Reversal learning of an avoidance response as a function of prior fear conditioning and fear extinction.

1965 ◽  
Vol 19 (2) ◽  
pp. 85-93 ◽  
Author(s):  
Morrie Baum
Keyword(s):  
Avoidance Response ◽  
Fear Conditioning ◽  
Reversal Learning ◽  
Fear Extinction

Improved reversal learning and altered fear conditioning in transgenic mice with regionally restricted p25 expression

2003 ◽  
Vol 18 (2) ◽  
pp. 423-431 ◽  
Author(s):  
Marco Angelo ◽  
Florian Plattner ◽  
Elaine E. Irvine ◽  
K. Peter Giese
Keyword(s):  
Transgenic Mice ◽  
Fear Conditioning ◽  
Reversal Learning

Translational Research from Animals to Humans

2016 ◽  
Author(s):  
Shigeru Morinobu ◽  
Shigeto Yamamoto ◽  
Manabu Fuchikami
Keyword(s):  
Animal Model ◽  
Fear Conditioning ◽  
Fear Extinction ◽  
Contextual Fear Conditioning ◽  
Behavioral Characteristics ◽  
Post Traumatic Stress ◽  
Contextual Fear ◽  
Glycine Transporter 1 ◽  
Post Traumatic ◽  
Prolonged Stress

To elucidate the pathophysiology of post-traumatic stress disorder (PTSD), the establishment of an appropriate animal model is necessary. In a series of studies, the authors validated single prolonged stress (SPS) as a model for PTSD. SPS-treated rats mimic the pathophysiological abnormalities and behavioral characteristics of PTSD, such as enhanced anxiety-like behavior, glucocorticoid negative feedback, and analgesia. In addition, the authors demonstrated enhanced freezing in response to contextual fear conditioning, and impaired extinction of fear memory, which was alleviated by D-cycloserine (DCS). In parallel, there was a decrease in extracellular glycine mediated by an increase in glycine transporter 1 in the hippocampus of SPS-treated rats after fear conditioning, which suggested that activation of N-methyl-D-asparate receptor by DCS during fear extinction training might alleviate the impaired fear extinction. This chapter summarizes PTSD-like symptoms in SPS and evaluates the validity of SPS as an animal model of PTSD.

scholarly journals Controlled cortical impact before or after fear conditioning does not affect fear extinction in mice

2015 ◽  
Vol 1606 ◽  
pp. 133-141 ◽  
Author(s):  
Demetrio Sierra-Mercado ◽  
Lauren M. McAllister ◽  
Christopher C.H. Lee ◽  
Mohammed R. Milad ◽  
Emad N. Eskandar ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Fear Extinction ◽  
Controlled Cortical Impact ◽  
Cortical Impact

scholarly journals GluN2D NMDA Receptors Gate Fear Extinction Learning and Interneuron Plasticity

2021 ◽  
Vol 13 ◽  
Author(s):  
Christophe J. Dubois ◽  
Siqiong June Liu
Keyword(s):  
Nmda Receptor ◽  
Fear Conditioning ◽  
Learning And Memory ◽  
Molecular Layer ◽  
Gaba Release ◽  
Long Term Potentiation ◽  
Fear Extinction ◽  
Fear Learning ◽  
Inhibitory Synapses ◽  
Extinction Learning

The cerebellum is critically involved in the formation of associative fear memory and in subsequent extinction learning. Fear conditioning is associated with a long-term potentiation at both excitatory and inhibitory synapses onto Purkinje cells. We therefore tested whether fear conditioning unmasks novel forms of synaptic plasticity, which enable subsequent extinction learning to reset cerebellar circuitry. We found that fear learning enhanced GABA release from molecular layer interneurons and this was reversed after fear extinction learning. Importantly an extinction-like stimulation of parallel fibers after fear learning is sufficient to induce a lasting decrease in inhibitory transmission (I-LTDstim) in the cerebellar cortex, a form of plasticity that is absent in naïve animals. While NMDA (N-methyl-D-aspartate) receptors are required for the formation and extinction of associative memory, the role of GluN2D, one of the four major NMDA receptor subunits, in learning and memory has not been determined. We found that fear conditioning elevates spontaneous GABA release in GluN2D KO as shown in WT mice. Deletion of GluN2D, however, abolished the I-LTDstim induced by parallel fiber stimulation after learning. At the behavioral level, genetic deletion of GluN2D subunits did not affect associative learning and memory retention, but impaired subsequent fear extinction learning. D-cycloserine, a partial NMDA receptor (NMDAR) agonist, failed to rescue extinction learning in mutant mice. Our results identify GluN2D as a critical NMDAR subunit for extinction learning and reveal a form of GluN2D-dependent metaplasticity that is associated with extinction in the cerebellum.

