The pros and cons of motor, memory, and emotion-related behavioral tests in the mouse traumatic brain injury model

Zhang, Ruoyu; Wang, Junming; Huang, Leo; Wang, Tom J.; Huang, Yinrou; Li, Zefu; He, Jinxin; Sun, Chen; Wang, Jing

doi:10.1080/01616412.2021.1956290

Cited by 9 publications

(9 citation statements)

References 166 publications

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“…Acute early activation of the KYNA pathway can prevent the development of depressive symptoms after mild TBI, and QUINA in serum can potentially be a biomarker of repetitive TBI [ 96 ]. Targeting TRP metabolism can help to elucidate its pathogenic role in various emotional changes induced by TBI [ 97 ].…”

Section: Acute Spinal Cord and Brain Injurymentioning

confidence: 99%

Tryptophan Metabolism in Central Nervous System Diseases: Pathophysiology and Potential Therapeutic Strategies

Huang¹,

Zhao²,

Zhang³

et al. 2023

Aging and disease

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The metabolism of L-tryptophan (TRP) regulates homeostasis, immunity, and neuronal function. Altered TRP metabolism has been implicated in the pathophysiology of various diseases of the central nervous system. TRP is metabolized through two main pathways, the kynurenine pathway and the methoxyindole pathway. First, TRP is metabolized to kynurenine, then kynurenic acid, quinolinic acid, anthranilic acid, 3-hydroxykynurenine, and finally 3-hydroxyanthranilic acid along the kynurenine pathway. Second, TRP is metabolized to serotonin and melatonin along the methoxyindole pathway. In this review, we summarize the biological properties of key metabolites and their pathogenic functions in 12 disorders of the central nervous system: schizophrenia, bipolar disorder, major depressive disorder, spinal cord injury, traumatic brain injury, ischemic stroke, intracerebral hemorrhage, multiple sclerosis, Alzheimer’s disease, Parkinson’s disease, amyotrophic lateral sclerosis, and Huntington’s disease. Furthermore, we summarize preclinical and clinical studies, mainly since 2015, that investigated the metabolic pathway of TRP, focusing on changes in biomarkers of these neurologic disorders, their pathogenic implications, and potential therapeutic strategies targeting this metabolic pathway. This critical, comprehensive, and up-to-date review helps identify promising directions for future preclinical, clinical, and translational research on neuropsychiatric disorders.

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Section: Acute Spinal Cord and Brain Injurymentioning

confidence: 99%

Tryptophan Metabolism in Central Nervous System Diseases: Pathophysiology and Potential Therapeutic Strategies

Huang¹,

Zhao²,

Zhang³

et al. 2023

Aging and disease

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“…We have also performed the rotarod test, beam walk test, and adhesive removal test to confirm the motor-sensory benefits of EA. The rotarod test has been reported to be the most efficient and reliable test for measuring the functional recovery of the TBI model ( Fujimoto et al, 2004 ; Zhang et al, 2022 ). The beam walking test was recognized to be an effective and sensitive method of assessing fine coordination and balance ( Luong et al, 2011 ; Zhang et al, 2022 ).…”

Section: Discussionmentioning

confidence: 99%

“…The rotarod test has been reported to be the most efficient and reliable test for measuring the functional recovery of the TBI model ( Fujimoto et al, 2004 ; Zhang et al, 2022 ). The beam walking test was recognized to be an effective and sensitive method of assessing fine coordination and balance ( Luong et al, 2011 ; Zhang et al, 2022 ). Moreover, the adhesive removal test was established in rats to determine the long-term effects of brain injury on sensory-motor behavior.…”

Section: Discussionmentioning

confidence: 99%

Electroacupuncture improves TBI dysfunction by targeting HDAC overexpression and BDNF-associated Akt/GSK-3β signaling

Hung

Chung

Luo

et al. 2022

Front. Cell. Neurosci.

