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An acute seizure prior to memory reactivation transiently impairs associative memory performance in C57BL/6J mice.

ABSTRACT: Memory deficits significantly decrease an individual's quality of life and are a pervasive comorbidity of epilepsy. Despite the various distinct processes of memory, the majority of epilepsy research has focused on seizures during the encoding phase of memory, therefore the effects of a seizure on other memory processes is relatively unknown. In the present study, we investigated how a single seizure affects memory reactivation in C57BL/6J adult mice using an associative conditioning paradigm. Initially, mice were trained to associate a tone (conditioned stimulus), with the presence of a shock (unconditioned stimulus). Flurothyl was then administered 1 h before, 1 h after, or 6 h before a memory reactivation trial. The learned association was then assessed by presenting a conditioned stimulus in a new context 24 h or 1 wk after memory reactivation. We found that mice receiving a seizure 1 h prior to reactivation exhibited a deficit in memory 24 h later but not 1 wk later. When mice were administered a seizure 6 h before or 1 h after reactivation, there were no differences in memory between seizure and control animals. Altogether, our study indicates that an acute seizure during memory reactivation leads to a temporary deficit in associative memory in adult mice. These findings suggest that the cognitive impact of a seizure may depend on the timing of the seizure relative to the memory process that is active.

SUBMITTER: Binder MS

PROVIDER: S-EPMC7433655 | biostudies-literature |

REPOSITORIES: biostudies-literature

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Project description:BackgroundTo date, there is only scare evidence characterizing the temporal features and progression of metabolic dysfunction in high-fat diet (HFD)-fed obese mice. Hence, its specific pathogenesis remains unclear.MethodsSixty 6-week-old male C57BL/6J mice were randomly divided into HFD and control diet (CD) groups and sacrificed at 1, 5, 9, 13, 17, and 21 weeks, respectively. At weekly intervals, intraperitoneal glucose tolerance testing (IPGTT) and intraperitoneal insulin tolerance testing (IPITT) were performed in both groups. A detailed time course in HFD-fed mice was investigated by evaluating the initiation of glucose homeostasis impairment, dyslipidemia, systemic insulin sensitivity, monocyte chemoattractant protein-1 (MCP-1) levels, epididymal white adipose tissue (eWAT) expansion, macrophage content changes, pro-inflammatory (M1)/anti-inflammatory (M2) macrophage imbalance, lipid accumulation in the liver, and β-cell morphometry in the pancreas.ResultsIn the HFD group, progressive weight gain and impairments in glucose metabolism (elevated fasting blood glucose and area under the curve (AUC) of IPGTT) were observed from the 3rd week, and a significantly elevated AUC of IPITT was first detected after week 7 of HFD feeding. As for dyslipidemia, after 9 weeks of feeding, the low-density lipoprotein cholesterol level and total cholesterol level in HFD group were significantly higher than those in the CD group (all P < 0.05), whereas no significant differences were shown in triglyceride level. Adipocyte size increased significantly in the HFD group in the 1st week, a phenotypic switch in eWAT from anti-inflammatory (M2) to pro-inflammatory (M1) macrophages was observed in the 5th week, and the metabolic inflammation was distinct in eWAT in the 9th week. Additionally, liver steatosis was considerably obvious at the 17th week and pancreatic β-cell morphometry did not change during 21 weeks of HFD feeding.ConclusionThe eWAT expansion was detected early in HFD-induced obese mice, which occurred prior to obvious insulin resistance.

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An acute seizure prior to memory reactivation transiently impairs associative memory performance in C57BL/6J mice.

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