Restoration of dopamine release deficits during object recognition memory acquisition attenuates cognitive impairment in a triple transgenic mice model of Alzheimer’s disease
Open accessAbstract
Previous findings indicate that the acquisition and consolidation of recognition memory involves dopaminergic activity. Although dopamine deregulation has been observed in Alzheimer's disease (AD) patients, the dysfunction of this neurotransmitter has not been investigated in animal models of AD. The aim of this study was to assess, by in vivo microdialysis, cortical and hippocampal dopamine, norepinephrine, and glutamate release during the acquisition of object recognition memory (ORM) in 5- and 10-mo-old triple-transgenic Alzheimer's disease mice (3xTg-AD) and to relate the extracellular changes to 24-h memory performance. Five- and 10-mo-old wild-type mice and 5-mo-old 3xTg-AD showed significant cortical but not hippocampal dopamine increase during object exploration. On a 24-h ORM test, these three groups displayed significant ORM. In contrast, 10-mo-old 3xTg-AD mice showed impaired dopamine release in the insular cortex during ORM acquisition, as well as significant impairment in ORM. In addition, cortical administration of a dopamine reuptake blocker produced an increase of dopamine levels in the 10-mo-old 3xTg-AD mice and attenuated the memory impairment. These data suggest that activation of the dopaminergic system in the insular cortex is involved in object recognition memory, and that dysfunction of this system contributes to the age-related decline in cognitive functioning of the 3xTg-AD mice.
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The increase of DA drive, evoked by dopaminergic drugs or stimulation of dopaminergic neurotransmission, improves synaptic plasticity dysfunctions, cognitive impairment and memory deficits in different experimental models of AD.
“the increase of DA drive -evoked by dopaminergic drugs or stimulation of the dopa minergic neurotransmission -improves synaptic plasticity dysfunctions, cognitive impairment and memory deficits in different experimental models of AD”
From Nilotinib restores memory function by preventing dopaminergic neuron degeneration in a mouse model of Alzheimer’s Disease (2021) · cites this paper as Guzmán-Ramos et al., 2012
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References 63 · Cited by 127
- Authors
- Guzmán-Ramos, K., Moreno-Castilla, P., Castro-Cruz, M., McGaugh, J. L., Martínez-Coria, H., LaFerla, F. M., & Bermúdez-Rattoni, F.
- Affiliations
- Universidad Nacional Autónoma de México (MX)
- University of California, Irvine (US)
- Venue
- Learning & Memory
- Publisher
- Cold Spring Harbor Laboratory
- Published
- 2012-09-14
- Volume
- 19
- Issue
- 10
- Pages
- 453-460
- ISSN
- 1072-0502 (ISSN-L)
- 1549-5485
- OpenAlex
- W2161451109
- Cited by
- 127
- References
- 63
- Citations by year
- 2026: 5 · 2025: 11 · 2024: 8 · 2023: 10 · 2022: 15 · 2021: 10 · 2020: 10 · 2019: 11 · 2018: 9 · 2017: 5 · 2016: 12 · 2015: 2 · 2014: 8 · 2013: 11
- Type
- posted content
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- Learning & Memory (publishedVersion)
- PubMed (publishedVersion)
- HighWire Press Open Archive (submittedVersion)
- Funders
- Consejo Nacional de Ciencia y Tecnología
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Life Sciences › Neuroscience › Cognitive Neuroscience › Memory and Neural Mechanisms
- Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
- Keywords
- Alzheimer's disease, object recognition memory, dopamine release, insula, triple transgenic mice, norepinephrine, glutamate, memory impairment, age-related cognitive decline, hippocampus
- MeSH terms
- Age Factors, Alzheimer Disease, Animals, Brain, Cognition Disorders, Disease Models, Animal, Dopamine, Exploratory Behavior, Humans, Male, Memory Disorders, Mice, Inbred C57BL, Mice, Transgenic, Mutation, Nomifensine, Norepinephrine, Photic Stimulation, Amyloid beta-Peptides, Amyloid beta-Protein Precursor, tau Proteins, Microdialysis, Glutamic Acid, Statistics, Nonparametric, Dopamine Uptake Inhibitors, Recognition, Psychology, Mice, Presenilin-1
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