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  • 1
    Online Resource
    Online Resource
    Hippocampal Inactivation Disrupts the Acquisition and Contextual Encoding of Fear Extinction
    Society for Neuroscience ; 2005
    In:  The Journal of Neuroscience Vol. 25, No. 39 ( 2005-09-28), p. 8978-8987
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 25, No. 39 ( 2005-09-28), p. 8978-8987
    Abstract: In recent studies, inactivation of the dorsal hippocampus before the retrieval of extinguished fear memories disrupted the context-dependent expression of these memories. In the present experiments, we examined the role of the dorsal hippocampus in the acquisition of extinction. After pairing an auditory conditional stimulus (CS) with an aversive footshock [unconditional stimulus (US)], rats received an extinction session in which the CS was presented without the US. In experiment 1, infusion of muscimol, a GABA A receptor agonist, into the dorsal hippocampus before the extinction training session decreased the rate of extinction. Moreover, when later tested for fear to the extinguished CS, all rats that had received hippocampal inactivation before extinction training demonstrated renewed fear regardless of the context in which testing took place. This suggests a role for the dorsal hippocampus in both acquiring the extinction memory and encoding the CS–context relationship that yields the context dependence of extinction. In experiment 2, inactivation of the dorsal hippocampus before testing also disrupted the context dependence of fear to the extinguished CS. In experiment 3, quantitative autoradiography revealed the boundaries of muscimol diffusion after infusion into the dorsal hippocampus. Together, these results reveal that the dorsal hippocampus is involved in the acquisition, contextual encoding, and context-dependent retrieval of fear extinction. Learning and remembering when and where aversive events occur is essential for adaptive emotional regulation.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.2246-05.2005
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2005
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 2
    Online Resource
    Online Resource
    Protein synthesis in the amygdala, but not the auditory thalamus, is required for consolidation of Pavlovian fear conditioning in rats
    Wiley ; 2003
    In:  European Journal of Neuroscience Vol. 18, No. 11 ( 2003-12), p. 3080-3088
    Details
    In: European Journal of Neuroscience, Wiley, Vol. 18, No. 11 ( 2003-12), p. 3080-3088
    Abstract: The amygdala is an essential neural substrate for Pavlovian fear conditioning. Nevertheless, long‐term synaptic plasticity in amygdaloid afferents, such as the auditory thalamus, may contribute to the formation of fear memories. We therefore compared the influence of protein synthesis inhibition in the amygdala and the auditory thalamus on the consolidation of Pavlovian fear conditioning in Long–Evans rats. Rats received three tone‐footshock trials in a novel conditioning chamber. Immediately after fear conditioning, rats were infused intra‐cranially with the protein synthesis inhibitor, anisomycin. Conditional fear to the tone and conditioning context was assessed by measuring freezing behaviour in separate retention tests conducted at least 24 h following conditioning. Post‐training infusion of anisomycin into the amygdala impaired conditional freezing to both the auditory and contextual stimuli associated with footshock. In contrast, intra‐thalamic infusions of anisomycin or a broad‐spectrum protein kinase inhibitor [1‐(5′‐isoquinolinesulphonyl)‐2‐methylpiperazine, H7] did not affect conditional freezing during the retention tests. Pre‐training intra‐thalamic infusion of the NMDA receptor antagonist 2‐amino‐5‐phosphonopentanoic acid (APV), which blocks synaptic transmission in the auditory thalamus, produced a selective deficit in the acquisition of auditory fear conditioning. Autoradiographic assays of cerebral [ 14 C]‐leucine incorporation revealed similar levels of protein synthesis inhibition in the amygdala and thalamus following intra‐cranial anisomycin infusions. These results reveal that the establishment of long‐term fear memories requires protein synthesis in the amygdala, but not the thalamus, after auditory fear conditioning. Forms of synaptic plasticity that depend on protein synthesis, such as long‐term potentiation, are likely candidates for the encoding and long‐term storage of fear memories in the amygdala.
    Type of Medium: Online Resource
    ISSN: 0953-816X , 1460-9568
    URL: Issue
    URL: Article
    DOI: 10.1111/ejn.2003.18.issue-11
    DOI: 10.1111/j.1460-9568.2003.03063.x
    Language: English
    Publisher: Wiley
    Publication Date: 2003
    detail.hit.zdb_id: 2005178-5
    SSG: 12
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  • 3
    Online Resource
    Online Resource
    Inactivation of the ventromedial prefrontal cortex reduces expression of conditioned fear and impairs subsequent recall of extinction
    Wiley ; 2006
    In:  European Journal of Neuroscience Vol. 24, No. 6 ( 2006-09), p. 1751-1758
    Details
    In: European Journal of Neuroscience, Wiley, Vol. 24, No. 6 ( 2006-09), p. 1751-1758
    Abstract: Anxiety disorders are thought to reflect deficits in the regulation of fear expression. Evidence from rodent studies implicates the ventromedial prefrontal cortex (vmPFC) in the regulation of conditioned fear. Lesions of the vmPFC have had differing effects on the acquisition and expression of conditioned fear, as well as on recall of extinction. The use of permanent lesions, however, makes it difficult to assess the phase of training in which the vmPFC is acting and can trigger recruitment of other structures, thereby masking lesion deficits. To overcome these problems, we temporarily inactivated the vmPFC of rats with tetrodotoxin (10 ng in a 0.5‐µl midline infusion) at one of four time points: prior to conditioning, prior to extinction, immediately after extinction or prior to recall of extinction. Consistent with lesion findings, inactivation of the vmPFC prior to acquisition had no effect but inactivation prior to extinction led to impaired recall of extinction the following day. In contrast to lesion findings, inactivation of the vmPFC decreased freezing at all time points, suggesting that some component of the vmPFC facilitates the expression of conditioned fear. These findings suggest that inactivation of the vmPFC can have opposite effects depending on the phase of training. The vmPFC appears to be involved both in stimulating the expression of conditioned fear and in serving as a site of extinction‐related plasticity that inhibits fear during recall of extinction.
