scholarly journals Role of the Dopaminergic System in the Striatum and Its Association With Functional Recovery or Rehabilitation After Brain Injury

2021 ◽  
Vol 15 ◽  
Author(s):  
Antonio Verduzco-Mendoza ◽  
Paul Carrillo-Mora ◽  
Alberto Avila-Luna ◽  
Arturo Gálvez-Rosas ◽  
Adriana Olmos-Hernández ◽  
...  
Keyword(s):  
Brain Injury ◽  
Functional Recovery ◽  
Dopaminergic System ◽  
Brain Structures ◽  
Receptor Activation ◽  
Important Goal ◽  
Dopaminergic Drugs ◽  
Beneficial Effects ◽  
Severe Tbi

Disabilities are estimated to occur in approximately 2% of survivors of traumatic brain injury (TBI) worldwide, and disability may persist even decades after brain injury. Facilitation or modulation of functional recovery is an important goal of rehabilitation in all patients who survive severe TBI. However, this recovery tends to vary among patients because it is affected by the biological and physical characteristics of the patients; the types, doses, and application regimens of the drugs used; and clinical indications. In clinical practice, diverse dopaminergic drugs with various dosing and application procedures are used for TBI. Previous studies have shown that dopamine (DA) neurotransmission is disrupted following moderate to severe TBI and have reported beneficial effects of drugs that affect the dopaminergic system. However, the mechanisms of action of dopaminergic drugs have not been completely clarified, partly because dopaminergic receptor activation can lead to restoration of the pathway of the corticobasal ganglia after injury in brain structures with high densities of these receptors. This review aims to provide an overview of the functionality of the dopaminergic system in the striatum and its roles in functional recovery or rehabilitation after TBI.

Transgenic overexpression of cardiac A1adenosine receptors mimics ischemic preconditioning

2000 ◽  
Vol 279 (3) ◽  
pp. H1071-H1078 ◽  
Author(s):  
R. Ray Morrison ◽  
Rachael Jones ◽  
Anne M. Byford ◽  
Alyssa R. Stell ◽  
Jason Peart ◽  
...  
Keyword(s):  
Infarct Size ◽  
Functional Recovery ◽  
Ischemic Preconditioning ◽  
Adenosine Receptors ◽  
Myocardial Function ◽  
Wild Type ◽  
Beneficial Effects ◽  
Pressure Development ◽  
Ldh Release

The role of A1adenosine receptors (A1AR) in ischemic preconditioning was investigated in isolated crystalloid-perfused wild-type and transgenic mouse hearts with increased A1AR. The effect of preconditioning on postischemic myocardial function, lactate dehydrogenase (LDH) release, and infarct size was examined. Functional recovery was greater in transgenic versus wild-type hearts (44.8 ± 3.4% baseline vs. 25.6 ± 1.7%). Preconditioning improved functional recovery in wild-type hearts from 25.6 ± 1.7% to 37.4 ± 2.2% but did not change recovery in transgenic hearts (44.8 ± 3.4% vs. 44.5 ± 3.9%). In isovolumically contracting hearts, pretreatment with selective A1 receptor antagonist 1,3-dipropyl-8-cyclopentylxanthine attenuated the improved functional recovery in both wild-type preconditioned (74.2 ± 7.3% baseline rate of pressure development over time untreated vs. 29.7 ± 7.3% treated) and transgenic hearts (84.1 ± 12.8% untreated vs. 42.1 ± 6.8% treated). Preconditioning wild-type hearts reduced LDH release (from 7,012 ± 1,451 to 1,691 ± 1,256 U · l−1 · g−1 · min−1) and infarct size (from 62.6 ± 5.1% to 32.3 ± 11.5%). Preconditioning did not affect LDH release or infarct size in hearts overexpressing A1AR. Compared with wild-type hearts, A1AR overexpression markedly reduced LDH release (from 7,012 ± 1,451 to 917 ± 1,123 U · l−1 · g−1 · min−1) and infarct size (from 62.6 ± 5.1% to 6.5 ± 2.1%). These data demonstrate that murine preconditioning involves endogenous activation of A1AR. The beneficial effects of preconditioning and A1AR overexpression are not additive. Taken with the observation that A1AR blockade equally eliminates the functional protection resulting from both preconditioning and transgenic A1AR overexpression, we conclude that the two interventions affect cardioprotection via common mechanisms or pathways.

