Lead exposure in late adolescence through adulthood impairs short-term spatial memory and the neuronal differentiation of adult-born cells in C57BL/6 male mice

Abstract Background: Nowadays, anesthetic drugs are widely used in anesthesia and surgical procedures and their effects on memory have been the focus of attention for a very long time. The effects of these common drugs include Dexmedetomidine (DEX) and Etomidate (ETO), on memory are controversial. In this study, the effects of these two drugs, co-administrated with heights stress, were evaluated on short-term and long-term spatial memory. 48 male mice were divided into 6 experimental groups consisting of Control, Control+heightstress (H.S), ETO, ETO+H.S, DEX+H.S. Drugs were administered Intra-peritoneal with doses of 0.3-0.4 mg/kg and 11 mg/kg for DEX and ETO respectively, and spatial memory was assessed using the Barnes Model.Results: DEX improved acquisition and retention of spatial reference memory, whereas ETO showed no such effects. In addition, DEX and ETO showed excitatory effects on short-term spatial memory, however DEX was more effective than ETO.Conclusion: the results suggested the neuoprotective, synaptic plasticity and memory improving effects of DEX on spatial reference and working memory. However, the precise neuronal and molecular mechanisms of these effects and their relation to the anti-stress system is still unknown and requires further research.

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Attenuation of zinc-enhanced inflammatory M1 phenotype of microglia by peridinin protects against short-term spatial-memory impairment following cerebral ischemia in mice

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2018.11.067 ◽

2018 ◽

Vol 507 (1-4) ◽

pp. 476-483 ◽

Cited By ~ 4

Author(s):

Yusuke Ueba ◽

Takaaki Aratake ◽

Ken-ichi Onodera ◽

Youichirou Higashi ◽

Tomoya Hamada ◽

...

Keyword(s):

Cerebral Ischemia ◽

Spatial Memory ◽

Memory Impairment ◽

Short Term ◽

M1 Phenotype

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Subchronic Oral Bromocriptine Methanesulfonate Enhances Open Field Novelty-Induced Behavior and Spatial Memory in Male Swiss Albino Mice

Neuroscience Journal ◽

10.1155/2013/948241 ◽

2013 ◽

Vol 2013 ◽

pp. 1-5

Author(s):

Olakunle James Onaolapo ◽

Adejoke Yetunde Onaolapo

Keyword(s):

Spatial Memory ◽

Open Field ◽

Cumulative Effect ◽

Male Mice ◽

Healthy Male ◽

Swiss Albino Mice ◽

Y Maze ◽

Field Assessment ◽

Albino Mice ◽

Neurobehavioral Effects

This study set out to assess the neurobehavioral effects of subchronic, oral bromocriptine methanesulfonate using the open field and the Y-maze in healthy male mice. Sixty adult Swiss albino mice were assigned into three groups. Controls received normal saline, while test groups received bromocriptine methanesulfonate at 2.5 and 5 mg/kg/day, respectively, for a period of 21 days. Neurobehavioral tests were carried out on days 1 and 21 after administration. Open field assessment on day 1 after administration revealed significant increase in grooming at 2.5 and 5 mg/kg, while horizontal and vertical locomotion showed no significant changes. Day 1 also showed no significant changes in Y-maze alternation. On day 21, horizontal locomotion, rearing, and grooming were increased significantly at 2.5 and 5 mg/kg doses after administration; also, spatial memory was significantly enhanced at 2.5 mg/kg. In conclusion, the study demonstrates the ability of oral bromocriptine to affect neurobehavior in normal mice. It also suggests that there is a cumulative effect of oral bromocriptine on the behaviors studied with more changes being seen after subchronic administration rather than after a single oral dose.

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The Dose-dependent Dual Effects of Corticosterone on Spatial Memory Ability After Traumatic Brain Injury Are Mediated by Two Corticosteroid Receptor Systems

10.21203/rs.3.rs-520614/v1 ◽

2021 ◽

Author(s):

Bin Zhang ◽

Mengshi Yang ◽

Qiongyu Yan ◽

Xiaojian Xu ◽

Fei Niu ◽

...