    Type of Medium: Online Resource
    ISSN: 0953-816X , 1460-9568
    URL: Issue
    URL: Article
    DOI: 10.1111/ejn.2006.24.issue-6
    DOI: 10.1111/j.1460-9568.2006.05014.x
    Language: English
    Publisher: Wiley
    Publication Date: 2006
    detail.hit.zdb_id: 2005178-5
    SSG: 12
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  • 4
    Online Resource
    Online Resource
    Recalling Safety: Cooperative Functions of the Ventromedial Prefrontal Cortex and the Hippocampus in Extinction
    Cambridge University Press (CUP) ; 2007
    In:  CNS Spectrums Vol. 12, No. 3 ( 2007-03), p. 200-206
    Details
    In: CNS Spectrums, Cambridge University Press (CUP), Vol. 12, No. 3 ( 2007-03), p. 200-206
    Abstract: Anxiety disorders are commonly treated with exposure-based therapies that rely on extinction of conditioned fear. Persistent fear and anxiety following exposure therapy could reflect a deficit in the recall of extinction learning. Animal models of fear learning have elucidated a neural circuit for extinction learning and recall that includes the amygdala, ventromedial prefrontal cortex (vmPFC), and hippocampus. Whereas the amygdala is important for extinction learning, the vmPFC is a site of neural plasticity that allows for the inhibition of fear during extinction recall. We suggest that the vmPFC receives convergent information from other brain regions, such as contextual information from the hippocampus, to determine the circumstances under which extinction or fear will be recalled. Imaging studies of human fear conditioning and extinction lend credence to this extinction network. Understanding the neural circuitry underlying extinction recall will lead to more effective therapies for disorders of fear and anxiety.
    Type of Medium: Online Resource
    ISSN: 1092-8529 , 2165-6509
    URL: Article
    DOI: 10.1017/S1092852900020915
    Language: English
    Publisher: Cambridge University Press (CUP)
    Publication Date: 2007
    detail.hit.zdb_id: 2149753-9
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  • 5
    Online Resource
    Online Resource
    Neurobiological correlates of state-dependent context fear
    Cold Spring Harbor Laboratory ; 2017
    In:  Learning & Memory Vol. 24, No. 9 ( 2017-09), p. 385-391
    Details
    In: Learning & Memory, Cold Spring Harbor Laboratory, Vol. 24, No. 9 ( 2017-09), p. 385-391
    Abstract: Retrieval of fear memories can be state-dependent, meaning that they are best retrieved if the brain states at encoding and retrieval are similar. Such states can be induced by activating extrasynaptic γ-aminobutyric acid type A receptors (GABA A R) with the broad α-subunit activator gaboxadol. However, the circuit mechanisms and specific subunits underlying gaboxadol's effects are not well understood. Here we show that gaboxadol induces profound changes of local and network oscillatory activity, indicative of discoordinated hippocampal–cortical activity, that were accompanied by robust and long-lasting state-dependent conditioned fear. Episodic memories typically are hippocampus-dependent for a limited period after learning, but become cortex-dependent with the passage of time. In contrast, state-dependent memories continued to rely on hippocampal GABAergic mechanisms for memory retrieval. Pharmacological approaches with α-subunit-specific agonists targeting the hippocampus implicated the prototypic extrasynaptic subunits (α 4 ) as the mediator of state-dependent conditioned fear. Together, our findings suggest that continued dependence on hippocampal rather than cortical mechanisms could be an important feature of state-dependent memories that contributes to their conditional retrieval.
