ArticleExperimental neurology2012
Substantia nigra vulnerability after a single moderate diffuse brain injury in the rat.
Article in Experimental neurology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.
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29 citing papers in PubMed, 48 citations in OpenAlex.
- Traumatic brain injury exacerbates alcohol consumption and neuroinflammation with decline in cognition and cholinergic activity.Translational psychiatry · 2025Article
- Lasting Impact: Exploring the Brain Mechanisms that Link Traumatic Brain Injury to Parkinson's Disease.Molecular neurobiology · 2025Review
- Adolescent mice exposed to TBI developed PD-like pathology in middle age.Translational psychiatry · 2025Article
- Long-Term Impact of Diffuse Traumatic Brain Injury on Neuroinflammation and Catecholaminergic Signaling: Potential Relevance for Parkinson's Disease Risk.Molecules (Basel, Switzerland) · 2024Article
- Dysregulation of the dopaminergic system secondary to traumatic brain injury: implications for mood and anxiety disorders.Frontiers in neuroscience · 2024Review
- Traumatic brain injury and the development of parkinsonism: Understanding pathophysiology, animal models, and therapeutic targets.Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie · 2022Review
- Time Course of Remote Neuropathology Following Diffuse Traumatic Brain Injury in the Male Rat.Experimental neurobiology · 2022Article
- Olfactory Bulb Excitotoxicity as a Gap-Filling Mechanism Underlying the Link Between Traumatic Brain Injury-Induced Secondary Neuronal Degeneration and Parkinson's Disease-Like Pathology.Neurochemical research · 2022Article
- Lifestyle Factors and Parkinson's Disease Risk in a Rural New England Case-Control Study.Parkinson's disease · 2021Article
- Spatial Distribution of Neuropathology and Neuroinflammation Elucidate the Biomechanics of Fluid Percussion Injury.Neurotrauma reports · 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
- Chronic risperidone administration leads to greater amphetamine-induced conditioned place preference.Neuropharmacology · 2020Article
- Approaches to Monitor Circuit Disruption after Traumatic Brain Injury: Frontiers in Preclinical Research.International journal of molecular sciences · 2020Review
- Neurotransmitter changes after traumatic brain injury: an update for new treatment strategies.Molecular psychiatry · 2019Review
- Incretin Mimetics as Rational Candidates for the Treatment of Traumatic Brain Injury.ACS pharmacology & translational science · 2019Article
- 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
- Does time heal all wounds? Experimental diffuse traumatic brain injury results in persisting histopathology in the thalamus.Behavioural brain research · 2018Article
- Traumatic brain injuries during development disrupt dopaminergic signaling.Experimental neurology · 2017Article
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9 authors at 2 institutions in 2 countries.
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Abstract
Dementia and parkinsonism are late-onset symptoms associated with repetitive head injury, as documented in multiple contact-sport athletes. Clinical symptomatology is the likely phenotype of chronic degeneration and circuit disruption in the substantia nigra (SN). To investigate the initiating neuropathology, we hypothesize that a single diffuse brain injury is sufficient to initiate SN neuropathology including neuronal loss, vascular disruption and microglial activation, contributing to neurodegeneration and altered dopamine regulation. Adult, male Sprague-Dawley rats were subjected to sham or moderate midline fluid percussion brain injury. Stereological estimates indicated a significant 44% loss of the estimated total neuron number in the SN at 28-days post-injury, without atrophy of neuronal nuclear volumes, including 25% loss of tyrosine hydroxylase positive neurons by 28-days post-injury. Multi-focal vascular compromise occurred 1-2 days post-injury, with ensuing microglial activation (significant 40% increase at 4-days). Neurodegeneration (silver-stain technique) encompassed on average 21% of the SN by 7-days post-injury and increased to 29% by 28-days compared to sham (1%). Whole tissue SN, but not striatum, dopamine metabolism was altered at 28-days post-injury, without appreciable gene or protein changes in dopamine synthesis or regulation elements. Together, single moderate diffuse brain injury resulted in SN neurovascular pathology potentially associated with neuroinflammation or dopamine dysregulation. Compensatory mechanisms may preserve dopamine signaling acutely, but subsequent SN damage with aging or additional injury may expose clinical symptomatology of motor ataxias and dementia.
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