ArticleBehavioral neuroscience2020
Involvement of the bed nucleus of the stria terminalis in initial conditioning and rapid reconditioning following extinction of contextual fear.
Article in Behavioral neuroscience, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Bed nucleus of the stria terminalis GABA neurons are necessary for changes in foraging behaviour following an innate threat.The European journal of neuroscience · 2023Article
- Effects of a cue associated with cocaine or food reinforcers on extinction and postextinction return of behavior.Behavioral neuroscience · 2022Article
- NMDA receptors in the CeA and BNST differentially regulate fear conditioning to predictable and unpredictable threats.Neurobiology of learning and memory · 2020Article
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Authors and funding
2 authors.
Funding
Abstract
Although a great deal is known about neurobiological mechanisms of initial conditioning and extinction, relatively little is known about mechanisms involved in the return of behavior following extinction. In this article, we examine the effects of temporarily inactivating the bed nucleus of the stria terminalis (BNST) on initial conditioning and postextinction reconditioning. We investigate effects in unsignaled contextual fear conditioning, in which animals initially receive strong contextual conditioning, followed by three sessions of nonreinforced context exposure (extinction), and then receive a single context-shock reconditioning trial. In 2 experiments with male Long Evans rats, we evaluated the effects of delivery of a muscimol/baclofen cocktail to the BNST prior to initial conditioning or reconditioning. In Experiment 1, we found that a single context-shock pairing results in more freezing following extinction than when it is the initial conditioning trial. This rapid reconditioning effect was impaired by BNST inactivation. In Experiment 2, we found that BNST inactivation also causes a deficit in freezing after strong initial conditioning. These findings suggest that the BNST is involved in both initial conditioning and postextinction reconditioning. We discuss implications of these findings for current thinking about BNST function in learning and memory processes. (PsycInfo Database Record (c) 2020 APA, all rights reserved).
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