Differential impairment of auditory and contextual fear conditioning by protein synthesis inhibition in C57BL/6N mice.

Stiedl, Oliver; Palve, Markki; Radulovic, Jelena; Birkenfeld, Karin; Spiess, Joachim

doi:10.1037/0735-7044.113.3.496

Cited by 47 publications

(40 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Some studies have shown that foreground conditioning results in stronger conditioning [62,77], while other studies have not found this effect [15,5,43,51,60,61]. Although no differences in freezing to the context were found between background and foreground conditioning in the current study, previous work in our lab has demonstrated that there are differences in the effects of foreground and background conditioning that are visible at one week, but not at 24 hours, post-training [32].…”

Section: Discussioncontrasting

confidence: 79%

“…When the foot shocks are administered without the auditory stimulus, in foreground conditioning, the context is more salient and becomes a foreground stimulus that elicits a CR [56,57]. Thus, it is unknown if nicotine withdrawal will disrupt foreground as well as background fear conditioning Interestingly, acquisition and consolidation of background contextual fear conditioning may involve different cellular substrates than acquisition and consolidation of foreground contextual fear conditioning [62,77]. Trifilieff and colleagues [81] demonstrated that consolidation of foreground contextual fear conditioning recruits distinct early and late phases of protein synthesis in the hippocampus and amygdala, while background contextual fear conditioning recruits only the early phase.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Nicotine withdrawal disrupts both foreground and background contextual fear conditioning but not pre-pulse inhibition of the acoustic startle response in C57BL/6 mice

André

Gulick

Portugal

et al. 2008

Behavioural Brain Research

View full text Add to dashboard Cite

Nicotine withdrawal is associated with multiple symptoms such as anxiety, increased appetite, and disrupted cognition in humans. Although animal models have provided insights into the somatic and affective symptoms of nicotine withdrawal, less research has focused on the effects of nicotine withdrawal on cognition. Therefore, in this study, C57BL/6 mice were used to test the effects of withdrawal from chronic nicotine on foreground and background contextual fear conditioning, which present the context as a primary or secondary stimulus, respectively. Mice withdrawn from 12 days of chronic nicotine (6.3 mg/kg/day) or saline were trained and tested in either foreground or background contextual fear conditioning; nicotine withdrawal-associated deficits in contextual fear conditioning were observed in both conditions. Mice were also tested for the effects of withdrawal on pre-pulse inhibition of the acoustic startle reflex (PPI), a measure of sensory gating, and on the acoustic startle reflex. Mice withdrawn from 12 days of chronic nicotine (6.3 or 12.6 mg/kg/day) or saline underwent one 30-minute PPI and startle session; no effect of withdrawal from chronic nicotine on PPI or startle was observed for either dose at 24 hours after nicotine removal. Therefore, mice were tested at different time points following withdrawal from 12.6 mg/kg/day chronic nicotine (8, 24, and 48 hours after nicotine removal). No effect of withdrawal from chronic nicotine was observed at any time point for PPI. Overall, these results demonstrate that nicotine withdrawal disrupts two methods of contextual learning but not sensory gating in C57BL/6 mice.

show abstract

Section: Discussioncontrasting

confidence: 79%

Section: Introductionmentioning

confidence: 99%

Nicotine withdrawal disrupts both foreground and background contextual fear conditioning but not pre-pulse inhibition of the acoustic startle response in C57BL/6 mice

André

Gulick

Portugal

et al. 2008

Behavioural Brain Research

View full text Add to dashboard Cite

show abstract

“…Context 2 was cleaned with 1% acetic acid before each experiment. A small amount of home cage embedding was transferred to context 2 to mimic home cage-like conditions and to reduce generalized fear (Stiedl et al, 1999a). The light intensity in context 2 was adjusted to ϳ420 lux.…”

Section: Methodsmentioning

confidence: 99%

Corticotropin-Releasing Factor Receptor 1 and Central Heart Rate Regulation in Mice during Expression of Conditioned Fear