    Type of Medium: Online Resource
    ISSN: 1549-5485
    URL: Article
    DOI: 10.1101/lm.045542.117
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2017
    detail.hit.zdb_id: 2022057-1
    SSG: 12
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  • 6
    Online Resource
    Online Resource
    Factors Regulating the Effects of Hippocampal Inactivation on Renewal of Conditional Fear After Extinction
    Cold Spring Harbor Laboratory ; 2004
    In:  Learning & Memory Vol. 11, No. 5 ( 2004-09), p. 598-603
    Details
    In: Learning & Memory, Cold Spring Harbor Laboratory, Vol. 11, No. 5 ( 2004-09), p. 598-603
    Abstract: After extinction of fear to a Pavlovian conditional stimulus (CS), contextual stimuli come to regulate the expression of fear to that CS. There is growing evidence that the context dependence of memory retrieval after extinction involves the hippocampus. In the present experiment, we examine whether hippocampal involvement in memory retrieval after extinction is related to the history of CS presentations in the context used for retrieval testing. We used infusions of muscimol to inactivate the dorsal hippocampus (DH) during postextinction retrieval tests that were conducted in contexts that differed in their history of CS presentations in that context. We found that DH inactivation affected the context-dependent retrieval of extinction (i.e., renewal) when testing occurred in a context that had no history of CS exposure, but not in a context that reliably predicted the CS. These results are discussed in terms of theories regarding the role of the hippocampus in contextual memory retrieval.
    Type of Medium: Online Resource
    ISSN: 1072-0502 , 1549-5485
    URL: Article
    DOI: 10.1101/lm.78704
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2004
    detail.hit.zdb_id: 2022057-1
    SSG: 12
    SSG: 5,2
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  • 7
    Online Resource
    Online Resource
    Differential Contributions of Glutamatergic Hippocampal→Retrosplenial Cortical Projections to the Formation and Persistence of Context Memories
    Oxford University Press (OUP) ; 2019
    In:  Cerebral Cortex Vol. 29, No. 6 ( 2019-06-01), p. 2728-2736
    Details
    In: Cerebral Cortex, Oxford University Press (OUP), Vol. 29, No. 6 ( 2019-06-01), p. 2728-2736
    Type of Medium: Online Resource
    ISSN: 1047-3211 , 1460-2199
    URL: Article
    DOI: 10.1093/cercor/bhy142
    Language: English
    Publisher: Oxford University Press (OUP)
    Publication Date: 2019
    detail.hit.zdb_id: 1483485-6
    SSG: 12
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  • 8
    Online Resource
    Online Resource
    Extinction of Remotely Acquired Fear Depends on an Inhibitory NR2B/PKA Pathway in the Retrosplenial Cortex
    Society for Neuroscience ; 2013
    In:  The Journal of Neuroscience Vol. 33, No. 50 ( 2013-12-11), p. 19492-19498
    Details
    In: The Journal of Neuroscience, Society for Neuroscience, Vol. 33, No. 50 ( 2013-12-11), p. 19492-19498
    Abstract: As memories age, their processing increasingly relies upon cortical rather than hippocampal circuits, but the adaptive significance and mechanisms of this shift are not fully understood. Here we investigated the behavioral features and cortical mechanisms underlying extinction of remotely versus recently acquired context fear in mice. Behaviorally, extinction and reinstatement were similar, but re-extinction of remote fear was significantly faster, suggesting time-dependent engagement of mechanisms specific for processing remote memory. Using pharmacological manipulations of NMDA receptors and associated signaling pathways in the in the retrosplenial cortex, we demonstrated that extinction of remote fear uniquely required NR2B-mediated downregulation of the cAMP-dependent protein kinase (PKA)/cAMP response element-binding protein pathway. Interestingly, NR2B/PKA interactions weakened independently of the age of the memory, but the functional significance of this molecular change was evident only as memory retrieval became PKA-dependent over time. Thus, cortical PKA signaling may provide a molecular signature of when a memory has become “remote,” and inhibition of this pathway may open the door for modulation of remote memories.
    Type of Medium: Online Resource
    ISSN: 0270-6474 , 1529-2401
    URL: Article
    DOI: 10.1523/JNEUROSCI.3338-13.2013
    Language: English
    Publisher: Society for Neuroscience
    Publication Date: 2013
    detail.hit.zdb_id: 1475274-8
    SSG: 12
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  • 9
    Online Resource
    Online Resource
    Contextual and Temporal Modulation of Extinction: Behavioral and Biological Mechanisms
    Elsevier BV ; 2006
    In:  Biological Psychiatry Vol. 60, No. 4 ( 2006-08), p. 352-360
    Details
    In: Biological Psychiatry, Elsevier BV, Vol. 60, No. 4 ( 2006-08), p. 352-360
    Type of Medium: Online Resource
    ISSN: 0006-3223
    URL: Article
    DOI: 10.1016/j.biopsych.2005.12.015
    RVK:
    XA 10000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 2006
    detail.hit.zdb_id: 1499907-9
    SSG: 12
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  • 10
    Online Resource
    Online Resource
    Hippocampal NMDA receptor subunits differentially regulate fear memory formation and neuronal signal propagation
    Wiley ; 2010
    In:  Hippocampus Vol. 20, No. 9 ( 2010-09), p. 1072-1082
    Details
    In: Hippocampus, Wiley, Vol. 20, No. 9 ( 2010-09), p. 1072-1082
    Type of Medium: Online Resource
    ISSN: 1050-9631
    URL: Article
    DOI: 10.1002/hipo.20705
    Language: English
    Publisher: Wiley
    Publication Date: 2010
    detail.hit.zdb_id: 1498049-6
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