Keyword(s):

Traumatic Brain Injury ◽

Brain Injury ◽

Spatial Memory ◽

Signaling Pathways ◽

Hippocampal Neurons ◽

High Dose ◽

Short Term ◽

Memory Ability ◽

Neurotoxic Effects ◽

Dose Dependent

Abstract Background: Our recent studies reported the opposite effects of mineralocorticoid receptor (MR) and glucocorticoid receptor (GR) on neuron survival after traumatic brain injury (TBI). However, as a mixed agonist for MR and GR, whether short term use of high-dose endogenous glucocorticoids exerts neurotoxic effects by excessive activation of GR, what is the set-point, and the possible signaling pathways remain unclear. This study examined the dose-dependent dual effects of corticosterone (CORT) on the spatial memory, the survival of hippocampal neurons and the possible receptor-mediated downstream signaling pathways after TBI.Methods: Based on controlled cortical impact (CCI) and CORT treatments, Sprague-Dawley rats (n=168) were randomly divided into the sham, CCI, CCI + CORT1 (0.3 mg/kg), CCI + CORT2 (3 mg/kg), CCI + CORT3 (30 mg/kg), CCI + CORT1 + spirolactone (spirolactone: 50 mg/kg/d), and CCI + CORT3 + RU486 (RU486: 50 mg/kg/d) groups. Brain tissues were collected on postinjury day 3 and processed for histology and western blot analysis.Results: On postinjury day 3, we tested the learning and memory ability, neuronal apoptosis in the hippocampus, activation levels of MR and GR, Bcl-2 family proteins, and apoptosis-related intracellular signaling pathways. We found that different doses of CORT exhibited dual effects on the survival of hippocampal neurons and the spatial memory. Lower doses of CORT (0.3, 3 mg/kg) significantly increased the activation of MR, upregulated the phosphorylation of Akt/CREB/Bad and the Bcl-2 expression, reduced the number of apoptotic neurons, and subsequently improved the spatial memory. In contrast, higher dose of CORT (30 mg/kg) exerted opposite effect by over activating GR, upregulating the expressions of P53/Bax, and inhibiting the Erk/CREB activities. Conclusion: The results suggest that there is a threshold between the neuroprotective and neurotoxic effects of endogenous GC, higher dose of which, even for short-term use, should also be avoided after TBI.

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Reduced Liver-Specific PGC1a Increases Susceptibility for Short-Term Diet-induced Weight Gain in Male Mice

10.1101/2020.12.04.412460 ◽

2020 ◽

Author(s):

E. Matthew Morris ◽

Roberto D. Noland ◽

Michael E. Ponte ◽

Michelle L. Montonye ◽

Julie A. Christianson ◽

...

Keyword(s):

Fatty Acid ◽

Weight Gain ◽

Energy Metabolism ◽

Energy Balance ◽

Fatty Acid Oxidation ◽

Positive Energy ◽

Acid Oxidation ◽

Male Mice ◽

Short Term

AbstractCentral integration of peripheral neural signals is one mechanism by which systemic energy homeostasis is regulated. Previous work described increased acute food intake following chemical reduction of hepatic fatty acid oxidation and ATP levels, which was prevented by common hepatic branch vagotomy (HBV). However, possible offsite actions of the chemical compounds confound the precise role of liver energy metabolism. Herein, we used a liver-specific PGC1a heterozygous (LPGC1a) mouse model, with associated reductions in mitochondrial fatty acid oxidation and respiratory capacity, to assess the role of liver energy metabolism in systemic energy homeostasis. LPGC1a male mice have 70% greater high-fat/high-sucrose (HFHS) diet-induced weight gain and 35% greater positive energy balance compared to wildtype (WT) (p<0.05). The greater energy balance was associated with altered feeding behavior and lower activity energy expenditure during HFHS in LPGC1a males. Importantly, no differences in HFHS-induced weight gain or energy metabolism was observed between female WT and LPGC1a mice. WT and LPGC1a mice underwent sham or HBV to assess whether vagal signaling was involved in HFHS-induced weight gain of male LPGC1a mice. HBV increased HFHS-induced weight gain (85%, p<0.05) in male WT, but not LPGC1a mice. As above, sham LPGC1a males gain 70% more weight during short-term HFHS feeding than sham WT (p<0.05). These data demonstrate a sexspecific role of reduced liver energy metabolism in acute diet-induced weight gain, and the need of more nuanced assessment of the role of vagal signaling in short-term diet-induced weight gain.Key Points SummaryReduced liver PGC1a expression results in reduced mitochondrial fatty acid oxidation and respiratory capacity in male mice.Male mice with reduced liver PGC1a expression (LPGC1a) demonstrate greater short-term high-fat/high-sucrose diet-induced weight gain compared to wildtype.Greater positive energy balance during HFHS feeding in male LPGC1a mice is associated with altered food intake patterns and reduced activity energy expenditure.Female LPGC1a mice do not have differences in short-term HFHS-induced body weight gain or energy metabolism compared to wildtype.Disruption of vagal signaling through common hepatic branch vagotomy increases short-term HFHS-induced weight gain in male wildtype mice, but does not alter male LPGC1a weight gain.

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