ArticleBrain research2011
Traumatic brain injury reduces striatal tyrosine hydroxylase activity and potassium-evoked dopamine release in rats.
Article in Brain research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.
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Who cites it
43 citing papers in PubMed, 65 citations in OpenAlex.
- Traumatic Brain Injury and Endocytosis: Reduced Rodent Hippocampal Endocytosis Proteins and Human Clathrin Light Chain Polymorphisms Are Associated with Impaired Neurological Outcomes After TBI.Molecular neurobiology · 2026Article
- Electrospun nanofiber scaffolds loaded with copper oxide for repairing traumatic brain injury through restoring copper homeostasis and regulating pyroptosis pathway.Burns & trauma · 2025Article
- Metabolic Diaschisis in Mild Traumatic Brain Injury.Journal of neurotrauma · 2024Article
- Elucidating the pivotal molecular mechanisms, therapeutic and neuroprotective effects of lithium in traumatic brain injury.Brain and behavior · 2024Review
- Enhancing cognitive function in chronic TBI: The Role of α7 nicotinic acetylcholine receptor modulation.Experimental neurology · 2024Article
- Dysregulation of the dopaminergic system secondary to traumatic brain injury: implications for mood and anxiety disorders.Frontiers in neuroscience · 2024Review
- Milnacipran Ameliorates Executive Function Impairments following Frontal Lobe Traumatic Brain Injury in Male Rats: A Multimodal Behavioral Assessment.Journal of neurotrauma · 2023Article
- Cannabidiol's neuroprotective properties and potential treatment of traumatic brain injuries.Frontiers in neurology · 2023Review
- Mechanical Stretching-Induced Traumatic Brain Injury Is Mediated by the Formation of GSK-3β-Tau Complex to Impair Insulin Signaling Transduction.Biomedicines · 2021Article
- Role of the Dopaminergic System in the Striatum and Its Association With Functional Recovery or Rehabilitation After Brain Injury.Frontiers in neuroscience · 2021Review
- Altered monoaminergic levels, spasticity, and balance disability following repetitive blast-induced traumatic brain injury in rats.Brain research · 2020Article
- Transcriptional Factors and Protein Biomarkers as Target Therapeutics in Traumatic Spinal Cord and Brain Injury.Current neuropharmacology · 2020Review
- Acrolein-mediated alpha-synuclein pathology involvement in the early post-injury pathogenesis of mild blast-induced Parkinsonian neurodegeneration.Molecular and cellular neurosciences · 2019Article
- GABAergic imbalance is normalized by dopamine DPsychopharmacology · 2019Article
- Novel therapies for combating chronic neuropathological sequelae of TBI.Neuropharmacology · 2019Review
- Lithium Improves Dopamine Neurotransmission and Increases Dopaminergic Protein Abundance in the Striatum after Traumatic Brain Injury.Journal of neurotrauma · 2018Article
- Executive (dys)function after traumatic brain injury: special considerations for behavioral pharmacology.Behavioural pharmacology · 2018Review
- Cocaine‑ and amphetamine‑regulated transcript (CART) is associated with dopamine and is protective against ischemic stroke.Molecular medicine reports · 2018Article
- Transcription factors Tp73, Cebpd, Pax6, and Spi1 rather than DNA methylation regulate chronic transcriptomics changes after experimental traumatic brain injury.Acta neuropathologica communications · 2018Article
- Spontaneous recovery of traumatic brain injury-induced functional deficits is not hindered by daily administration of lorazepam.Behavioural brain research · 2018Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
There is increasing evidence that traumatic brain injury (TBI) induces hypofunction of the striatal dopaminergic system, the mechanisms of which are unknown. In this study, we analyzed the activity of striatal tyrosine hydroxylase (TH) in rats at 1 day, 1 week, and 4 weeks after TBI using the controlled cortical impact model. There were no changes in the level of TH phosphorylated at serine 40 site (pser40TH) at 1 day or 4 weeks. At 1 week, injured animals showed decreased pser40TH to 73.9±7.3% (p≤0.05) of sham injured rats. The in vivo TH activity assay showed no significant difference between injured and sham rats at 1 day. However, there was a decreased activity in injured rats to 62.1±8.2% (p≤0.05) and 68.8±6.2% (p≤0.05) of sham injured rats at 1 and 4 weeks, respectively. Also, the activity of protein kinase A, which activates TH, decreased at 1 week (injured: 87.8±2.8%, sham: 100.0±4.2%, p≤0.05). To study the release activity of dopamine after injury, potassium (80 mM)-evoked dopamine release was measured by microdialysis in awake, freely moving rats. Dialysates were collected and analyzed by high-performance liquid chromatography. There were no significant differences in dopamine release at 1 day and 4 weeks between sham and injured groups. At 1 week, there was a significant decrease (injured: 0.067±0.015 μM, sham: 0.127±0.027 μM, p≤0.05). These results suggest that TBI-induced dopamine neurotransmission deficits are, at least in part, attributable to deficits in TH activity.
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