A cFos activation map of remote fear memory attenuation

Silva, Bianca A.; Burns, Allison M.; Gräff, Johannes

doi:10.1007/s00213-018-5000-y

Cited by 104 publications

(100 citation statements)

References 66 publications

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“…The lack of group differences during conditioning also suggests that there were no intrinsic effects of the hM4Di virus in the absence of CNO. We then replicated previous work showing that with the passage of time, fear memories are processed to a lesser extent within the HPC and rely on neocortical storage (Teixeira et al, 2006;Lesburgueres et al, 2011;Silva et al, 2018;DeNardo et al, 2019). When fear memory recall following conditioning was tested after 1 d, we observed a more pronounced recruitment of cellular activity compared to the PL.…”

Section: Discussionsupporting

confidence: 87%

Odor Modulates the Temporal Dynamics of Fear Memory Consolidation

Grella

Fortin

McKissick

et al. 2019

Preprint

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Number of words in the abstract: 267 Number of characters w spaces (main text excluding abstract, references & fig legends): 54,606 Grella et al., 2ABSTRACT Systems consolidation (SC) theory proposes that recent, contextually rich memories are stored in the hippocampus (HPC). As these memories become remote, they are believed to rely more heavily on cortical structures within the prefrontal cortex (PFC), where they lose much of their contextual detail and become schematized. Odor is a particularly evocative cue for intense remote memory recall and despite these memories being remote, they are highly contextual. In instances such as post-traumatic stress disorder (PTSD), intense remote memory recall can occur years after trauma, which seemingly contradicts SC. We hypothesized that odor may shift the organization of salient or fearful memories such that when paired with an odor at the time of encoding, they are delayed in the de-contextualization process that occurs across time, and retrieval may still rely on the HPC, where memories are imbued with contextually rich information, even at remote time points. We investigated this by tagging odor-and non-odorassociated fear memories in male c57BL/6 mice and assessed recall and c-Fos expression in the dorsal CA1 (dCA1) and prelimbic cortex (PL) 1 d or 21 d later. In support of SC, our data showed that recent memories were more dCA1-dependent whereas remote memories were more PL-dependent. However, we also found that odor influenced this temporal dynamic biasing the memory system from the PL to the dCA1 when odor cues were present.Behaviorally, inhibiting the dCA1 with activity-dependent DREADDs had no effect on recall at 1 d and unexpectedly caused an increase in freezing at 21 d. Together, these findings demonstrate that odor can shift the organization of fear memories at the systems level.Grella et al., 3

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Section: Discussionsupporting

confidence: 87%

Odor Modulates the Temporal Dynamics of Fear Memory Consolidation

Grella

Fortin

McKissick

et al. 2019

Preprint

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“…Although we examined the underlying mechanism of fear memory in cerebellar cortex, PCspecific STAT3 deletion may have a more widespread impact on the brain's fear memory 13 network in general. Previous studies have shown that removal of only a few highly interconnected areas (high-degree nodes) of the fear network was enough to disrupt fear memory consolidation (Vetere et al, 2017, Silva et al, 2019. Under this assumption, we performed immunohistochemistry for detecting c-fos expressions in the brain after auditory long-term fear memory retrieval tests.…”

Section: Increased Neural Activity Of Fear-related Regions In the Stamentioning

confidence: 99%

Ablation of STAT3 in Purkinje Cells Reorganizes Cerebellar Synaptic Plasticity in Long-Term Fear Memory Network

Han

Kwon

Kim

et al. 2020

Preprint

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Emotional memory processing, such as fear memory, engages a large neuronal network of brain regions including the cerebellum. However, the molecular and cellular mechanisms of the cerebellar cortex modulating the fear memory network is largely unknown. Here, we illustrate a novel mechanism by which synaptic signaling in cerebellar Purkinje cells (PCs) via STAT3 regulates long-term fear memory. Firstly, we generated PC-specific STAT3 knockout (STAT3PKO) mice. Transcriptome analyses revealed that STAT3 deletion results in transcriptional changes that lead to an increase in the expression of glutamate receptors. The amplitude of AMPA receptor-mediated excitatory postsynaptic currents at parallel fiber to PC synapses was larger in STAT3PKO mice than in wild-type littermates. Conditioning at the parallel fiber induced long-term depression of parallel fiber-PC synapses in STAT3PKO mice while the same manipulation induced long-term potentiation in wild-type littermates. Interestingly, STAT3PKO mice showed an aberrantly enhanced long-term fear memory. Neuronal activity in fear-related regions increased in fear-conditioned STAT3PKO mice. Our data suggest that STAT3-dependent molecular regulation in PCs is indispensable for proper expression of fear memory processing.

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“…This prediction based on anatomical connectivity is supported by transient neuronal synchronization across these structures and functional studies showing that inactivation of the RE affects especially those behaviors, which depend on prefrontal–hippocampal communication, such as spatial working memory and long‐term spatial and contextual memory consolidation (Ali et al, ; Barker & Warburton, ; Ferraris et al, ; Griffin, ; Hallock, Wang, & Griffin, ; Hembrook & Mair, ; Hembrook, Onos, & Mair, ; Roy, Svensson, Mazeh, & Kocsis, ; Vetere et al, ; Xu & Sudhof, ). In addition, the RE has been implicated in attention, behavioral flexibility and impulse control but also more basic functions such as circadian regulation, nociception and fear (see Cassel et al, for review; Prasad, Macgregor, & Chudasama, ; Silva, Burns, & Graff, ; Vetere et al, ).…”

Section: Introductionmentioning

confidence: 99%

Afferent connections of the thalamic nucleus reuniens in the mouse

Scheel

Wulff

Malsen

2019

J of Comparative Neurology

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The nucleus reuniens (RE) is part of the midline thalamus and one of the major sources of thalamic inputs to the hippocampal formation and the medial prefrontal cortex. However, it not only sends strong efferents to these areas but is also heavily innervated by both brain regions. Based on its connectivity and supported by functional studies the RE has been suggested to represent a major hub in reciprocal hippocampal–prefrontal communication. Indeed, inactivation studies have demonstrated that this nucleus is particularly important for cognitive behaviors which depend on prefrontal–hippocampal communication, such as working memory or memory consolidation. However, besides its central role in mediating hippocampal–prefrontal communication, the RE is target of a multitude of other cortical and subcortical afferents, which likely modulate its function. So far, however, studies that have systematically investigated the afferents of the RE have only been performed in rats. Because of the unique role of the mouse as a genetically accessible model system for mammalian brain circuit analysis we have mapped the afferent connectivity of the mouse RE using retrograde Fluoro‐Gold tracing. Comparison with similar data from rats indicated a very high level of similarity in prefrontal and hippocampal afferents but some differences in afferent connectivity with other brain regions. In particular, our results suggest interspecies differences regarding the integration of the RE in circuits of fear, aversion, and defense.

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A cFos activation map of remote fear memory attenuation

Cited by 104 publications

References 66 publications

Odor Modulates the Temporal Dynamics of Fear Memory Consolidation

Odor Modulates the Temporal Dynamics of Fear Memory Consolidation

Ablation of STAT3 in Purkinje Cells Reorganizes Cerebellar Synaptic Plasticity in Long-Term Fear Memory Network

Afferent connections of the thalamic nucleus reuniens in the mouse

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