scholarly journals Role of Thalamus in Recovery of Traumatic Brain Injury

2016 ◽  
Vol 07 (S 01) ◽  
pp. S076-S079 ◽  
Author(s):  
Ashok Munivenkatappa ◽  
Amit Agrawal
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Structures ◽  
Thalamic Nuclei ◽  
Posttraumatic Symptoms ◽  
Injured Brain ◽  
Recovery Mechanisms ◽  
The Brain ◽  
Degree Of Recovery

ABSTRACTDegree of recovery after traumatic brain injury is highly variable that lasts for many weeks to months. The evidence of brain structures involved in recovery mechanisms is limited. This review highlights evidence of the brain structure particularly thalamus in neuroplasticity mechanism. Thalamus with its complex global networking has potential role in refining the cortical and other brain structures. Thalamic nuclei activation both naturally or by neurorehabilitation in injured brain can enhance and facilitate the improvement of posttraumatic symptoms. This review provides evidence from literature that thalamus plays a key role in recovery mechanism after injury. The study also emphasize that thalamus should be specifically targeted in neurorehabilitation following brain injury.

scholarly journals Intracerebroventricular injection of ouabain causes mania-like behavior in mice through D2 receptor activation

2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Alexander Lopachev ◽  
Anna Volnova ◽  
Anna Evdokimenko ◽  
Denis Abaimov ◽  
Yulia Timoshina ◽  
...  
Keyword(s):  
Mouse Model ◽  
Histological Analysis ◽  
Dopaminergic System ◽  
D2 Receptor ◽  
Brain Structures ◽  
Receptor Activation ◽  
Intracerebroventricular Injection ◽  
Fast Scan Cyclic Voltammetry ◽  
The Central Nervous System ◽  
Brain Ventricle

Abstract Intracerebroventricular (ICV) administration of ouabain, an inhibitor of the Na, K-ATPase, is an approach used to study the physiological functions of the Na, K-ATPase and cardiotonic steroids in the central nervous system, known to cause mania-like hyperactivity in rats. We describe a mouse model of ouabain-induced mania-like behavior. ICV administration of 0.5 µl of 50 µM (25 pmol, 14.6 ng) ouabain into each lateral brain ventricle results in increased locomotor activity, stereotypical behavior, and decreased anxiety level an hour at minimum. Fast-scan cyclic voltammetry showed that administration of 50 µM ouabain causes a drastic drop in dopamine uptake rate, confirmed by elevated concentrations of dopamine metabolites detected in the striatum 1 h after administration. Ouabain administration also caused activation of Akt, deactivation of GSK3β and activation of ERK1/2 in the striatum of ouabain-treated mice. All of the abovementioned effects are attenuated by haloperidol (70 µg/kg intraperitoneally). Observed effects were not associated with neurotoxicity, since no dystrophic neuron changes in brain structures were demonstrated by histological analysis. This newly developed mouse model of ouabain-induced mania-like behavior could provide a perspective tool for studying the interactions between the Na,K-ATPase and the dopaminergic system.

scholarly journals Early Dynamics of Cerebrospinal CD14+ Monocytes and CD15+ Granulocytes in Patients after Severe Traumatic Brain Injury: A Cohort Study

2015 ◽  
Vol 2015 ◽  
pp. 1-7
Author(s):  
Lukas Kurt Postl ◽  
Viktoria Bogner ◽  
Martijn van Griensven ◽  
Marc Beirer ◽  
Karl Georg Kanz ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Cohort Study ◽  
Brain Injury ◽  
Serum Albumin ◽  
Significant Influence ◽  
Severe Traumatic Brain Injury ◽  
Elective Surgery ◽  
Flow Analysis ◽  
Severe Tbi

In traumatic brain injury (TBI) the analysis of neuroinflammatory mechanisms gained increasing interest. In this context certain immunocompetent cells might play an important role. Interestingly, in the actual literature there exist only a few studies focusing on the role of monocytes and granulocytes in TBI patients. In this regard it has recently reported that the choroid plexus represents an early, selective barrier for leukocytes after brain injury. Therefore the aim of this study was to evaluate the very early dynamics of CD14+ monocytes and CD15+ granulocyte in CSF of patients following severe TBI with regard to the integrity of the BBB. Cytometric flow analysis was performed to analyze the CD14+ monocyte and CD15+ granulocyte population in CSF of TBI patients. The ratio of CSF and serum albumin as a measure for the BBB’s integrity was assessed in parallel. CSF samples of patients receiving lumbar puncture for elective surgery were obtained as controls. Overall 15 patients following severe TBI were enrolled. 10 patients were examined as controls. In patients, the monocyte population as well as the granulocyte population was significantly increased within 72 hours after TBI. The BBB’s integrity did not have a significant influence on the cell count in the CSF.

scholarly journals The pattern of hospital-community-home (HCH) nursing in tracheostomy patients with severe traumatic brain injury: is it feasible?

