Background: Episodic memories are encoded within hippocampal and neocortical circuits. Retrieving these memories is assumed to involve reactivation of neural ensembles that were established during learning. Although it has been possible to follow the activity of individual neurons shortly after learning, it has not been possible to examine their activity weeks later during retrieval. We addressed this issue by using a stable form of GFP (H2B-GFP) to permanently tag neurons that are active during contextual fear conditioning.

Results: H2B-GFP expression in transgenic mice was increased by learning and could be regulated by doxycycline (DOX). Using this system, we found a large network of neurons in the hippocampus, amygdala, and neocortex that were active during context fear conditioning and subsequent memory retrieval 2 days later. Reactivation was contingent on memory retrieval and was not observed when animals were trained and tested in different environments. When memory was retrieved several weeks after learning, reactivation was altered in the hippocampus and amygdala but remained unchanged in the cortex.

Conclusions: Retrieving a recently formed context fear memory reactivates neurons in the hippocampus, amygdala, and cortex. Several weeks after learning, the degree of reactivation is altered in hippocampal and amygdala networks but remains stable in the cortex.

Download full-text PDF

Source
http://dx.doi.org/10.1016/j.cub.2012.11.019DOI Listing

Publication Analysis

Top Keywords

hippocampus amygdala
12
reactivation neural
8
neural ensembles
8
neurons hippocampus
8
context fear
8
memory retrieval
8
weeks learning
8
reactivation altered
8
reactivation
5
memory
5

Similar Publications

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

Laboratory for Neuropathology, KU Leuven, Leuven, Belgium.

Background: In 43-63% of symptomatic Alzheimer's disease (AD) patients, there is an observed accumulation of misfolded alpha-synuclein (αSyn). Two primary αSyn subtypes have been identified based on the underlying spreading pattern of this pathology: caudo-rostral and amygdala-predominant. Interactions between pathological TDP-43, Tau, and αSyn can aggravate their spread and aggregation.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

College of Public Health, University of Kentucky, Lexington, KY, USA.

Background: Brain arteriolosclerosis (B-ASC) is a pathologic hallmark characterized by dysmorphic brain arteriolar wall thickening. B-ASC is a common finding at autopsy in aged persons - some degree of B-ASC is seen in >80% of brains beyond age 80 years - and is associated with cognitive impairment. Hypertension and diabetes are widely recognized as risk factors for B-ASC.

View Article and Find Full Text PDF

Background: The mesolimbic system plays a crucial role in weight regulation and cognition. Previous studies suggest that the pathology of Alzheimer's disease (AD) can lead to the atrophy of the mesolimbic system and body mass index (BMI) decline. It remains unknown whether BMI is associated with the the mesolimbic system in AD.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

Mayo Clinic, Jacksonville, FL, USA.

Background: Inclusions of TAR DNA binding protein of 43kDa (TDP-43) constitute the main characteristic pathology in the majority (∼97%) of amyotrophic lateral sclerosis (ALS) cases and approximately 50% of patients with frontotemporal lobar degeneration (FTLD). TDP-43 is a nuclear RNA binding protein; however, in disease, it becomes hyperphosphorylated and/or insoluble, hindering its nuclear function in maintaining RNA homeostasis. Importantly, the incidence of TDP-43 proteinopathy extends to aging brains (LATE) and may be concomitant with Alzheimer's disease (AD) neuropathological changes (LATE/AD) in up to 70% of AD patients.

View Article and Find Full Text PDF

Basic Science and Pathogenesis.

Alzheimers Dement

December 2024

Laboratory for Neuropathology, KU Leuven, Leuven, Belgium.

Background: Limbic-predominant age-related TDP-43 encephalopathy (LATE) has been recently recognized as a cause of dementia in the elderly. LATE and Alzheimer's disease (AD) share similar clinical presentations, and their neuropathological changes-LATE-NC and ADNC-commonly co-occur in the brains of individuals with dementia. Frontotemporal degeneration (FTLD-TDP) represents another group of TDP-43-associated neurodegenerative diseases.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!