The effects of neurotoxic hippocampal lesions on two effects of context after fear extinction.

Frohardt, Russell J.; Guarraci, Fay A.; Bouton, Mark E.

doi:10.1037/0735-7044.114.2.227

Cited by 119 publications

(172 citation statements)

References 45 publications

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“…Contextual fear extinction was impaired in mice with a reduced HC (strain 9XCA/ Wah). Like fear conditioning, extinction has been proposed to be a form of new learning rather than an erasure of existing memories (for review, see Bouton, 1993), and it is dependent on hippocampal function (Wilson et al, 1995;Frohardt et al, 2000) (see also Fox and Holland, 1998). In addition, extinction is NMDA receptor dependent (Lee and Kim, 1998;Santini et al, 2001) (but see Berman and Dudai, 2001) and requires protein synthesis (Flood et al, 1977;Berman and Dudai, 2001;Vianna et al, 2001), similar to fear conditioning.…”

Section: Discussionmentioning

confidence: 99%

Selective Modification of Short-Term Hippocampal Synaptic Plasticity and Impaired Memory Extinction in Mice with a Congenitally Reduced Hippocampal Commissure

Schimanski¹,

Wahłsten

Nguyen

2002

J. Neurosci.

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The hippocampus is critical for forming new long-term memories, but the contributions of the hippocampal commissure (HC) to memory function and hippocampal synaptic plasticity are unclear. To shed light on this issue, we characterized behavioral memory and hippocampal synaptic plasticity in two inbred mouse strains. BALB/cWah1 mice display a range of corpus callosal defects and an intact HC, whereas 9XCA/Wah mice exhibit a complete absence of corpus callosum and a greatly reduced HC. No differences between strains were found in long-term potentiation (LTP) within two synaptic pathways in hippocampal slices. However, paired-pulse facilitation was deficient in area CA1 of slices from 9XCA/Wah, and it was rescued by decreasing extracellular [Ca 2ϩ ], suggesting that presynaptic calcium dynamics may be altered in this strain. In addition, contextual fear extinction was impaired in 9XCA/Wah mice, but performance on cued fear extinction and on 24 hr memory tests for cued and contextual fear conditioning were not significantly different between strains. Thus, an intact HC is critical for normal extinction of contextual fear. Intact interhemispheric connectivity is not required for acquisition or expression of cued and contextual fear conditioning. LTP was normal in slices from mice that lacked an intact HC, and this was correlated with normal performance on fear conditioning tests. In contrast, impaired short-term synaptic plasticity was correlated with defective contextual memory extinction in mice lacking an intact HC. Thus, the HC in mice is vital for particular aspects of memory function and for short-term synaptic modification in specific hippocampal circuits. Key words: hippocampal commissure; memory; learning; LTP; fear conditioning; extinction; agenesis; mouse strains; synaptic plasticityThe classic case study of H.M., a patient with surgical transection of the medial temporal lobes, demonstrated that the hippocampus is critical for the formation of new declarative memories (Scoville and Milner, 1957). Studies of human commissurotomy patients indicate that the main interhemispheric communication pathway between hippocampi, the hippocampal commissure (HC), is important for normal memory function. Indeed, patients with a transected HC show greater recognition memory deficits than those with an intact HC (Phelps et al., 1991). Patients with transection of both the corpus callosum (CC) and the HC also showed poor memory performance (Zaidel and Sperry, 1974). These findings indicate that an intact CC and HC are required for normal memory function.In two common inbred mouse strains, BALB/c and 129, agenesis of the CC occurs in Ͻ50% of these mice, whereas the remainder appear to have normal forebrain commissures (see Fig.

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Section: Discussionmentioning

confidence: 99%

Selective Modification of Short-Term Hippocampal Synaptic Plasticity and Impaired Memory Extinction in Mice with a Congenitally Reduced Hippocampal Commissure

Schimanski¹,

Wahłsten

Nguyen

2002

J. Neurosci.

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“…110 Consistent with this general framework, reinstatement of extinguished fear, a context-specific phenomenon thought to be mediated primarily by context-US associations, is disrupted by pretraining radiofrequency lesions of fimbria-fornix 111 or pretraining electrolytic lesions of hippocampus. 112 Hippocampal involvement in renewal is more complex. Studies involving permanent, pretraining lesions of fimbria-fornix 111 or hippocampus 112,113 have reported inconsistent effects, but studies employing temporary inactivation of hippocampus via localized infusions of the GABA A receptor agonist muscimol have reported specific deficits.…”

Section: Neural Mechanismsmentioning

confidence: 99%

“…112 Hippocampal involvement in renewal is more complex. Studies involving permanent, pretraining lesions of fimbria-fornix 111 or hippocampus 112,113 have reported inconsistent effects, but studies employing temporary inactivation of hippocampus via localized infusions of the GABA A receptor agonist muscimol have reported specific deficits. When animals are tested in a novel context (AAB or ABC renewal) and muscimol is infused into hippocampus before test, renewal is not observed (i.e., freezing is equally low in all contexts).…”

