ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013
Blockade of stimulus convergence in amygdala neurons disrupts taste associative learning.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 14 citations in OpenAlex.
- A neural mechanism for learning from delayed postingestive feedback.bioRxiv : the preprint server for biology · 2024Article
- Engram mechanisms of memory linking and identity.Nature reviews. Neuroscience · 2024Review
- The Functional and Neurobiological Properties of Bad Taste.Physiological reviews · 2019Review
- The Insula and Taste Learning.Frontiers in molecular neuroscience · 2017Review
- A molecular mechanism underlying gustatory memory trace for an association in the insular cortex.eLife · 2015Article
- Synaptic tagging during memory allocation.Nature reviews. Neuroscience · 2014Review
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Humans and non-human animals learn associations of temporally contingent stimuli to better cope with the changing environment. In animal models of classical conditioning, a neutral conditioned stimulus (CS) predicts an aversive unconditioned stimulus (US). Several lines of indirect evidence indicate that this learning may rely on stimulus convergence in a subset of neurons, but this hypothesis has not been directly tested. In the current study, we tested this hypothesis using a pharmacogenetic approach, the cAMP response element-binding protein (CREB)/Allatostatin Receptor system, to target a subset of amygdala neurons receiving convergent stimuli in mice during conditioned taste aversion. Virally infected basolateral amygdala neurons with higher CREB levels were predominantly active during CS presentation. Blocking stimulus convergence in infected neurons by silencing them during US disrupted taste associative memory. Moreover, silencing infected neurons only during CS also disrupted associative memory formation. These results provide support for the notion that convergent inputs of CS and US in a subpopulation of neurons are critical for associative memory formation.
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Registered trials
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