Influence of diurnal phase on behavioral tests of sensorimotor performance, anxiety, learning and memory in mice

AbstractBehavioral measurements in mice are critical tools used to evaluate the effects of interventions. Whilst mice are nocturnal animals, many studies conduct behavioral tests during the day. To better understand the effects of diurnal rhythm on mouse behaviors, we compared the results from behavioral tests conducted in the active and inactive phases. C57BL/6 mice were used in this study; we focus on sensorimotor performance, anxiety, learning and memory. Overall, our results show mice exhibit slightly higher cutaneous sensitivity, better long-term contextual memory, and a greater active avoidance escape response during the active phase. We did not observe significant differences in motor coordination, anxiety, or spatial learning and memory. Furthermore, apart from the elevated-O-maze, there was no remarkable sex effect among these tests. This study provides information on the effects of different diurnal phases on types of behavior and demonstrates the importance of the circadian cycle on learning and memory. Although we did not detect differences in anxiety and spatial learning/memory, diurnal rhythm may interact with other factors to influence these behaviors.

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A Long-Term Enriched Environment Ameliorates the Accelerated Age-Related Memory Impairment Induced by Gestational Administration of Lipopolysaccharide: Role of Plastic Mitochondrial Quality Control

Frontiers in Cellular Neuroscience ◽

10.3389/fncel.2020.559182 ◽

2021 ◽

Vol 14 ◽

Author(s):

Zhan-Qiang Zhuang ◽

Zhe-Zhe Zhang ◽

Yue-Ming Zhang ◽

He-Hua Ge ◽

Shi-Yu Sun ◽

...

Keyword(s):

Learning And Memory ◽

Spatial Learning ◽

Memory Impairment ◽

Spatial Learning And Memory ◽

Mitochondrial Quality Control ◽

Protein Levels ◽

Age Related ◽

Old Mice ◽

Lps Treatment

Studies have shown that gestational inflammation accelerates age-related memory impairment in mother mice. An enriched environment (EE) can improve age-related memory impairment, whereas mitochondrial dysfunction has been implicated in the pathogenesis of brain aging. However, it is unclear whether an EE can counteract the accelerated age-related memory impairment induced by gestational inflammation and whether this process is associated with the disruption of mitochondrial quality control (MQC) processes. In this study, CD-1 mice received daily intraperitoneal injections of lipopolysaccharide (LPS, 50 μg/kg) or normal saline (CON group) during gestational days 15–17 and were separated from their offspring at the end of normal lactation. The mothers that received LPS were divided into LPS group and LPS plus EE (LPS-E) treatment groups based on whether the mice were exposed to an EE until the end of the experiment. At 6 and 18 months of age, the Morris water maze test was used to evaluate spatial learning and memory abilities. Quantitative reverse transcription polymerase chain reaction and Western blot were used to measure the messenber RNA (mRNA) and protein levels of MQC-related genes in the hippocampus, respectively. The results showed that all the aged (18 months old) mice underwent a striking decline in spatial learning and memory performances and decreased mRNA/protein levels related to mitochondrial dynamics (Mfn1/Mfn2, OPA1, and Drp1), biogenesis (PGC-1α), and mitophagy (PINK1/parkin) in the hippocampi compared with the young (6 months old) mice. LPS treatment exacerbated the decline in age-related spatial learning and memory and enhanced the reduction in the mRNA and protein levels of MQC-related genes but increased the levels of PGC-1α in young mice. Exposure to an EE could alleviate the accelerated decline in age-related spatial learning and memory abilities and the accelerated changes in MQC-related mRNA or protein levels resulting from LPS treatment, especially in aged mice. In conclusion, long-term exposure to an EE can counteract the accelerated age-related spatial cognition impairment modulated by MQC in CD-1 mother mice that experience inflammation during pregnancy.

