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Sustained attention performance in rats with intracortical infusions of 192 IgG-saporin-induced cortical cholinergic deafferentation: Effects of Physostigmine and FG 7142.
Abstract
Rats with extensive lesions of cortical cholinergic afferents as a result of infusions of 192 IgG-saporin into the basal forebrain show persistent impairments in sustained attention performance (J. McGaughy, T. Kaiser, & M. Sarter, 1996). However, the administration of neither the cholinesterase inhibitor physostigmine nor the benzodiazepine receptor partial inverse agonist FG 7142 attenuated the lesion-induced impairments in performance. The present study demonstrated that less extensive cortical cholinergic deafferentation, produced by intracortical infusions of a relatively small concentration of 192 IgG-saporin, resulted in a significant impairment in sustained attention. However, the administration of neither physostigmine (0.01-0.1 mg/kg) nor FG 7142 (0.1-1.0 mg/kg) benefited the performance of the animals. Because neither compound selectively augments performance-associated increases in acetylcholine release from residual neurons, beneficial effects on cortical cholinergic deafferentation-based impairments in attention may remain limited.
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“Persistent spiking may contribute to the generation of responses in the sustained attention task (Sarter et al, 2005; McGaughy and Sarter, 1998).”
From Modes and models of forebrain cholinergic neuromodulation of cognition (2011) · cites this paper as McGaughy and Sarter, 1998
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The cognitive neuroscience of sustained attention: where top-down meets bottom-up.
Sarter, M., Givens, B., & Bruno, J. P. (2001) · Brain Research Reviews · doi:10.1016/s0165-0173(01)00044-3 · Cited by 1,194
Self-citationModes and models of forebrain cholinergic neuromodulation of cognition
Hasselmo, M. E., & Sarter, M. (2011) · Neuropsychopharmacology · doi:10.1038/npp.2010.104 · Cited by 733
Self-citationSarter, M., Hasselmo, M. E., Bruno, J. P., & Givens, B. (2005) · Brain Research Reviews · doi:10.1016/j.brainresrev.2004.08.006 · Cited by 667
Self-citationAdenosine and sleep–wake regulation
Basheer, R., Strecker, R. E., Thakkar, M. M., & McCarley, R. W. (2004) · Progress in Neurobiology · doi:10.1016/j.pneurobio.2004.06.004 · Cited by 620
Hasselmo, M. E., & McGaughy, J. (2004) · Progress in Brain Research · doi:10.1016/s0079-6123(03)45015-2 · Cited by 525
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Metadata
- Authors
- McGaughy, J., & Sarter, M.
- Affiliations
- The Ohio State University (US)
- Venue
- Behavioral Neuroscience
- Published
- 1998
- Volume
- 112
- Issue
- 6
- Pages
- 1519-1525
- ISSN
- 0735-7044 (ISSN-L)
- 1939-0084
- OpenAlex
- W2046080212
- Cited by
- 147
- References
- 0
- Citations by year
- 2026: 1 · 2024: 1 · 2022: 3 · 2021: 2 · 2020: 2 · 2019: 3 · 2018: 3 · 2017: 3 · 2016: 3 · 2015: 6 · 2014: 9 · 2013: 8 · 2012: 9
- FWCI
- 2.64
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Behavioral Neuroscience (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5r01ag010173-10)
- National Institute on Aging (AG10 173)
- National Institute of Mental Health (MH01072, K02MH001072)
- National Institute of Neurological Disorders and Stroke (NS32938, R01NS032938)
- Topics
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neurotransmitter Receptor Influence on Behavior
- Health Sciences › Medicine › Pharmacology (medical) › Cholinesterase and Neurodegenerative Diseases
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Nicotinic Acetylcholine Receptors Study
- Keywords
- sustained attention, physostigmine, FG 7142, cholinesterase inhibitors, acetylcholine release, basal forebrain lesions, attention deficits, rats
- MeSH terms
- Saporins, Afferent Pathways, Animals, Immunotoxins, Appetitive Behavior, Attention, Brain Mapping, Carbolines, Cerebral Cortex, Cholinergic Fibers, Discrimination Learning, Immunoglobulin G, Male, N-Glycosyl Hydrolases, Physostigmine, Plant Proteins, Rats, Inbred Strains, Prosencephalon, GABA Antagonists, Rats, Ribosome Inactivating Proteins, Type 1
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