Time-dependent behavioral recovery after sepsis in rats
- PMID: 18542919
- DOI: 10.1007/s00134-008-1129-1
Time-dependent behavioral recovery after sepsis in rats
Abstract
Objective: To evaluate the cognitive performance in rats that survived sepsis induced by cecal ligation and puncture (CLP) after 10, 30 and 60 days.
Design: Prospective, controlled experiment.
Setting: Animal basic science laboratory.
Subjects: Male Wistar rats, weighing 300-350 g.
Interventions: The rats were sham-operated or submitted to CLP (sepsis group) with "basic support" (saline, s.c. at 50 mL/kg immediately and 12 h after CLP plus ceftriaxone, s.c. at 30 mg/kg and clindamycin, s.c. at 25 mg/kg 6, 12 and 18 h after CLP).
Measurements and main results: The animals underwent six behavioral tasks 10, 30 and 60 days after surgery: (a) habituation to the open field; (b) inhibitory avoidance task; (c) continuous multiple trials step-down inhibitory avoidance task; (d) object recognition; (e) elevated plus-maze; and (f) forced swimming test. We demonstrated that survivors 10 days after CLP presented deficits on the habituation to the open field, step-down inhibitory avoidance, continuous multiple-trials step-down inhibitory avoidance, object recognition and forced swimming. After 30 days of sepsis induction, survivors maintained deficits on the step-down inhibitory avoidance, continuous multiple-trials step-down inhibitory avoidance and forced swimming. However, after 60 days all behavior deficits were reversed.
Conclusions: These results indicate that the impairment of memory and learning, demonstrated 10 days after the induction of sepsis, persist 30 days after the CLP. The cognitive impairments did not persist after 60 days suggesting that this model can help in the understanding of the biological mechanisms associated with sepsis-induced sickness behavior.
Comment in
-
Time-dependent behavioral recovery after sepsis in rats.Intensive Care Med. 2009 Mar;35(3):576; author reply 577. doi: 10.1007/s00134-008-1369-0. Epub 2008 Dec 16. Intensive Care Med. 2009. PMID: 19083198 No abstract available.
Similar articles
-
Cognitive impairment in sepsis survivors from cecal ligation and perforation.Crit Care Med. 2005 Jan;33(1):221-3; discussion 262-3. doi: 10.1097/01.ccm.0000150741.12906.bd. Crit Care Med. 2005. PMID: 15644673
-
Behavioral deficits in sepsis-surviving rats induced by cecal ligation and perforation.Braz J Med Biol Res. 2007 Jun;40(6):831-7. doi: 10.1590/s0100-879x2007000600013. Braz J Med Biol Res. 2007. PMID: 17581683
-
Antioxidant treatment prevented late memory impairment in an animal model of sepsis.Crit Care Med. 2007 Sep;35(9):2186-90. doi: 10.1097/01.ccm.0000281452.60683.96. Crit Care Med. 2007. PMID: 17855835
-
What animal models can tell us about long-term cognitive dysfunction following sepsis: A systematic review.Neurosci Biobehav Rev. 2021 May;124:386-404. doi: 10.1016/j.neubiorev.2020.12.005. Epub 2020 Dec 9. Neurosci Biobehav Rev. 2021. PMID: 33309906
-
A review of behavioral methods for the evaluation of cognitive performance in animal models: Current techniques and links to human cognition.Physiol Behav. 2022 Feb 1;244:113652. doi: 10.1016/j.physbeh.2021.113652. Epub 2021 Nov 18. Physiol Behav. 2022. PMID: 34801559 Review.
Cited by
-
Amelioration of Neurochemical Alteration and Memory and Depressive Behavior in Sepsis by Allopurinol, a Tryptophan 2,3-Dioxygenase Inhibitor.CNS Neurol Disord Drug Targets. 2024;23(12):1499-1515. doi: 10.2174/0118715273282363240415045927. CNS Neurol Disord Drug Targets. 2024. PMID: 38712373
-
Cognitive dysfunction is sustained after rescue therapy in experimental cerebral malaria, and is reduced by additive antioxidant therapy.PLoS Pathog. 2010 Jun 24;6(6):e1000963. doi: 10.1371/journal.ppat.1000963. PLoS Pathog. 2010. PMID: 20585569 Free PMC article.
-
Dimethyl Fumarate Limits Neuroinflammation and Oxidative Stress and Improves Cognitive Impairment After Polymicrobial Sepsis.Neurotox Res. 2018 Oct;34(3):418-430. doi: 10.1007/s12640-018-9900-8. Epub 2018 Apr 30. Neurotox Res. 2018. PMID: 29713994
-
The Methylglyoxal/RAGE/NOX-2 Pathway is Persistently Activated in the Hippocampus of Rats with STZ-Induced Sporadic Alzheimer's Disease.Neurotox Res. 2022 Apr;40(2):395-409. doi: 10.1007/s12640-022-00476-9. Epub 2022 Feb 2. Neurotox Res. 2022. PMID: 35106732
-
Aversive memory in sepsis survivor rats.J Neural Transm (Vienna). 2011 Feb;118(2):213-7. doi: 10.1007/s00702-010-0502-8. Epub 2010 Oct 24. J Neural Transm (Vienna). 2011. PMID: 20972806
References
Publication types
MeSH terms
LinkOut - more resources
Full Text Sources
Medical
Miscellaneous