Basal forebrain cholinergic lesions disrupt increments but not decrements in conditioned stimulus processing
Open accessAbstract
Magnocellular neurons in the basal forebrain provide the major cholinergic innervation of cortex. Recent research suggests that this cholinergic system plays an important role in the regulation of attentional processes. The present study examined the ability of rats with selective immunotoxic lesions of these neurons (made with 192 IgG- saporin) to modulate attention within an associative learning framework. Each rat was exposed to conditioned stimuli (CS) that were either consistent or inconsistent predictors of subsequent cues. Intact control rats showed increased CS associability when that cue was an inconsistent predictor of a subsequent cue, whereas lesioned rats were impaired in increasing attention to the CS when its established relation to another cue was modified. In a separate experiment designed to test latent inhibition, it was shown that removal of the corticopetal cholinergic neurons spared a decrement in associability that occurs when rats are extensively preexposed to a CS prior to conditioning. These data indicate that the cholinergic innervation of cortex is critical for incrementing, but not for decrementing attentional processing. The specific behavioral tests used to assess the role of the basal forebrain cholinergic system in the present study were previously used to identify a role for the amygdala central nucleus in attention (Holland and Gallagher, 1993b). Those studies, together with the results in this report, indicate that regulation of attentional processes during associative learning may be mediated by projections from the amygdala to the basal forebrain cholinergic system.
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Prediction error and attentional salience are mediated by separate but interacting neurotransmitter systems, dopamine and acetylcholine.
“key drivers of earning -prediction error and attentional salience 18 are mediated by separate but interacting neurotransmitter systems (dopamine and acetylcholine) 20,21 .”
From Computational psychiatry: a Rosetta Stone linking the brain to mental illness (2014) · cites this paper as [20]
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- Authors
- Chiba, A., Bucci, D., Holland, P., & Gallagher, M.
- Affiliations
- University of North Carolina at Chapel Hill (US)
- ORCID
- Gallagher, M
- Venue
- The Journal of Neuroscience
- Publisher
- Society for Neuroscience
- Published
- 1995-11-01
- Volume
- 15
- Issue
- 11
- Pages
- 7315-7322
- ISSN
- 0270-6474 (ISSN-L)
- 1529-2401
- PMC
- PMC6578087
- OpenAlex
- W1854670164
- Cited by
- 257
- References
- 36
- Citations by year
- 2026: 1 · 2024: 1 · 2023: 2 · 2022: 3 · 2021: 2 · 2020: 1 · 2019: 4 · 2018: 5 · 2017: 3 · 2016: 12 · 2015: 9 · 2014: 11 · 2013: 7 · 2012: 10
- FWCI
- 6.21
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- Locations
- Journal of Neuroscience (publishedVersion, cc-by-nc-sa)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Carolina Digital Repository (University of North Carolina at Chapel Hill) (submittedVersion)
- UNC Libraries
- Funders
- National Institutes of Health (1k05mh001149-01a1)
- National Institute on Aging (P01AG009973, P0-AG09973)
- National Institute of Mental Health (F32-MH1099, KO5-MH01149)
- Topics
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuroscience and Neuropharmacology Research
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Keywords
- basal forebrain cholinergic system, attention, associative learning, saporin, latent inhibition, amygdala projections, attentional modulation
- MeSH terms
- Saporins, Animals, Antibodies, Monoclonal, Immunotoxins, Association Learning, Attention, Behavior, Animal, Conditioning, Classical, Cues, Male, Neural Inhibition, N-Glycosyl Hydrolases, Parasympathetic Nervous System, Rats, Inbred Strains, Prosencephalon, Cholinergic Agents, Rats, Ribosome Inactivating Proteins, Type 1
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