Abstract
IntroductionSurvivors from sepsis have presented with long-term cognitive impairment, including alterations in memory, attention, concentration, and global loss of cognitive function. Thus, we evaluated the effects of memory enhancers in sepsis-surviving rats.MethodsThe rats underwent cecal ligation and perforation (CLP) (sepsis group) with 'basic support' (saline at 50 mL/kg immediately and 12 hours after CLP plus ceftriaxone at 30 mg/kg and clindamycin at 25 mg/kg 6, 12, and 18 hours after CLP) or sham-operated (control group). After 10 or 30 days, rats were submitted to an inhibitory avoidance task. After task training, animals received injections of saline, epinephrine, naloxone, dexamethasone, or glucose. Twenty-four hours afterwards, animals were submitted to the inhibitory avoidance test.ResultsWe demonstrated that memory enhancers reversed impairment in the sepsis group 10 and 30 days after sepsis induction. This effect was of lower magnitude when compared with sham animals 10 days, but not 30 days, after sepsis.ConclusionsUsing different pharmacologic approaches, we conclude that the adrenergic memory formation pathways are responsive in sepsis-surviving animals.
Highlights
Survivors from sepsis have presented with longterm cognitive impairment, including alterations in memory, attention, concentration, and global loss of cognitive function
We demonstrated that memory enhancers reversed impairment in the sepsis group 10 and 30 days after sepsis induction
Using different pharmacologic approaches, we conclude that the adrenergic memory formation pathways are responsive in sepsis-surviving animals
Summary
Survivors from sepsis have presented with longterm cognitive impairment, including alterations in memory, attention, concentration, and global loss of cognitive function. It has been demonstrated that survivors from sepsis presented longterm cognitive impairment, including alterations in memory, attention, concentration, and global loss of cognitive function [2]. Opioid receptors are involved in memory modulation, and post-training injections of the opioid antagonist naloxone (NAL) enhance retention of inhibitory avoidance in rats [9]. In this context, we investigated whether some of the molecular mechanisms associated with memory formation are preserved in sepsis survivors using the posttraining administration of EPI, NAL, dexamethasone (DEX), and glucose (GLU) in a step-down inhibitory avoidance task in rats
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