Stiedl¹,

Meyer²,

Jahn³

et al. 2004

J Pharmacol Exp Ther

Self Cite

View full text Add to dashboard Cite

The present study was performed to 1) determine heart rate (HR) effects mediated through central corticotropin-releasing factor receptor subtypes 1 (CRF 1 ) and 2 (CRF 2 ) and 2) to investigate the contribution of endogenous CRF to baseline HR and its fear-induced adjustment in freely moving mice. CRF ligands were injected into both lateral ventricles (i.c.v.) 15 min before the presentation of a conditioned auditory fear stimulus (CS). Initial behavioral results suggest an ovine CRF (oCRF)-mediated enhanced baseline fear and mildly enhanced conditioned auditory fear. In contrast, i.c.v. injection of oCRF (35-210 ng/mouse) dose-dependently decreased baseline HR, increased HR variability, and attenuated the CS-induced tachycardia. This effect is suggested to depend on a combined activation of sympathetic and parasympathetic activity referred to as enhanced sympathovagal antagonism. An extreme bradycardia was elicited by oCRF injection into the lower brainstem. All HR effects were probably mediated by CRF 1 because injection of the CRF 2 -selective agonist mouse urocortin II was ineffective, and the baseline bradycardia by i.c.v. CRF was preserved in CRF 2 -deficient mice. Injection of various CRF receptor antagonists including the CRF 2 -selective antisauvagine-30 did not affect the conditioned HR response. This finding suggests that endogenous CRF does not contribute to the fear-mediated tachycardia. Thus, the hypothesis of an involvement of CRF in HR responses of mice to acute aversive stimulation is rejected. Pharmacological evidence points at the involvement of CRF 1 in enhanced sympathovagal antagonism, a pathological state contributing to elevated cardiac risk, whereas the physiological role of the brain CRF system in cardiovascular regulation remains to be determined.

show abstract

“…If undisturbed, an induction of the transcription factors c-fos, c-jun, and NGFI-A occurs in the BLA during this initial phase of memory formation (e.g., Campeau et al 1991;Beck and Fibiger 1995;Rosen et al 1998). Studies in various behavioral paradigms (Grecksch and Matthies 1980;Tiunova et al 1998) including fear conditioning (Stiedl et al 1999) have furthermore suggested the existence of a second time window of protein synthesis several hours after training that is critical for memory consolidation. However, little is known about the molecular and cellular processes or the genes that are expressed during this time window.…”

mentioning

confidence: 99%

Identification of Genes Expressed in the Amygdala During the Formation of Fear Memory

Stork

Stork²,

Pape³

et al. 2001

Learn. Mem.

View full text Add to dashboard Cite

In this study we describe changes of gene expression that occur in the basolateral complex of the mouse amygdala (BLA) during the formation of fear memory. Through the combination of a behavioral training scheme with polymerase chain reaction-based expression analysis (subtractive hybridization and virtual Northern analysis) we were able to identify various gene products that are increased in expression after Pavlovian fear conditioning and are of potential significance for neural plasticity and information storage in the amygdala. In particular, a key enzyme of monoamine metabolism, aldehyde reductase, and the protein sorting and ubiquitination factor Praja1, showed pronounced and learning-specific induction six hours after fear conditioning training. Aldehyde reductase and Praja1, including a novel alternatively spliced isoform termed Praja1a, were induced in the BLA depending on the emotional stimulus presented and showed different expression levels in response to associative conditioning, training stress, and experience of conditioned fear. Stress and fear were further found to induce various signal transduction factors (transthyretin, phosphodiesterase1, protein kinase inhibitor-␣) and structural reorganization factors (e.g., E2-ubiquitin conjugating enzyme, neuroligin1, actin, UDP-galactose transporter) during training. Our results show that the formation of Pavlovian fear memory is associated with changes of gene expression in the BLA, which may contribute to neural plasticity and the processing of information about both conditioned and unconditioned fear stimuli.[The Praja1a sequence has been deposited in GenBank data base under accession no. AF335250.]

show abstract

Differential impairment of auditory and contextual fear conditioning by protein synthesis inhibition in C57BL/6N mice.

Cited by 47 publications

References 30 publications

Nicotine withdrawal disrupts both foreground and background contextual fear conditioning but not pre-pulse inhibition of the acoustic startle response in C57BL/6 mice

Nicotine withdrawal disrupts both foreground and background contextual fear conditioning but not pre-pulse inhibition of the acoustic startle response in C57BL/6 mice

Corticotropin-Releasing Factor Receptor 1 and Central Heart Rate Regulation in Mice during Expression of Conditioned Fear

Identification of Genes Expressed in the Amygdala During the Formation of Fear Memory

Contact Info

Product

Resources

About