Section: Neural Mechanismsmentioning

confidence: 99%

“…In most experiments there is no effect of these manipulations 112,113,118 but there is one report of a decrease in freezing across an extinction training session following pretraining electrolytic lesions 113 and one report of a disruption of within-session extinction following pre-extinction training infusions of muscimol. 114 Two recent physiological studies by Garcia and co-workers indicate that long-term potentiation (LTP) is induced in the output pathways of the dorsal 119 and ventral 120 hippocampus by extinction training; that extinction is impaired by application of depotentiation-inducing low-frequency stimulation to the dorsal hippocampus following extinction training; 119 and that application of LTP-inducing high-frequency stimulation to the dorsal hippocampus shortly after depotentiation induction restores extinction behavior.…”

Section: Neural Mechanismsmentioning

confidence: 99%

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Mechanisms of fear extinction

2006

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Excessive fear and anxiety are hallmarks of a variety of disabling anxiety disorders that affect millions of people throughout the world. Hence, a greater understanding of the brain mechanisms involved in the inhibition of fear and anxiety is attracting increasing interest in the research community. In the laboratory, fear inhibition most often is studied through a procedure in which a previously fear conditioned organism is exposed to a fear-eliciting cue in the absence of any aversive event. This procedure results in a decline in conditioned fear responses that is attributed to a process called fear extinction. Extensive empirical work by behavioral psychologists has revealed basic behavioral characteristics of extinction, and theoretical accounts have emphasized extinction as a form of inhibitory learning as opposed to an erasure of acquired fear. Guided by this work, neuroscientists have begun to dissect the neural mechanisms involved, including the regions in which extinction-related plasticity occurs and the cellular and molecular processes that are engaged. The present paper will cover behavioral, theoretical and neurobiological work, and will conclude with a discussion of clinical implications. Molecular Psychiatry (2007) 12, 120-150.

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“…Contextual information can resolve this ambiguity because rats trained in context A and extinguished in context B will display a renewed conditioned response if they are retested in context A (the ABA design) or another context C (the ABC design). Bouton and colleagues (Wilson et al 1995;Frohardt et al 2000) were the first to examine the contribution of the hippocampal formation to context-specific extinction. Using the ABA design, they found no evidence that relatively complete damage to the hippocampal formation disrupted context-specific extinction.…”

Section: Conditional Discrimination Type IImentioning

confidence: 99%

Context representations, context functions, and the parahippocampal–hippocampal system

Rudy¹

2009

Learn. Mem.

266

309

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Psychologists and neurobiologists have a long-standing interest in understanding how the context surrounding the events of our lives is represented and how it influences our behavior. The hippocampal formation emerged very early as a major contributor to how context is represented and functions. There is a large literature examining its contribution that on the surface reveals an array of conflicting outcomes and controversy. This review reveals that these conflicts can be resolved by building Nadel and Willner's dual-process theory of context representations. Two general conclusions emerge: (1) There are two neural systems that can support context representations and functions-a neocortical system composed primarily of perirhinal and postrhinal cortices and a hippocampal system that includes perirhinal, postrhinal, entorhinal cortices, and the hippocampal formation. (2) These two systems are not equivalent-some context representations and functions are uniquely supported by the hippocampal system. These conclusions are discussed in the context of canonical ideas about the special properties of the hippocampal system that enable it to make unique contributions to memory.Everything we experience happens somewhere. The term ''context'' is often used to denote this ''somewhere.'' In the analysis of learning and memory, the context is like the setting for a stage play (Medin and Reynolds 1985). It provides the background for the real action in the drama-the main events. More importantly, as a consequence of learning and memory processes, the context often helps to select appropriate behaviors and determine the explicit and implicit content of our thoughts. Thus, it is not surprising that psychologists have a long-standing empirical and theoretical interest in understanding just what makes up a representation of context and how context representations interact with the main events of our lives to influence our behavior (see Balsam and Tomie 1985).More recently, neurobiologists have increased their interest in the problem of linking context representations and functions to brain systems. The hippocampal formation emerged quite early as a major focal point among many researchers. As a result, there is a substantial literature linking the hippocampal formation and context. However, on the surface, this research yields a dismaying set of conflicting results, with many findings that the hippocampal formation plays a critical role in supporting the influence of context on memory and behavior and many other findings that it does not.The goal of this article is to bring some clarity and order to this state of affairs. I start by providing a working definition of ''context'' that implicitly underpins its experimental analysis. I then describe several different functions of context that have been studied in the laboratory and are assumed to be theoretically important. I then introduce and build on a dual-process theory of context representations that was put forth several years ago by Lynn Nadel, Jeffrey Willner, and colleague...

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The effects of neurotoxic hippocampal lesions on two effects of context after fear extinction.

Cited by 119 publications

References 45 publications

Selective Modification of Short-Term Hippocampal Synaptic Plasticity and Impaired Memory Extinction in Mice with a Congenitally Reduced Hippocampal Commissure

Selective Modification of Short-Term Hippocampal Synaptic Plasticity and Impaired Memory Extinction in Mice with a Congenitally Reduced Hippocampal Commissure

Mechanisms of fear extinction

Context representations, context functions, and the parahippocampal–hippocampal system

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