ArticleJournal of neurotrauma2015
Altered regulation of protein kinase a activity in the medial prefrontal cortex of normal and brain-injured animals actively engaged in a working memory task.
Article in Journal of neurotrauma, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 24 citations in OpenAlex.
- The relationship between muscle strength and working memory in older adults: fNIRS-based evidence.Frontiers in psychology · 2026Article
- Temporal characterisation and electrophysiological implications of TBI-induced serine/threonine kinase activity in mouse cortex.Cellular and molecular life sciences : CMLS · 2025Article
- Correlation of muscle strength, working memory, and activities of daily living in older adults.Frontiers in aging neuroscience · 2024Article
- Combined Use of Guanfacine andNeurotrauma reports · 2024Article
- Scientific rationale for the use of α2A-adrenoceptor agonists in treating neuroinflammatory cognitive disorders.Molecular psychiatry · 2023Review
- Scientific Rationale for the Treatment of Cognitive Deficits from Long COVID.Neurology international · 2023Review
- The Aversive Lens: Stress effects on the prefrontal-cingulate cortical pathways that regulate emotion.Neuroscience and biobehavioral reviews · 2023Review
- Does muscle strength predict working memory? A cross-sectional fNIRS study in older adults.Frontiers in aging neuroscience · 2023Article
- Correlates of physical activity levels, muscle strength, working memory, and cognitive function in older adults.Frontiers in aging neuroscience · 2023Article
- Hypothesis: Tau pathology is an initiating factor in sporadic Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2021Review
- Guanfacine's mechanism of action in treating prefrontal cortical disorders: Successful translation across species.Neurobiology of learning and memory · 2020Review
- Phosphodiesterase PDE4D Is Decreased in Frontal Cortex of Aged Rats and Positively Correlated With Working Memory Performance and Inversely Correlated With PKA Phosphorylation of Tau.Frontiers in aging neuroscience · 2020Article
- Alzheimer's-like pathology in aging rhesus macaques: Unique opportunity to study the etiology and treatment of Alzheimer's disease.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Traumatic Brain Injury Induces Alterations in Cortical Glutamate Uptake without a Reduction in Glutamate Transporter-1 Protein Expression.Journal of neurotrauma · 2017Article
- Glucose-Dependent Insulinotropic Polypeptide Ameliorates Mild Traumatic Brain Injury-Induced Cognitive and Sensorimotor Deficits and Neuroinflammation in Rats.Journal of neurotrauma · 2016Article
- Article
- Chronic Stress Weakens Connectivity in the Prefrontal Cortex: Architectural and Molecular Changes.Chronic stress (Thousand Oaks, Calif.)Review
- Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Cyclic adenosine monophosphate (cAMP)-dependent protein kinase A (PKA) signaling is required for short- and long-term memory. In contrast, enhanced PKA activity has been shown to impair working memory, a prefrontal cortex (PFC)-dependent, transient form of memory critical for cognition and goal-directed behaviors. Working memory can be impaired after traumatic brain injury (TBI) in the absence of overt damage to the PFC. The cellular and molecular mechanisms that contribute to this deficit are largely unknown. In the present study, we examined whether altered PKA signaling in the PFC as a result of TBI is a contributing mechanism. We measured PKA activity in medial PFC (mPFC) tissue homogenates prepared from sham and 14-day postinjury rats. PKA activity was measured both when animals were inactive and when actively engaged in a spatial working memory task. Our results demonstrate, for the first time, that PKA activity in the mPFC is actively suppressed in uninjured animals performing a working memory task. By comparison, both basal and working memory-related PKA activity was elevated in TBI animals. Inhibition of PKA activity by intra-mPFC administration of Rp-cAMPS into TBI animals had no influence on working memory performance 30 min postinfusion, but significantly improved working memory when tested 24 h later. This improvement was associated with reduced glutamic acid decarboxylase 67 messenger RNA levels. Taken together, these results suggest that TBI-associated working memory dysfunction may result, in part, from enhanced PKA activity, possibly leading to altered expression of plasticity-related genes in the mPFC.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.