ArticleNeuroscience2011
Altered adrenergic receptor signaling following traumatic brain injury contributes to working memory dysfunction.
Article in Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
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Who cites it
31 citing papers in PubMed, 53 citations in OpenAlex.
- Alpha-2 adrenergic challenge with guanfacine one month after mild traumatic brain injury: altered working memory and BOLD response.International journal of psychophysiology : official journal of the International Organization of Psychophysiology · 2011Trial
- Neuronal and glial networks interact with traumatic brain injury to modulate cognition in ABCD study.NPJ systems biology and applications · 2026Article
- Lasting Impact: Exploring the Brain Mechanisms that Link Traumatic Brain Injury to Parkinson's Disease.Molecular neurobiology · 2025Review
- Effects of a Serotonin Receptor Peptide on Behavioral Pattern Separation in Sham- vs. Mild Traumatic Brain Injured Rats.Endocrinology, diabetes and metabolism journal · 2024Article
- Dysregulated brain-gut axis in the setting of traumatic brain injury: review of mechanisms and anti-inflammatory pharmacotherapies.Journal of neuroinflammation · 2024Review
- 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
- Astrocytes in Post-traumatic Stress Disorder.Neuroscience bulletin · 2022Review
- DNA methylation under the major depression pathway predicts pediatric quality of life four-month post-pediatric mild traumatic brain injury.Clinical epigenetics · 2021Article
- Guanfacine's mechanism of action in treating prefrontal cortical disorders: Successful translation across species.Neurobiology of learning and memory · 2020Review
- Excitation of prefrontal cortical neurons during conditioning enhances fear memory formation.Scientific reports · 2020Article
- Noradrenergic α1-Adrenoceptor Actions in the Primate Dorsolateral Prefrontal Cortex.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Methylphenidate Treatment of Cognitive Dysfunction in Adults After Mild to Moderate Traumatic Brain Injury: Rationale, Efficacy, and Neural Mechanisms.Frontiers in neurology · 2019Review
- Untangling PTSD and TBI: Challenges and Strategies in Clinical Care and Research.Current neurology and neuroscience reports · 2018Review
- Executive (dys)function after traumatic brain injury: special considerations for behavioral pharmacology.Behavioural pharmacology · 2018Review
- Continuous Infusion of Phenelzine, Cyclosporine A, or Their Combination: Evaluation of Mitochondrial Bioenergetics, Oxidative Damage, and Cytoskeletal Degradation following Severe Controlled Cortical Impact Traumatic Brain Injury in Rats.Journal of neurotrauma · 2018Article
- Evidence for altered brain reactivity to norepinephrine in Veterans with a history of traumatic stress.Neurobiology of stress · 2018Article
- Networks of Cultured iPSC-Derived Neurons Reveal the Human Synaptic Activity-Regulated Adaptive Gene Program.Cell reports · 2017Article
- Catecholamines and cognition after traumatic brain injury.Brain : a journal of neurology · 2016Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
The prefrontal cortex is highly vulnerable to traumatic brain injury (TBI) and its structural and/or functional alterations as a result of TBI can give rise to persistent working memory (WM) dysfunction. Using a rodent model of TBI, we have described profound WM deficits following TBI that are associated with increases in prefrontal catecholamine (both dopamine and norepinephrine) content. In this study, we examined if enhanced norepinephrine signaling contributes to TBI-associated WM dysfunction. We demonstrate that administration of α1 adrenoceptor antagonists, but not α2A agonist, at 14 days post-injury significantly improved WM performance. mRNA analysis revealed increased levels of α1A, but not α1B or α1D, adrenoceptor in the medial prefrontal cortex (mPFC) of brain-injured rats. As α1A and 1B adrenoceptor promoters contain putative cAMP response element (CRE) sequences, we therefore examined if CRE-binding protein (CREB) actively engages these sequences in order to increase receptor gene transcription following TBI. Our results show that the phosphorylation of CREB is enhanced in the mPFC at time points during which increased α1A mRNA expression was observed. Chromatin immunoprecipitation (ChIP) assays using mPFC tissue from injured animals indicated increased phospho-CREB binding to the CRE sites of α1A, but not α1B, promoter compared to that observed in uninjured controls. To address the translatability of our findings, we tested the efficacy of the FDA-approved α1 antagonist Prazosin and observed that this drug improves WM in injured animals. Taken together, these studies suggest that enhanced CREB-mediated expression of α1 adrenoceptor contributes to TBI-associated WM dysfunction, and therapies aimed at reducing α1 signaling may be useful in the treatment of TBI-associated WM deficits in humans.
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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.