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Treadmill exercise prevents decline in spatial learning and memory in APP/PS1 transgenic mice through improvement of hippocampal long-term potentiation

Behavioural Brain Research ◽

10.1016/j.bbr.2010.12.030 ◽

2011 ◽

Vol 218 (2) ◽

pp. 308-314 ◽

Cited By ~ 94

Author(s):

Hui-li Liu ◽

Gang Zhao ◽

Kui Cai ◽

Hai-hua Zhao ◽

Li-de Shi

Keyword(s):

Transgenic Mice ◽

Learning And Memory ◽

Spatial Learning ◽

Treadmill Exercise ◽

Long Term Potentiation ◽

Spatial Learning And Memory ◽

Term Potentiation

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Long-term green tea catechin administration prevents spatial learning and memory impairment in senescence-accelerated mouse prone-8 mice by decreasing Aβ1-42 oligomers and upregulating synaptic plasticity–related proteins in the hippocampus

Neuroscience ◽

10.1016/j.neuroscience.2009.07.014 ◽

2009 ◽

Vol 163 (3) ◽

pp. 741-749 ◽

Cited By ~ 105

Author(s):

Q. Li ◽

H.F. Zhao ◽

Z.F. Zhang ◽

Z.G. Liu ◽

X.R. Pei ◽

...

Keyword(s):

Synaptic Plasticity ◽

Learning And Memory ◽

Green Tea ◽

Spatial Learning ◽

Memory Impairment ◽

Spatial Learning And Memory ◽

Green Tea Catechin ◽

Related Proteins ◽

Senescence Accelerated Mouse

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Post-weaning mice fed exclusively milk have deficits in induction of long-term depression in the CA1 hippocampal region and spatial learning and memory

Neuroscience Research ◽

10.1016/j.neures.2012.05.006 ◽

2012 ◽

Vol 73 (4) ◽

pp. 292-301 ◽

Cited By ~ 3

Author(s):

Hideaki Nishie ◽

Ryouhei Miyata ◽

Ryu Fujikawa ◽

Ken-ichi Kinoshita ◽

Yoshikage Muroi ◽

...

Keyword(s):

Learning And Memory ◽

Spatial Learning ◽

Spatial Learning And Memory ◽

Hippocampal Region ◽

Long Term Depression

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Effect of Short- and Long-Term Administration of Baclofen on Spatial Learning and Memory in Rats

Physiological Research ◽

10.33549/physiolres.933554 ◽

2018 ◽

pp. 133-141 ◽

Cited By ~ 1

Author(s):

M. HOLAJOVA ◽

M. FRANEK

Keyword(s):

Learning And Memory ◽

Spatial Learning ◽

Receptor Agonist ◽

Gabab Receptor ◽

Spatial Learning And Memory ◽

Adult Rats ◽

Treatment Groups ◽

Term Administration ◽

Short And Long Term

Baclofen is the only clinically available metabotropic GABAB receptor agonist. In our experiment, we tested the hypothesis that long-term baclofen administration can impair learning and memory in rats. The experiment consisted of three parts. In the first part of the study the drug was administered simultaneously with the beginning of the behavioral tests. In the second and third part of the experiment baclofen was administered daily for 14 days and for one month before the tests. In each part of the experiment, adult rats were randomly divided into four treatment groups. Three groups were given an injection of baclofen at doses of 1 mg/kg, 5 mg/kg, 10 mg/kg, while the fourth group was injected with saline. The injections were given after each session. Spatial learning and memory were tested using the Morris water maze, involving three types of tests: Acquisition, Probe, and Re-acquisition. This work reveals that baclofen did not affect spatial learning at any of the tested doses and regardless of the length of administration. Memory was observed to be affected, but only at the highest dose of baclofen and only temporarily. This conclusion is in line with previously published clinical cases.

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The Contribution of Stem Cell Factor and Granulocyte Colony-Stimulating Factor in Reducing Neurodegeneration and Promoting Neural Network Reorganization after Traumatic Brain Injury

10.21203/rs.2.17381/v2 ◽

2020 ◽

Author(s):

Junchi He ◽

Thomas Russell ◽

Xuecheng Qiu ◽

Fei Hao ◽

Michele Kyle ◽

...

