The entorhinal cortex (EC) has been shown to be an integral piece of the hippocampal memory system. It sits in a unique position within the brain with strong, intricate, reciprocal connectivity with the hippocampus as well as a vast array of neocortical regions. Topographical patterns of afferent and efferent projections suggest that the EC can be divided into the medial and lateral regions, each of which can be further divided into dorsal, intermediate, and lateral bands. These EC sub-regions, with variable anatomical features, indicate a multifaceted role of the EC in memory processing. The present article reviews rodent behavioral studies which tested the effect of manipulation to EC sub-regions in several different memory paradigms. An analysis of the specific targets of EC manipulations reveals an important role of the caudomedial EC for spatial memory. In recognition memory paradigms, damage to the lateral EC impairs recognition of the combined information of objects, locations, and environmental contexts relevant to the content of an experience; whereas damage to medial EC preferentially impairs the recognition of the spatial arrangement of objects relevant to the spatial location of an experience. Fewer studies have examined the impact of EC manipulations on contextual memory and temporal associative memory, the results of which are fairly conflicting and possible confounds are explored. Our summary provides further support for the functional dissociation within the EC for learning and memory and generates several ideas for future investigations.
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http://dx.doi.org/10.1016/j.nlm.2014.08.006 | DOI Listing |
Background: A significant proportion of individuals maintain healthy cognitive function despite having extensive Alzheimer's disease (AD) pathology, known as cognitive resilience. Understanding the molecular mechanisms that protect these individuals can identify therapeutic targets for AD dementia. This study aims to define molecular and cellular signatures of cognitive resilience, protection and resistance, by integrating genetics, bulk RNA, and single-nucleus RNA sequencing data across multiple brain regions from AD, resilient, and control individuals.
View Article and Find Full Text PDFAlzheimer's disease (AD) is a neurodegenerative disease characterized by progressive impairments in episodic and spatial memory, as well as circuit and network-level dysfunction. While functional impairments in medial entorhinal cortex (MEC) and hippocampus (HPC) have been observed in patients and rodent models of AD, it remains unclear how communication between these regions breaks down in disease, and what specific physiological changes are associated with the onset of memory impairment. We used silicon probes to simultaneously record neural activity in MEC and hippocampus before or after the onset of spatial memory impairment in the 3xTg mouse model of AD pathology.
View Article and Find Full Text PDFBMC Rheumatol
January 2025
Department of Clinical Sciences, Diagnostic Radiology, Lund, Lund University, Lund, Sweden.
Background: Systemic lupus erythematosus (SLE) often presents with neuropsychiatric (NP) involvement, including cognitive impairment and depression. Past magnetic resonance imaging (MRI) research in SLE patients showed smaller hippocampal volumes but did not investigate other medial temporal lobe (MTL) regions. Our study aims to compare MTL subregional volumes in SLE patients to healthy individuals (HI) and explore MTL subregional volumes in relation to neuropsychiatric SLE (NPSLE) manifestations.
View Article and Find Full Text PDFGeorgian Med News
November 2024
2Institute of Botany after A. Takhtajyan NAS RA, Yerevan, Armenia.
Parkinson disease (PD) is a common neurodegenerative condition. It affects the central nervous system, and it impairs cognitive processes, motor skills and other functions. The aim of this study was to determine the synaptic processes in medial Entorhinal cortex (mENT) under High frequency stimulation of Basolateral Amygdala on the model of Parkinson's disease under the influence of Hydrocortisone.
View Article and Find Full Text PDFCell Rep
January 2025
Nash Family Department of Neuroscience, The Friedman Brain Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA. Electronic address:
Temporal lobe epilepsy (TLE) causes pervasive and progressive memory impairments, yet the specific circuit changes that drive these deficits remain unclear. To investigate how hippocampal-entorhinal dysfunction contributes to progressive memory deficits in epilepsy, we performed simultaneous in vivo electrophysiology in the hippocampus (HPC) and medial entorhinal cortex (MEC) of control and epileptic mice 3 or 8 weeks after pilocarpine-induced status epilepticus (Pilo-SE). We found that HPC synchronization deficits (including reduced theta power, coherence, and altered interneuron spike timing) emerged within 3 weeks of Pilo-SE, aligning with early-onset, relatively subtle memory deficits.
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