scholarly journals SUN-235 Deficient Fear Extinction in PRKAR1A-Defective Mice

2020 ◽  
Vol 4 (Supplement_1) ◽  
Author(s):  
Margaret Keil ◽  
Enrica Paradiso ◽  
Rita S Keil ◽  
Maddalena Ugolini ◽  
Evan Harris ◽  
...  
Keyword(s):  
Gene Expression ◽  
Fear Conditioning ◽  
Conditioned Fear ◽  
Critical Role ◽  
Fear Memory ◽  
Brain Regions ◽  
Fear Extinction ◽  
Carney Complex ◽  
Bdnf Gene ◽  
Extinction Learning

Abstract Background: The role of the cAMP/PKA signaling in molecular pathways involved in fear memory is well established: PKA is required for fear memory formation and is a constraint for fear extinction. Previously we reported that a Prkar1a heterozygote (HZ) mouse that was developed in our lab to investigate Carney complex (CNC), the disease caused by PRKAR1A mutations, showed brain region-specific increased PKA activity that was associated with anxiety-like behavioral phenotype and threat bias (Keil, 2010, 2013). We hypothesized that Prkar1a+/- (HZ) mice would have deficits in fear extinction behavior. Brain derived neurotrophic factor (BDNF) has a critical role in formation of fear memory and its transcription is regulated by PKA/CREB. A mouse model with down regulation of PKA provides an opportunity for the first time to investigate the effect of altered PKA signaling on fear conditioning and extinction. Method: Fear conditioning, fear extinction learning, and fear extinction recall were tested in adult male HZ and wild-type (WT) mice as follows: fear conditioning training followed 24hr later by extinction training (new context), then 24hr later by extinction recall training. Percentage of time freezing was used to assess conditioned fear response. We measured BDNF gene expression in brain regions after completion of extinction recall training. Results: As expected, fear conditioning (learning) behavior was similar in HZ and WT mice. However, HZ mice showed a significant deficit in the early phase of fear extinction learning compared to WT. There was no difference in extinction recall between genotypes. Alterations in BDNF gene expression in the prefrontal cortex and amygdala was associated with deficit in fear extinction. Conclusion: Mice with a downregulation of Prkar1a gene demonstrate intact fear conditioning but impaired fear extinction learning, consistent with prior studies that report that PKA inhibition is necessary to facilitate extinction learning. Prkar1a+/- mice provide a valuable model to investigate impaired fear extinction to identify mechanisms for therapeutic targets for anxiety and trauma-related disorders.

scholarly journals Regular Music Exposure in Juvenile Rats Facilitates Conditioned Fear Extinction and Reduces Anxiety after Foot Shock in Adulthood

2019 ◽  
Vol 2019 ◽  
pp. 1-10
Author(s):  
Si Chen ◽  
Tuo Liang ◽  
Fiona H. Zhou ◽  
Ye Cao ◽  
Chao Wang ◽  
...  
Keyword(s):  
Fear Conditioning ◽  
Conditioned Fear ◽  
Conditioning Session ◽  
Fear Extinction ◽  
Extinction Training ◽  
Anterior Cingulate ◽  
Stressful Event ◽  
Sprague Dawley ◽  
Positive Role ◽  
Juvenile Rats

Music exposure is known to play a positive role in learning and memory and can be a complementary treatment for anxiety and fear. However, whether juvenile music exposure affects adult behavior is not known. Two-week-old Sprague-Dawley rats were exposed to music for 2 hours daily or to background noise (controls) for a period of 3 weeks. At 60 days of age, rats were subjected to auditory fear conditioning, fear extinction training, and anxiety-like behavior assessments or to anterior cingulate cortex (ACC) brain-derived neurotrophic factor (BDNF) assays. We found that the music-exposed rats showed significantly less freezing behaviors during fear extinction training and spent more time in the open arm of the elevated plus maze after fear conditioning when compared with the control rats. Moreover, the BDNF levels in the ACC in the music group were significantly higher than those of the controls with the fear conditioning session. This result suggests that music exposure in juvenile rats decreases anxiety-like behaviors, facilitates fear extinction, and increases BDNF levels in the ACC in adulthood after a stressful event.

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