2020 ◽  
Author(s):  
Xiangyi Yin ◽  
Jie Wu ◽  
Lihui Zhou ◽  
Chunyan Ni ◽  
Minyan Xiao ◽  
...  
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Nursing Care ◽  
Severe Traumatic Brain Injury ◽  
Barthel Index ◽  
Control Group ◽  
Severe Tbi

Abstract Background Tracheostomy is very common in patients with severe traumatic brain injury (TBI), and long-term nursing care are needed for those patients. We aimed to evaluate the effects of hospital-community-home (HCH) nursing in those patients. Methods Tracheostomy patients with severe TBI were included. Glasgow coma score (GCS), Karnofsky, Self-Anxiety Scale (SAS) and Barthel assessment at the discharge and two months after discharge were evaluated. Results A total of 60 patients were included. There weren’t significant differences between two groups in the GCS, Karnofsky, SAS and Barthel index at discharge((all p > 0.05), the GCS, Karnofsky and Barthel index was all significantly increased after two months follow-up for two groups (all p < 0.05), and the GCS, Karnofsky and Barthel index at two months follow-up in HCH group was significantly higher than that of control group(all p < 0.05), but the SAS at two months follow-up in HCH group was significantly less than that of control group(p = 0.009). The incidence of block of artificial tracheal cannula and readmission in HCH group were significant less than that of control group (all p < 0.05). Conclusion HCH nursing care is feasible in tracheostomy patients with severe TBI, future studies are needed to further evaluate the role of HCH nursing care.

Abstract 111: Myeloid Specific Deletion of CD36 Increases Microglia-Like CD45 Low Subset and Exacerbates Stroke-Induced Brain Injury

Stroke ◽  
2020 ◽  
Vol 51 (Suppl_1) ◽  
Author(s):  
Keun Woo Park ◽  
Mustafa Balkaya ◽  
Jiwon Yang ◽  
Sunghee Cho
Keyword(s):  
Brain Injury ◽  
Immune Cells ◽  
Infarct Volume ◽  
Recovery Process ◽  
Stroke Recovery ◽  
Beneficial Effects ◽  
Transient Focal Ischemia ◽  
Inflammation Resolution

Objective: CD36 regulates biological and pathological processes including inflammation, resolution, phagocytosis, and angiogenesis. Highly expressed in monocytes/macrophages (MM), MM CD36 has been implicated in both detrimental and beneficial effects in acute stroke outcome and recovery. Using myeloid specific deficiency of CD36 (CD36KO MM ) mice, the present study addresses the role of MM CD36 on subset composition of MM in the acute and recovery phases of stroke. Methods: WT (CD36 fl/fl ) and CD36KO MM (M/F, 12w old) mice were subjected to transient focal ischemia. Brain immune cells were collected at 3d, 7d and 2m (n=8-12/timepoint). Infarct volume and hemispheric swelling were measured at 3d (n=13/genotype). In the isolated brain immune cells, CD11b+ cells were further distinguished by CD45 Hi and CD45 Low subsets. The extent of MM trafficking was determined by an intravenous infusion of control GFP+ splenocytes into the stroked WT and CD36KO MM mice 1d prior to sacrifice and MM subset analyses. Results: Compared to WT mice, CD36KO MM mice showed no difference in CD45 Low subset at 3d, 7d and 2m after stroke. However, CD36KO MM mice displayed a significant reduction of CD45 Hi subset, presumably infiltrating cells, at these time points (n=4-8 /group, P<0.01). Adoptive transfer of control GFP+ splenocytes to stroked CD36KO MM mice resulted in an increase of GFP+ cells in CD45 Low but a profound reduction in CD45 Hi subset. Despite the near absence of CD45 Hi and increased CD45 Low population in the post-ischemic brain, CD36KO MM mice displayed exacerbation of brain injury (15.1±13.7 vs 25.8±17.5 mm 3 , p<0.05) and brain swelling (12.1±10.3 vs 18.4±12.7 %, p=0.1). Conclusion: The observed reduction of CD45 Hi subset and exacerbation of brain injury in CD36KO MM mice suggests a beneficial role of infiltrated CD45 Hi MMs in limiting stroke injury. The sustained trafficking at 2m indicates potential involvement of MM CD36 in the recovery process. Further studies to assess long-term outcomes of CD36KO MM mice will provide critical insights on the role of macrophage CD36 in stroke recovery.

