In a natural environment, avoidance of a particular food source is mostly determined by a previous intake experience during which sensory stimuli such as food odor, become aversive through a simple associative conditioned learning. Conditioned odor aversion learning (COA) is a food conditioning paradigm that results from the association between a tasteless scented solution (conditioned stimulus, CS) and a gastric malaise (unconditioned stimulus, US) that followed its ingestion. In the present experimental conditions, acquisition of COA also led to acquisition of aversion toward the context in which the CS was presented (conditioned context aversion, CCA). Previous data have shown that the entorhinal cortex (EC) is involved in the memory processes underlying COA acquisition and context fear conditioning, but whether EC lesion modulates CCA acquisition has never be investigated. To this aim, male Long-Evans rats with bilateral EC lesion received CS-US pairings in a particular context with different interstimulus intervals (ISI). The results showed that the establishment of COA with long ISI obtained in EC-lesioned rats is associated with altered CCA learning. Since ISI has been suggested to be the determining factor in the odor- and context-US association, our results show that the EC is involved in the processes that control both associations relative to ISI duration.
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http://dx.doi.org/10.3389/fnins.2015.00342 | 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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