by year
- 2025: 4 · 2024: 4 · 2023: 5 · 2022: 5 · 2021: 10 · 2020: 6 · 2019: 8 · 2018: 11 · 2017: 5 · 2016: 12 · 2015: 21 · 2014: 19 · 2013: 19 · 2012: 23
- FWCI
- 8.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Journal of Neuroscience (publishedVersion)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Keywords
- acute stress, long-term potentiation, basolateral amygdala, medial prefrontal cortex, stress-induced memory impairment, hippocampal CA1, synaptic plasticity, stress and learning
- MeSH terms
- Acute Disease, Amygdala, Analysis of Variance, Animals, Behavior, Animal, Electric Stimulation, Hippocampus, Male, Neural Pathways, Neuronal Plasticity, Stress, Physiological, Theta Rhythm, Receptors, N-Methyl-D-Aspartate, Rats, Sprague-Dawley, Prefrontal Cortex, Long-Term Potentiation, Excitatory Postsynaptic Potentials, Rats
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