ArticleNeuroscience letters2007
Traumatic brain injury stimulates hippocampal catechol-O-methyl transferase expression in microglia.
Article in Neuroscience letters, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 48 citations in OpenAlex.
- Targeting Catechol-O-Methyltransferase Induces Mitochondrial Dysfunction and Enhances the Efficacy of Radiotherapy in Glioma.Cancer research · 2024Article
- Long-Term Impact of Diffuse Traumatic Brain Injury on Neuroinflammation and Catecholaminergic Signaling: Potential Relevance for Parkinson's Disease Risk.Molecules (Basel, Switzerland) · 2024Article
- Systemic Elevation of n-3 Polyunsaturated Fatty Acids (n-3-PUFA) Is Associated with Protection against Visual, Motor, and Emotional Deficits in Mice following Closed-Head Mild Traumatic Brain Injury.Molecular neurobiology · 2021Article
- Adulthood systemic inflammation accelerates the trajectory of age-related cognitive decline.Aging · 2021Article
- Progressive long-term spatial memory loss following repeat concussive and subconcussive brain injury in mice, associated with dorsal hippocampal neuron loss, microglial phenotype shift, and vascular abnormalities.The European journal of neuroscience · 2021Article
- Differential Effects of Pergolide and Bromocriptine on Working Memory Performance and Brain Activation after Mild Traumatic Brain Injury.Journal of neurotrauma · 2021Article
- Dopamine: an immune transmitter.Neural regeneration research · 2020Review
- Penetrating Ballistic-Like Brain Injury Leads to MicroRNA Dysregulation, BACE1 Upregulation, and Amyloid Precursor Protein Loss in Lesioned Rat Brain Tissues.Frontiers in neuroscience · 2020Article
- TSG-6 in conditioned media from adipose mesenchymal stem cells protects against visual deficits in mild traumatic brain injury model through neurovascular modulation.Stem cell research & therapy · 2019Article
- Adipose Stem Cell-Based Clinical Strategy for Neural Regeneration: A Review of Current Opinion.Stem cells international · 2019Review
- Concentrated Conditioned Media from Adipose Tissue Derived Mesenchymal Stem Cells Mitigates Visual Deficits and Retinal Inflammation Following Mild Traumatic Brain Injury.International journal of molecular sciences · 2018Article
- Impact of Traumatic Brain Injury on Dopaminergic Transmission.Cell transplantation · 2017Review
- Catecholaminergic based therapies for functional recovery after TBI.Brain research · 2016Review
- 2-Methoxyestradiol, an endogenous 17β-estradiol metabolite, inhibits microglial proliferation and activation via an estrogen receptor-independent mechanism.American journal of physiology. Endocrinology and metabolism · 2016Article
- A Novel Closed-Head Model of Mild Traumatic Brain Injury Using Focal Primary Overpressure Blast to the Cranium in Mice.Journal of neurotrauma · 2016Article
- Mild Traumatic Brain Injury Produces Neuron Loss That Can Be Rescued by Modulating Microglial Activation Using a CB2 Receptor Inverse Agonist.Frontiers in neuroscience · 2016Article
- Motor, visual and emotional deficits in mice after closed-head mild traumatic brain injury are alleviated by the novel CB2 inverse agonist SMM-189.International journal of molecular sciences · 2014Article
- Cerebral glucose metabolism in an immature rat model of pediatric traumatic brain injury.Journal of neurotrauma · 2013Article
- Addressing neuropsychiatric disturbances during rehabilitation after traumatic brain injury: current and future methods.Dialogues in clinical neuroscience · 2011Review
- Targeting Dopamine in Acute Traumatic Brain Injury.The open drug discovery journal · 2010Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Outcome following traumatic brain injury (TBI) is in large part determined by the combined action of multiple processes. In order to better understand the response of the central nervous system to injury, we utilized an antibody array to simultaneously screen 507 proteins for altered expression in the injured hippocampus, a structure critical for memory formation. Array analysis indicated 41 candidate proteins have altered expression levels 24h after TBI. Of particular interest was catechol-O-methyl transferase (COMT), an enzyme involved in metabolizing catecholamines released following neuronal activity. Altered catecholamine signaling has been observed after brain injury, and may contribute to the cognitive dysfunctions and behavioral deficits often experienced after TBI. Our data shows that COMT expression in the injured ipsilateral hippocampus was elevated for at least 14 d after controlled cortical impact injury. We found strong co-localization of COMT immunoreactivity with the microglia marker Iba1 near the injury site. Since dopamine transporter expression has been reported to be down-regulated after brain injury, COMT-mediated catecholamine metabolism may play a more prominent role in terminating catecholamine signaling in injured areas.
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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.