Regulation of Synaptic Plasticity Genes during Consolidation of Fear Conditioning

Ressler, Kerry J.; Paschall, Gayla Y.; Zhou, Xiaoliu; Davis, Michael

doi:10.1523/jneurosci.22-18-07892.2002

Cited by 197 publications

(159 citation statements)

References 60 publications

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“…158 In our latest study we replicated the acquisition finding, reporting a decrease in gephyrin protein and the surface expression of GABA A receptors 2 and 6 h after fear acquisition, respectively. Following extinction training, gephyrin mRNA, gephyrin protein and GABA A receptor binding increased at 2, 4 and 6 h, respectively.…”

Section: Neurotransmitter Systemssupporting

confidence: 69%

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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Section: Neurotransmitter Systemssupporting

confidence: 69%

Mechanisms of fear extinction

2006

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“…Aversive stimulation has been shown to induce a second stage of protein synthesis that reaches a significantly increased level 4-8 h after stimulus presentation (Grecksch and Matthies 1980;Freeman et al 1995;Quevedo et al 1999;Ressler et al 2002). Therefore, we administered ANI at 3, 6, and 18 h after sampling.…”

Section: Discussionmentioning

confidence: 99%

“…However, in the search for the molecular constituents of such a "memory trace" in the brain, the behavioral tasks used have focused on associative learning (e.g., fear conditioning and avoidance learning). Under certain conditions it has also been reported that two or more stages of protein synthesis are involved in memory consolidation (Grecksch and Matthies 1980;Freeman et al 1995;Quevedo et al 1999;Ressler et al 2002). However, classical (fear) conditioning and avoidance learning require negative reinforcement.…”

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confidence: 99%

Social recognition memory requires two stages of protein synthesis in mice

Richter¹,

Wolf²,

Engelmann³

2005

Learn. Mem.

104

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Olfactory recognition memory was tested in adult male mice using a social discrimination task. The testing was conducted to begin to characterize the role of protein synthesis and the specific brain regions associated with activity in this task. Long-term olfactory recognition memory was blocked when the protein synthesis inhibitor anisomycin was injected 20 min before, immediately after, or 6 h after sampling. No effect was observed when anisomycin was administered 3 h or 18 h after sampling. Immunohistochemical analysis of Fos expression revealed that sampling-like exposure to a juvenile increased the activity of a subset of cells in the accessory olfactory bulb and the brain areas that are associated with it. Additionally, increased Fos expression was measured in the main olfactory bulb and the piriform cortex, whereas no signs of activation were seen in the cortical nucleus of the amygdala, all components of the main olfactory system. No increases in Fos immunoreactivity were observed after 4 h. Our data suggest that long-lasting olfactory recognition memory requires two stages of protein synthesis. The first stage takes place within 1–2 h and the second stage between 6–7 h after sampling. The first but not the second stage is paralleled by an increase in the number of Fos-immunoreactive cells in brain areas associated with both the main and accessory olfactory systems. It therefore appears that the role of the second stage of protein synthesis in recognition memory depends on the integrity of the first stage of protein synthesis

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“…Electrophysiological and c-fos immunoreactivity studies in rodents have indeed demonstrated that the habenula is activated in response to various aversive stressors, including stimulation of the tail, restraint, novel environments, and footshock (Benabid and Jeaugey, 1989;Wirtshafter et al, 1994;Gao et al, 1996;Smith et al, 1997). We have previously reported that the habenula also showed increased expression of synaptic plasticity genes associated with long-term changes in neuronal activity in response to stress associated with fear conditioning (Ressler et al, 2002). Along with evidence indicating the habenula's role in regulating monoamine transmission, these results suggest that stress may induce long-term structural changes in the habenula which influences subsequent monoamine-dependent behaviors.…”

Section: Introductionmentioning

confidence: 95%

Lesions of the habenula produce stress- and dopamine-dependent alterations in prepulse inhibition and locomotion

Heldt

Ressler

2006

Brain Research

Self Cite

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The habenula complex modulates the a ctivity of dopamine and serotonin systems in the brain. An important question remains whether there is a link between habenula dysfunction and monoaminerelated disorders, such as schizophrenia. In this study, we describe an interaction between habenula lesions and stress that produces long-lasting effects on behavior. Mice received control lesions or bilateral electrolytic lesions of the habenula and were tested for fear-potentiated startle and freezing measures of conditioned fear. They w ere also tested for prepulse inhibition (PPI) and locomotor activity in the presence or absence of a dopaminergic agonist (apomorphine) or an atypical antipsychotic with mixed dopamine/serotonin antagonist properties (clozapine). There were no detectable effects of habenula lesions on fear conditioning and no effects on PPI in the absence o f stress. However, following conditioned fear stress, habenula-lesioned animals showed decreased PPI which normalized with clozapine. Lesioned animals also showed diminished activity at baseline, with hyperlocomotion following apomorphine. These data support the hypothesis that the habenula may be normally involved in stress-dependent regulation of monoamine systems.

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Regulation of Synaptic Plasticity Genes during Consolidation of Fear Conditioning

Cited by 197 publications

References 60 publications

Mechanisms of fear extinction

Mechanisms of fear extinction

Social recognition memory requires two stages of protein synthesis in mice

Lesions of the habenula produce stress- and dopamine-dependent alterations in prepulse inhibition and locomotion

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