Dorsal hippocampus infusions of <scp>CNQX</scp> into the dentate gyrus disrupt expression of trace fear conditioning

Pierson, Jamie L.; Pullins, Shane E.; Quinn, Jennifer J.

doi:10.1002/hipo.22413

Cited by 22 publications

(26 citation statements)

References 61 publications

(87 reference statements)

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“…However, use of the terms fear learning, fear conditioning, fear-motivated learning, fear memory, and fear extinction has become so widespread that many readers interested in these subjects might well skip altogether an article whose title does not contain those words. So they will be used here as they are in most other recent accounts of the subject (95,98,115,116,182,294,296,299,378,403,421,462,463,468,475,501,524,653).…”

Section: B Fear-motivated Learningmentioning

confidence: 99%

Fear Memory

Izquierdo

Furini

Myskiw

2016

Physiological Reviews

380

259

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Fear memory is the best-studied form of memory. It was thoroughly investigated in the past 60 years mostly using two classical conditioning procedures (contextual fear conditioning and fear conditioning to a tone) and one instrumental procedure (one-trial inhibitory avoidance). Fear memory is formed in the hippocampus (contextual conditioning and inhibitory avoidance), in the basolateral amygdala (inhibitory avoidance), and in the lateral amygdala (conditioning to a tone). The circuitry involves, in addition, the pre-and infralimbic ventromedial prefrontal cortex, the central amygdala subnuclei, and the dentate gyrus. Fear learning models, notably inhibitory avoidance, have also been very useful for the analysis of the biochemical mechanisms of memory consolidation as a whole. These studies have capitalized on in vitro observations on long-term potentiation and other kinds of plasticity. The effect of a very large number of drugs on fear learning has been intensively studied, often as a prelude to the investigation of effects on anxiety. The extinction of fear learning involves to an extent a reversal of the flow of information in the mentioned structures and is used in the therapy of posttraumatic stress disorder and fear memories in general.

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Section: B Fear-motivated Learningmentioning

confidence: 99%

Fear Memory

Izquierdo

Furini

Myskiw

2016

Physiological Reviews

380

259

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“…Trace fear conditioning is similar to delay fear conditioning, except that there is a stimulus-free interval separating the conditioned stimulus (CS) and the unconditioned stimulus (US) presented. Trace fear conditioning depends upon an intact hippocampus (Pierson et al 2015).…”

Section: Impaired Hippocampal-dependent Behavior In Eef2k-ko Micementioning

confidence: 99%

eEF2K/eEF2 Pathway Controls the Excitation/Inhibition Balance and Susceptibility to Epileptic Seizures

et al. 2016

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Alterations in the balance of inhibitory and excitatory synaptic transmission have been implicated in the pathogenesis of neurological disorders such as epilepsy. Eukaryotic elongation factor 2 kinase (eEF2K) is a highly regulated, ubiquitous kinase involved in the control of protein translation. Here, we show that eEF2K activity negatively regulates GABAergic synaptic transmission. Indeed, loss of eEF2K increases GABAergic synaptic transmission by upregulating the presynaptic protein Synapsin 2b and α5-containing GABAA receptors and thus interferes with the excitation/inhibition balance. This cellular phenotype is accompanied by an increased resistance to epilepsy and an impairment of only a specific hippocampal-dependent fear conditioning. From a clinical perspective, our results identify eEF2K as a potential novel target for antiepileptic drugs, since pharmacological and genetic inhibition of eEF2K can revert the epileptic phenotype in a mouse model of human epilepsy.

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“…However, one possibility is that the effects of hippocampal pharamcological manipulations on trace conditioning are highly dependent on target region. Indeed, one study found that blockade of DH AMPA receptors within the dentate gyrus, but not CA1, disrupted trace fear retrieval (Pierson, Pullins, & Quinn, 2015). Therefore, to better understand the role of the hippocampus in trace conditioning, close attention will not only need to be paid to dorsal/ventral regional differences, but also to spatially relevant inputs to the trisinaptic circuit.…”

Section: Declarative Memory and Trace Conditioningmentioning

confidence: 99%

The role of working memory and declarative memory in trace conditioning

Connor

Gould

2016

Neurobiology of Learning and Memory

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Translational assays of cognition that are similarly implemented in both lower and higher-order species, such as rodents and primates, provide a means to reconcile preclinical modeling of psychiatric neuropathology and clinical research. To this end, Pavlovian conditioning has provided a useful tool for investigating cognitive processes in both lab animal models and humans. This review focuses on trace conditioning, a form of Pavlovian conditioning typified by the insertion of a temporal gap (i.e., trace interval) between presentations of a conditioned stimulus (CS) and an unconditioned stimulus (US). This review aims to discuss pre-clinical and clinical work investigating the mnemonic processes recruited for trace conditioning. Much work suggests that trace conditioning involves unique neurocognitive mechanisms to facilitate formation of trace memories in contrast to standard Pavlovian conditioning. For example, the hippocampus and prefrontal cortex (PFC) appear to play critical roles in trace conditioning. Moreover, cognitive mechanistic accounts in human studies suggest that working memory and declarative memory processes are engaged to facilitate formation of trace memories. The aim of this review is to integrate cognitive and neurobiological accounts of trace conditioning from preclinical and clinical studies to examine involvement of working and declarative memory.

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Dorsal hippocampus infusions of CNQX into the dentate gyrus disrupt expression of trace fear conditioning

Cited by 22 publications

References 61 publications

Fear Memory

Fear Memory

eEF2K/eEF2 Pathway Controls the Excitation/Inhibition Balance and Susceptibility to Epileptic Seizures

The role of working memory and declarative memory in trace conditioning

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