scholarly journals Protective Role of Melatonin in Neonatal Diseases

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Eloisa Gitto ◽  
Lucia Marseglia ◽  
Sara Manti ◽  
Gabriella D’Angelo ◽  
Ignazio Barberi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Free Radicals ◽  
Brain Injury ◽  
Antioxidant Status ◽  
Protective Role ◽  
Oxygen Radical ◽  
Perinatal Brain Injury ◽  
Beneficial Effects ◽  
Prophylactic Use

Oxidative stress contributes to the severity of several newborn conditions to the extent that Saugstad coined the phrase “oxygen radical diseases of neonatology.” In order to counteract free radicals damage many strategies to augment antioxidant status in ill-term and preterm infants have been proposed and several medications have been experimented with mixed results. Several studies have tested the efficacy of melatonin to counteract oxidative damage in diseases of newborns such as chronic lung disease, perinatal brain injury, necrotizing enterocolitis, and retinopathy of prematurity, giving promising results. The peculiar perinatal susceptibility to oxidative stress indicates that prophylactic use of antioxidants as melatonin could help to prevent or at least reduce oxidative stress related diseases in newborns. However, more studies are needed to confirm these beneficial effects.

scholarly journals Role of CCL2 (MCP-1) in Traumatic Brain Injury (TBI): Evidence from Severe TBI Patients and CCL2−/− Mice

2009 ◽  
Vol 30 (4) ◽  
pp. 769-782 ◽  
Author(s):  
Bridgette D Semple ◽  
Nicole Bye ◽  
Mario Rancan ◽  
Jenna M Ziebell ◽  
M Cristina Morganti-Kossmann
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Brain Damage ◽  
Closed Head Injury ◽  
Lesion Volume ◽  
Cellular Mechanisms ◽  
Cytokine Network ◽  
Secondary Brain Damage ◽  
Severe Tbi

Cerebral inflammation involves molecular cascades contributing to progressive damage after traumatic brain injury (TBI). The chemokine CC ligand-2 (CCL2) (formerly monocyte chemoattractant protein-1, MCP-1) is implicated in macrophage recruitment into damaged parenchyma after TBI. This study analyzed the presence of CCL2 in human TBI, and further investigated the role of CCL2 in physiological and cellular mechanisms of secondary brain damage after TBI. Sustained elevation of CCL2 was detected in the cerebrospinal fluid (CSF) of severe TBI patients for 10 days after trauma, and in cortical homogenates of C57Bl/6 mice, peaking at 4 to 12 h after closed head injury (CHI). Neurological outcome, lesion volume, macrophage/microglia infiltration, astrogliosis, and the cerebral cytokine network were thus examined in CCL2-deficient (−/−) mice subjected to CHI. We found that CCL2−/− mice showed altered production of multiple cytokines acutely (2 to 24 h); however, this did not affect lesion size or cell death within the first week after CHI. In contrast, by 2 and 4 weeks, a delayed reduction in lesion volume, macrophage accumulation, and astrogliosis were observed in the injured cortex and ipsilateral thalamus of CCL2−/− mice, corresponding to improved functional recovery as compared with wild-type mice after CHI. Our findings confirm the significant role of CCL2 in mediating post-traumatic secondary brain damage.

Self-regulation and social and behavioral functioning following childhood traumatic brain injury

2006 ◽  
Vol 12 (5) ◽  
pp. 609-621 ◽  
Author(s):  
KALAICHELVI GANESALINGAM ◽  
ANN SANSON ◽  
VICKI ANDERSON ◽  
KEITH OWEN YEATES
Keyword(s):  
Traumatic Brain Injury ◽  
Brain Injury ◽  
Injury Severity ◽  
Group Membership ◽  
Important Determinant ◽  
Self Regulation ◽  
Behavioral Functioning ◽  
Severe Tbi ◽  
The Impact

This study examined the impact of childhood traumatic brain injury (TBI) on self-regulation and social and behavioral functioning, and the role of self-regulation as a predictor of children's social and behavioral functioning. Participants included 65 children with moderate to severe TBI and 65 children without TBI, all between 6 and 11 years of age. Self-regulation and social and behavioral functioning were assessed 2 to 5 years following injury. Children with TBI displayed deficits in self-regulation and social and behavioral functioning, after controlling for socioeconomic status (SES), although the magnitude of the deficits was not related to injury severity. Self-regulation accounted for significant variance in children's social and behavioral functioning, after controlling for SES and group membership. Self-regulation may be an important determinant of children's social and behavioral functioning following TBI. (JINS, 2006,12, 609–621.)

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