Acquired traumatic brain injury (TBI) is frequently accompanied by persistent cognitive symptoms, including executive function disruptions and memory deficits. The Morris Water Maze (MWM) is the most widely-employed laboratory behavioral test for assessing cognitive deficits in rodents after experimental TBI. Numerous protocols exist for performing the test, which has shown great robustness in detecting learning and memory deficits in rodents after infliction of TBI. We review applications of the MWM for the study of cognitive deficits following TBI in pre-clinical studies, describing multiple ways in which the test can be employed to examine specific aspects of learning and memory. Emphasis is placed on dependent measures that are available and important controls that must be considered in the context of TBI. Finally, caution is given regarding interpretation of deficits as being indicative of dysfunction of a single brain region (hippocampus), as experimental models of TBI most often result in more diffuse damage that disrupts multiple neural pathways and larger functional networks that participate in complex behaviors required in MWM performance.
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http://dx.doi.org/10.1016/j.neubiorev.2018.03.010 | DOI Listing |
CNS Neurosci Ther
January 2025
Department of Anatomy, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou, Henan, China.
Objectives: Endoplasmic reticulum (ER) stress-induced protein homeostasis perturbation is a core pathological element in the pathogenesis of neurodegenerative diseases. This study aims to clarify the unique role played by C/EBP homologous protein (CHOP) as a biomarker of the unfolded protein response (UPR) in the etiology of chronic pain and related cognitive impairments following chronic constrictive nerve injury (CCI).
Methods: The memory capability following CCI was assessed utilizing the Morris water maze (MWM) and fear conditioning test (FCT).
J Am Heart Assoc
January 2025
Department of Neurosurgery, Center of Pituitary Tumor, Ruijin Hospital Shanghai Jiao Tong University School of Medicine Shanghai China.
Background: Carotid endarterectomy (CEA) is widely used to treat carotid artery stenosis (CAS). However, the effects of CEA on unilateral CAS-induced cognitive impairment and the underlying mechanism remain poorly understood.
Methods And Results: Thirteen patients diagnosed with unilateral severe CAS underwent pre- and post-CEA assessments, including fluoro-2-deoxy-d-glucose positron emission tomography/magnetic resonance imaging, cognitive assessments, and routine blood tests before and after CEA.
Br J Pharmacol
January 2025
Institute of Neurobiology, Xi'an Jiaotong University Health Science Center, Xi'an, China.
Background And Purpose: Autophagy-lysosomal pathway dysfunction leads to postoperative cognitive dysfunction (POCD). Dexmedetomidine (Dex) improves POCD, and we probed the effects of Dex on autophagy-lysosomal pathway dysfunction in a POCD model.
Experimental Approach: A POCD mouse model was established and intraperitoneally injected with Dex.
J Alzheimers Dis
January 2025
Key Laboratory of Basic Pharmacology of Guizhou Province, School of Pharmacy, Zunyi Medical University, Zunyi, China.
Background: One of the hallmark pathological characteristics of Alzheimer's disease (AD) is amyloid-β (Aβ) accumulated in brain, which is mainly derived from the proteolytic processing of amyloid-β protein precursor (AβPP). The ubiquitin-proteasome system is able to reduce Aβ generation by ubiquitination and degradation of AβPP. Icariin (ICA), a flavonoid isolated from Maxim.
View Article and Find Full Text PDFNeurochem Int
January 2025
Department of Pharmacology and Chemical Biology, Shanghai Jiao Tong University School of Medicine, 280 South Chongqing Road, Shanghai 200025, PR China. Electronic address:
Microglia-mediated neuroinflammation plays a critical role in neuronal damage in neurodegenerative disorders such as Alzheimer's disease. Evidence shows that voltage-gated potassium (Kv) channels regulate microglial activation. We previously reported that copper dyshomeostasis causes neuronal injury via activating microglia.
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