Journal
NAUNYN-SCHMIEDEBERGS ARCHIVES OF PHARMACOLOGY
Volume 395, Issue 12, Pages 1573-1585Publisher
SPRINGER
DOI: 10.1007/s00210-022-02286-4
Keywords
Inflammation; Immune challenge; Lymnaea stagnalis; Learning; memory; Aerial respiration; Homeostasis
Categories
Funding
- Natural Sciences and Engineering Research Council of Canada
- Regione EmiliaRomagna L.R. N. 20/2002 PROGETTI DI RICERCA SUI METODI ALTERNATIVI ALL'UTILIZZO DI ANIMALI
- FAR 2016 Department of Life Sciences, University of Modena and Reggio Emilia
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By studying the pond snail as an invertebrate model system, we found that LPS-induced inflammation can cause sickness and impair cognitive function, but can be restored by aspirin.
By employing a reductionistic (but not simplistic) approach using an established invertebrate model system, the pond snail Lymnaea stagnalis, we investigated whether (1) lipopolysaccharide (LPS)-induced inflammation would cause a sickness state and impair cognitive function, and-if so-(2) would aspirin (acetylsalicylic acid-ASA) restore the impaired cognition. To test our hypotheses, we first determined if the injection of 25 mg (6.25 mu g/mL) of Escherichia coli-derived LPS serotype O127:B8 altered homeostatic behavior, aerial respiration, and then determined if LPS altered memory formation when this behavior was operantly conditioned. Next, we determined if ASA altered the LPS-induced changes in both aerial respiration and cognitive functions. LPS induced a sickness state that increased aerial respiration and altered the ability of snails to form or recall long-term memory. ASA reverted the LPS-induced sickness state and thus allowed long-term memory both to be formed and recalled. We confirmed our hypotheses and provided the first evidence in an invertebrate model system that an injection of LPS results in a sickness state that obstructs learning and memory, and this impairment can be prevented by a non-steroidal anti-inflammatory.
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