The Morris water maze and the radial-arm maze are two of the most frequently employed behavioral tasks used to assess spatial memory in rodents. In this study, we describe two new behavioral tasks in a radial-arm water maze enabling to combine the advantages of the Morris water maze and the radial-arm maze. In both tasks, spatial and nonspatial learning was assessed and the only task parameter that varied was the nature of the information available which was either spatial (various distal extra-maze cues) or nonspatial (visual intra-maze patterns). In experiment 1, 129T2/Sv mice were able to learn three successive pairwise discriminations [(1) A+/B-, (2) B+/C-, (3) C+/A-] with the same efficiency in both modalities (i.e. spatial and nonspatial modalities). Probe-trials at the end of each of these discriminations revealed particular features of this transverse-patterning-like procedure. In experiment 2, another group of 129T2/Sv mice was submitted to a delayed matching-to-sample working memory task. Mice were able to learn the task and were then able to show resistance to temporal interference as long as 60 min in the spatial modality but they failed to acquire the task in the nonspatial modality. The fact that the nonspatial information was exactly the same in both experiments highlights the existence of an interaction between the cognitive requirements of the task and the nature of the information.
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http://dx.doi.org/10.1016/j.cogbrainres.2004.06.016 | DOI Listing |
Neuromolecular Med
January 2025
Department of Neurology, Puren Hospital Affliated to Wuhan University of Science and Technology, No. 1, Benxi Street, Wuhan City, 430081, Hubei Province, China.
Sleep deprivation (SD) impairs learning and memory. Investigating the role of epigenetic modifications, such as 5-methylcytosine (mC), in SD is crucial. This study established an SD mouse model and assessed the mRNA levels of mC-related genes in brain tissue to identify potential candidates.
View Article and Find Full Text PDFNeurochem Res
January 2025
Department of Radiology, the Second Affiliated Hospital of Kunming Medical University, No.374 Yunnan-Burma Road, Wuhua District, Kunming, Yunnan, 650101, PR China.
Objective: Post-resuscitation brain injury is a common sequela after cardiac arrest (CA). Increasing sirtuin1 (SIRT1) has been involved in neuroprotection in oxygen-glucose deprivation (OGD) neurons, and we investigated its mechanism in post-cardiopulmonary resuscitation (CPR) rat brain injury by mediating p65 deacetylation modification to mediate hippocampal neuronal ferroptosis.
Methods: Sprague-Dawley rat CA/CPR model was established and treated with Ad-SIRT1 and Ad-GFP adenovirus vectors, or Erastin.
Alzheimers Dement
December 2024
Department of Neurosciences, University of California San Diego, La Jolla, CA, USA.
Background: Alzheimer's disease (AD) is the most common tauopathy and characterized by the progressive accumulation of Aß and tau. Tau is expressed in two major isoforms containing either 3 or 4 c-terminal repeats labeled as 3R and 4R tau. While these two isoforms occur in roughly equimolar ratios in AD, most research focus and mouse models of tau center only the 4Rtau protein and not 3Rtau.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Institut de recherches cliniques de Montréal (IRCM), Montréal, QC, Canada.
Background: Soluble Aβ oligomers (AβOs) induce synapse dysfunction, leading to cognitive impairment and memory deficits in Alzheimer's disease (AD). Our laboratory and several research groups characterized neurexin family members' physiological roles, pivotal synaptic adhesion molecules for development, plasticity, and maintenance. Beyond their normal functions, we found neurexins binding to AβOs causes AβO-induced neurexin dysregulation.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
Chiang Mai University/Neurophysiology Unit/Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai, Thailand.
Background: Our studies suggest that iron-overloaded rats developed neurotoxicity and cognitive impairment (1,2). An increase in brain mitochondrial fission and brain mitophagy have been considered as one of underlying mechanisms in brain with iron-overloaded condition (3,4). Hence, a pharmacological intervention focused on preventing brain mitochondrial pathologies is required.
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