Keyword(s):

Frontal Cortex ◽

Learning And Memory ◽

Spatial Learning ◽

Spatial Learning And Memory ◽

Granulocyte Colony Stimulating Factor ◽

Hippocampal Ca1 ◽

Severe Tbi ◽

Apical Dendrites ◽

Stimulating Factor

Abstract Background Traumatic brain injury (TBI) is a major cause of death and disability in young adults worldwide. TBI-induced long-term cognitive deficits represent a growing clinical problem. Stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) are involved in neuroprotection and neuronal plasticity. However, the knowledge concerning reparative efficacy of SCF+G-CSF treatment in post-acute TBI recovery remains incomplete. This study aims to determine the efficacy of SCF+G-CSF on post-acute TBI recovery in young adult mice. The controlled cortical impact model of TBI was used for inducing a severe damage in the motor cortex of the right hemisphere in 8-week-old male C57BL mice. SCF+G-CSF treatment was initiated 3 weeks after induction of TBI. Results Severe TBI led to persistent motor functional deficits (Rota-Rod test) and impaired spatial learning and memory (Morris water maze test). SCF+G-CSF treatment significantly improved the severe TBI-impaired spatial learning and memory 6 weeks after treatment. TBI also caused significant increases of Fluoro-Jade C positive degenerating neurons in bilateral frontal cortex, striatum and hippocampus, and significant reductions in MAP2 + apical dendrites and overgrowth of SMI312 + axons in peri-TBI cavity frontal cortex and in the ipsilateral hippocampal CA1 at 24 weeks post-TBI. SCF+G-CSF treatment significantly reduced TBI-induced neurodegeneration in the contralateral frontal cortex and hippocampal CA1, increased MAP2 + apical dendrites in the peri-TBI cavity frontal cortex, and prevented TBI-induced axonal overgrowth in both the peri-TBI cavity frontal cortex and ipsilateral hippocampal CA1. Conclusions These findings reveal a novel pathology of axonal overgrowth after TBI and demonstrate a therapeutic potential of SCF+G-CSF in ameliorating TBI-induced long-term neuronal pathology, neural network malformation, and impairments in spatial learning and memory.

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The Contribution of Stem Cell Factor and Granulocyte-Colony Stimulating Factor in Reducing Neurodegeneration and Promoting Neural Network Reorganization after Traumatic Brain Injury

10.21203/rs.2.17381/v1 ◽

2019 ◽

Author(s):

Junchi He ◽

Thomas Russell ◽

Xuecheng Qiu ◽

Fei Hao ◽

Michele Kyle ◽

...

Keyword(s):

Frontal Cortex ◽

Learning And Memory ◽

Spatial Learning ◽

Spatial Learning And Memory ◽

Granulocyte Colony Stimulating Factor ◽

Colony Stimulating Factor ◽

Hippocampal Ca1 ◽

Severe Tbi ◽

Stimulating Factor

Abstract Background Traumatic brain injury (TBI) is a major cause of death and disability in young adults worldwide. TBI-induced long-term cognitive deficits represent a growing clinical problem.Stem cell factor (SCF) and granulocyte-colony stimulating factor (G-CSF)play a role in neuroprotection and neuronal plasticity.However, the knowledge concerning reparative efficacy of SCF+G-CSF treatment in post-acute TBI recovery remains incomplete. This study aims to determine the effectsof stem cell factor (SCF) and granulocyte colony-stimulating factor (G-CSF) on post-TBI recovery in young adult mice. The controlled cortical impact model of TBI was used for inducing a severe damage in the motor cortex of the right hemisphere in 8-week-old male C57BL mice. The combination treatment of SCF and G-CSF (SCF+G-CSF) was initiated 3 weeks after induction of TBI. Results Severe TBI led to persistent motor functional deficits (Rota-Rod test) and impaired spatial learning and memory (Morris water maze test). SCF+G-CSF treatment significantly improved the severe TBI-impaired spatial learning and memory at 6 weeks post-treatment.TBI also caused significant increases of Fluoro-Jade C positive degenerating neurons in bilateral frontal cortex, striatum and hippocampus, and significant reductions in MAP2+apical dendrites and overgrowth of SMI312+axons in peri-TBI cavity frontal cortex and in the ipsilateral hippocampal CA1 at 24 weeks post-TBI. SCF+G-CSF treatment significantly reduced TBI-induced neurodegeneration in the contralateral frontal cortex and hippocampal CA1, increased MAP2+apical dendrites in the peri-TBI cavity frontal cortex, and prevented TBI-induced axonal overgrowth in both the peri-TBI cavity frontal cortex and ipsilateral hippocampal CA1. Conclusions These findings reveal a novel pathology of axonal overgrowth after TBI and demonstrate a therapeutic potential of SCF+G-CSF in ameliorating TBI-induced long-term neuronal pathology, neural network malformation, and impairments in spatial learning and memory.

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