Fear Extinction
Mostrando 13-23 de 23 artigos, teses e dissertações.
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13. Factors Regulating the Effects of Hippocampal Inactivation on Renewal of Conditional Fear After Extinction
After extinction of fear to a Pavlovian conditional stimulus (CS), contextual stimuli come to regulate the expression of fear to that CS. There is growing evidence that the context dependence of memory retrieval after extinction involves the hippocampus. In the present experiment, we examine whether hippocampal involvement in memory retrieval after extinctio
Cold Spring Harbor Laboratory Press.
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14. CB1 Cannabinoid Receptors Modulate Kinase and Phosphatase Activity During Extinction of Conditioned Fear in Mice
Cannabinoid receptors type 1 (CB1) play a central role in both short-term and long-term extinction of auditory-cued fear memory. The molecular mechanisms underlying this function remain to be clarified. Several studies indicated extracellular signal-regulated kinases (ERKs), the phosphatidylinositol 3-kinase with its downstream effector AKT, and the phosphat
Cold Spring Harbor Laboratory Press.
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15. Thickness of ventromedial prefrontal cortex in humans is correlated with extinction memory
The ventromedial prefrontal cortex (vmPFC) has been implicated in fear extinction [Phelps, E. A., Delgado, M. R., Nearing, K. I. & Ledoux, J. E. (2004) Neuron 43, 897-905; Herry, C. & Garcia, R. (2003) Behav. Brain Res. 146, 89-96]. Here, we test the hypothesis that the cortical thickness of vmPFC regions is associated with how well healthy humans retain the
National Academy of Sciences.
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16. AX+, BX- Discrimination Learning in the Fear-Potentiated Startle Paradigm: Possible Relevance to Inhibitory Fear Learning in Extinction
The neural mechanisms of fear suppression most commonly are studied through the use of extinction, a behavioral procedure in which a feared stimulus (i.e., one previously paired with shock) is nonreinforced repeatedly, leading to a reduction or elimination of the fear response. Although extinction is perhaps the most convenient index of fear inhibition, a gr
Cold Spring Harbor Laboratory Press.
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17. Lesions of Rat Infralimbic Cortex Enhance Recovery and Reinstatement of an Appetitive Pavlovian Response
The prefrontal cortex (PFC) has a well-established role in the inhibition of inappropriate responding, and evidence suggests that the infralimbic (IL) region of the rat medial PFC (MPFC) may be involved in some aspects of extinction of conditioned fear. MPFC lesions including, but not those sparing the IL cortex increase spontaneous recovery of extinguished
Cold Spring Harbor Laboratory Press.
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18. Retrieval of memory for fear-motivated training initiates extinction requiring protein synthesis in the rat hippocampus
Evidence that protein synthesis inhibitors induce amnesia in a variety of species and learning paradigms indicates that the consolidation of newly acquired information into stable memories requires the synthesis of new proteins. Because extinction of a response also requires acquisition of new information, extinction, like original learning, would be expecte
The National Academy of Sciences.
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19. Intrinsic Neuronal Excitability Is Reversibly Altered by a Single Experience in Fear Conditioning
Learning is known to cause alterations in intrinsic cellular excitability but, to date, these changes have been seen only after multiple training trials. A powerful learning task that can be quickly acquired and extinguished with a single trial is fear conditioning. Rats were trained and extinguished on a hippocampus-dependent form of fear conditioning to de
American Physiological Society.
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20. Nonassociative learning processes determine expression and extinction of conditioned fear in mice
Freezing to a tone following auditory fear conditioning is commonly considered as a measure of the strength of the tone-shock association. The decrease in freezing on repeated nonreinforced tone presentation following conditioning, in turn, is attributed to the formation of an inhibitory association between tone and shock that leads to a suppression of the e
Cold Spring Harbor Laboratory Press.
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21. The L-type calcium channel blocker nifedipine impairs extinction, but not reduced contingency effects, in mice
We recently reported that fear extinction, a form of inhibitory learning, is selectively blocked by systemic administration of L-type voltage-gated calcium channel (LVGCC) antagonists, including nifedipine, in mice. We here replicate this finding and examine three reduced contingency effects after vehicle or nifedipine (40 mg/kg) administration. In the first
Cold Spring Harbor Laboratory Press.
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22. Improvements in Hippocampal-Dependent Learning and Decremental Attention in 5-HT3 Receptor Overexpressing Mice
The 5-HT3 receptor for serotonin is expressed within limbic structures and is known to modulate neurotransmitter release, suggesting that this receptor may influence learning and memory. Perturbations in serotonergic neurotransmission lead to changes in the ability to attend, learn, and remember. To examine the role of 5-HT3 receptors in learning, memory, an
Cold Spring Harbor Laboratory Press.
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23. Working memory and fear conditioning
Previous studies of associative learning implicate higher-level cognitive processes in some forms of classical conditioning. An ongoing debate is concerned with the extent to which attention and awareness are necessary for trace but not delay eye-blink conditioning [Clark, R. E. & Squire, L. R. (1998) Science 280, 77–81; Lovibond, P. F. & Shanks, D. (2002)
The National Academy of Sciences.