GLORIA

GEOMAR Library Ocean Research Information Access

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
Filter
  • Cold Spring Harbor Laboratory  (3)
  • 1
    Online Resource
    Online Resource
    Cold Spring Harbor Laboratory ; 2017
    In:  Learning & Memory Vol. 24, No. 9 ( 2017-09), p. 385-391
    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
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2017
    detail.hit.zdb_id: 2022057-1
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 2
    Online Resource
    Online Resource
    Cold Spring Harbor Laboratory ; 2016
    In:  Learning & Memory Vol. 23, No. 11 ( 2016-11), p. 631-638
    In: Learning & Memory, Cold Spring Harbor Laboratory, Vol. 23, No. 11 ( 2016-11), p. 631-638
    Abstract: Understanding how episodic memories are formed and retrieved is necessary if we are to treat disorders in which they malfunction. Muscarinic acetylcholine receptors (mAChR) in the hippocampus and cortex underlie memory formation, but there is conflicting evidence regarding their role in memory retrieval. Additionally, there is no consensus on which mAChR subtypes are critical for memory processing. Using pharmacological and genetic approaches, we found that (1) encoding and retrieval of contextual memory requires mAChR in the dorsal hippocampus (DH) and retrosplenial cortex (RSC), (2) memory formation requires hippocampal M 3 and cooperative activity of RSC M 1 and M 3, and (3) memory retrieval is more impaired by inactivation of multiple M 1 –M 4 mAChR in DH or RSC than inactivation of individual receptor subtypes. Contrary to the view that acetylcholine supports learning but is detrimental to memory retrieval, we found that coactivation of multiple mAChR is required for retrieval of both recently and remotely acquired context memories. Manipulations with higher receptor specificity were generally less potent than manipulations targeting multiple receptor subtypes, suggesting that mAChR act in synergy to regulate memory processes. These findings provide unique insight into the development of therapies for amnestic symptoms, suggesting that broadly acting, rather than receptor-specific, mAchR agonists and positive allosteric modulators may be the most effective therapeutic approach.
    Type of Medium: Online Resource
    ISSN: 1549-5485
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2016
    detail.hit.zdb_id: 2022057-1
    SSG: 12
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
  • 3
    In: Learning & Memory, Cold Spring Harbor Laboratory, Vol. 16, No. 4 ( 2009-04), p. 273-278
    Abstract: Extinction of fear requires learning that anticipated aversive events no longer occur. Animal models reveal that sustained phosphorylation of the extracellular signal-regulated kinase (Erk) in hippocampal CA1 neurons plays an important role in this process. However, the key signals triggering and regulating the activity of Erk are not known. By varying the degree of expected and delivered aversive reinforcement, we demonstrate that Erk specifically responds to prediction errors of contextual aversive events. An increase of somatonuclear phospho-Erk (pErk) within principal CA1 neurons was observed only when the expectation of contextual foot shock was violated, but not when the context was consistently nonreinforced or reinforced by foot shock. The rate of error detection, Erk signaling, and fear extinction markedly depended on shock expectancy and the aversive valence of the context, as revealed by comparison of groups trained with single, continuous, or partial reinforcement. On the basis of these findings, the hippocampal Erk response to prediction errors of aversive outcome is proposed as a unique mechanism of fear extinction. Improving the detection and processing of these errors has the potential to attenuate fear responses in patients with anxiety disorders.
    Type of Medium: Online Resource
    ISSN: 1072-0502 , 1549-5485
    Language: English
    Publisher: Cold Spring Harbor Laboratory
    Publication Date: 2009
    detail.hit.zdb_id: 2022057-1
    SSG: 12
    SSG: 5,2
    Location Call Number Limitation Availability
    BibTip Others were also interested in ...
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...