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BackgroundAcupuncture or electroacupuncture (EA) appears to be a potential treatment in acute clinical traumatic brain injury (TBI); however, it remains uncertain whether acupuncture affects post-TBI histone deacetylase (HDAC) expression or impacts other biochemical/neurobiological events.Materials and methodsWe used behavioral testing, Western blot, and immunohistochemistry analysis to evaluate the cellular and molecular effects of EA at LI4 and LI11 in both weight drop-impact acceleration (WD)- and controlled cortical impact (CCI)-induced TBI models.ResultsBoth WD- and CCI-induced TBI caused behavioral dysfunction, increased cortical levels of HDAC1 and HDAC3 isoforms, activated microglia and astrocytes, and decreased cortical levels of BDNF as well as its downstream mediators phosphorylated-Akt and phosphorylated-GSK-3β. Application of EA reversed motor, sensorimotor, and learning/memory deficits. EA also restored overexpression of HDAC1 and HDAC3, and recovered downregulation of BDNF-associated signaling in the cortex of TBI mice.ConclusionThe results strongly suggest that acupuncture has multiple benefits against TBI-associated adverse behavioral and biochemical effects and that the underlying mechanisms are likely mediated by targeting HDAC overexpression and aberrant BDNF-associated Akt/GSK-3 signaling.

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“…The time spent and the distance traveled in the center, and the periphery of the box was examined. 39…”

Section: Open Field Testmentioning

confidence: 99%

“…The EPM is one of the most widely used tests to assess anxiety-like behavior in mice. 39,40 The apparatus consists of a pair of open arms (50 cm × 5 cm) perpendicular to a pair of arms with walls but no ceiling (50 cm × 10 cm × 40 cm) and a central area connected (10 cm × 10 cm). The maze is located 50 cm above the ground.…”

Section: Elevated Plus-maze (Epm)mentioning

confidence: 99%

An enriched environment improves long-term functional outcomes in mice after intracerebral hemorrhage by mechanisms that involve the Nrf2/BDNF/glutaminase pathway

Jia

Wang

Ren

et al. 2023

J Cereb Blood Flow Metab

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Post-stroke depression exacerbates neurologic deficits and quality of life. Depression after ischemic stroke is known to some extent. However, depression after intracerebral hemorrhage (ICH) is relatively unknown. Increasing evidence shows that exposure to an enriched environment (EE) after cerebral ischemia/reperfusion injury has neuroprotective effects in animal models, but its impact after ICH is unknown. In this study, we investigated the effect of EE on long-term functional outcomes in mice subjected to collagenase-induced striatal ICH. Mice were subjected to ICH with the standard environment (SE) or ICH with EE for 6 h/day (8:00 am–2:00 pm). Depressive, anxiety-like behaviors and cognitive tests were evaluated on day 28 with the sucrose preference test, tail suspension test, forced swim test, light-dark transition experiment, morris water maze, and novel object recognition test. Exposure to EE improved neurologic function, attenuated depressive and anxiety-like behaviors, and promoted spatial learning and memory. These changes were associated with increased expression of transcription factor Nrf2 and brain-derived neurotrophic factor (BDNF) and inhibited glutaminase activity in the perihematomal tissue. However, EE did not change the above behavioral outcomes in Nrf2−/− mice on day 28. Furthermore, exposure to EE did not increase BDNF expression compared to exposure to SE in Nrf2−/− mice on day 28 after ICH. These findings indicate that EE improves long-term outcomes in sensorimotor, emotional, and cognitive behavior after ICH and that the underlying mechanism involves the Nrf2/BDNF/glutaminase pathway.

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The pros and cons of motor, memory, and emotion-related behavioral tests in the mouse traumatic brain injury model

Cited by 9 publications

References 166 publications

Tryptophan Metabolism in Central Nervous System Diseases: Pathophysiology and Potential Therapeutic Strategies

Tryptophan Metabolism in Central Nervous System Diseases: Pathophysiology and Potential Therapeutic Strategies

Electroacupuncture improves TBI dysfunction by targeting HDAC overexpression and BDNF-associated Akt/GSK-3β signaling

An enriched environment improves long-term functional outcomes in mice after intracerebral hemorrhage by mechanisms that involve the Nrf2/BDNF/glutaminase pathway

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