Post-stroke recovery: the role of activity-dependent release of brain-derived neurotrophic factor

2014 ◽  
Vol 14 (11) ◽  
pp. 1335-1344 ◽  
Author(s):  
Antonio Berretta ◽  
Yu-Chieh Tzeng ◽  
Andrew N Clarkson
Keyword(s):  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Stroke Recovery ◽  
Post Stroke ◽  
Activity Dependent

Abstract W P96: Optogenetic Neuronal Stimulation Enhances Neurotrophin Expression in the Contralesional Motor Cortex After Stroke

Stroke ◽  
2014 ◽  
Vol 45 (suppl_1) ◽  
Author(s):  
Michelle Y Cheng ◽  
Eric H Wang ◽  
Corinne L Bart ◽  
Alex R Bautista ◽  
Wyatt J Woodson ◽  
...  
Keyword(s):  
Motor Cortex ◽  
Functional Recovery ◽  
Primary Motor Cortex ◽  
Recovery Process ◽  
Cortical Reorganization ◽  
Stroke Recovery ◽  
Post Stroke ◽  
Neuronal Stimulation ◽  
Activity Dependent

Objective: Functional recovery after stroke has been observed and is currently attributed to both brain remodeling and plasticity. One form of cortical reorganization involves the balance of interhemispheric interactions between ipsilesional and contralesional cortex. Stimulation of ipsilesional primary motor cortex (iM1) has been shown to be beneficial, however, the role of the contralesional M1 (cM1) remains controversial. Recently we showed that optogenetic stimulations of iM1 post-stroke promote functional recovery. In this study, we investigate the role of contralesional cortex in recovery by optogenetically stimulating iM1 or cM1 and examine the involvement of activity-dependent neurotrophins. Methods: Thy-1-ChR2-YFP line-18 transgenic male mice were used. Mice underwent stereotaxic surgery to implant a fiber cannula in either iM1 or cM1, followed by an intraluminal middle cerebral artery suture occlusion. Optogenetic stimulation began at day5 post-stroke and continued until day14 post-stroke. Sensorimotor behavior tests were used to assess their recovery at day 0, 2, 7, 10 and 14 post-stroke. Mice were sacrificed at day15 post-stroke and neurotrophin expressions were examined using quantitative PCR. Results: Repeated iM1 stimulations promoted functional recovery at day14 post-stroke, with improved motor performance on the rotating beam test (p<0.01). Real-time PCR revealed significant increases of neurotrophin expressions in contralesional M1 at day15 post-stroke, including brain-derived neurotrophic factor (BDNF) (p<0.05), nerve growth factor (NGF) (p<0.05) and neurotrophin 3 (NTF3) (p<0.05). BDNF and NTF3 expression were also significantly increased in the contralesional S1 of stimulated mice (p<0.05). Conclusion: Our data suggest that activity-dependent neurotrophins in the contralesional cortex may be an important mechanism mediating stroke recovery. Current studies include specific stimulation and inhibition of the iM1 or cM1 post-stroke to elucidate the neurocircuitry mediating stroke recovery. In addition, the expression of neurotrophins will be examined in these studies to elucidate their role in the recovery process.

The Influence of Val66Met Polymorphism in Brain-Derived Neurotrophic Factor on Stroke Recovery Outcome: A Systematic Review and Meta-analysis

2021 ◽  
pp. 154596832110141
Author(s):  
Xuan Liu ◽  
Jun-Chao Fang ◽  
Xin-Yue Zhi ◽  
Qiu-Yu Yan ◽  
Hong Zhu ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Genetic Model ◽  
Meta Analysis ◽  
Brain Derived Neurotrophic Factor ◽  
Recessive Model ◽  
Stroke Recovery ◽  
Stroke Severity ◽  
Val66met Polymorphism ◽  
Asian Patients ◽  
Caucasian Patients

Background and purpose. A single nucleotide polymorphism at nucleotide 196 (G/A) in the human brain-derived neurotrophic factor ( BDNF) gene produces an amino acid substitution (valine to methionine) at codon 66(Val66Met). It is unclear whether carriers of this substitution may have worse functional outcomes after stroke. We aimed to explore the distribution of Val66Met polymorphism and evaluate the effect of different genotypes on stroke functional recovery. Methods. Several databases were searched using the keywords BDNF or brain-derived neurotrophic factor, codon66, G196A, rs6265, or Val66Met, and stroke. Results. A total of 25 articles were relevant to estimate the distribution of alleles; 5 reports were applied in the meta-analysis to assess genetic differences on recovery outcomes. The genetic model analysis showed that the recessive model should be used; we combined data for AA versus GA+GG (GG—Val/Val, GA—Val/Met, AA—Met/Met). The results showed that stroke patients with AA might have worse recovery outcomes than those with GA+GG (odds ratio = 1.90; 95% CI: 1.17-3.10; P = .010; I2 = 69.2%). Overall, the A allele may be more common in Asian patients (48.6%; 95% CI: 45.8%-51.4%, I2 = 54.2%) than Caucasian patients (29.8%; 95% CI: 7.5%-52.1%; I2 = 99.1%). However, in Caucasian patients, the frequency of the A allele in Iranians (87.9%; 95% CI: 83.4%-92.3%) was quite higher than that in other Caucasians (18.7%; 95% CI: 16.6%-20.9%; I2 = 0.00%). Conclusion. Val66Met AA carriers may have worse rehabilitation outcomes than GA+GG carriers. Further studies are needed to determine the effect of Val66Met polymorphism on stroke recovery and to evaluate this relationship with ethnicity, sex, age, stroke type, observe duration, stroke severity, injury location, and therapies.

Role of brain-derived neurotrophic factor in the control of D3 receptor expression

1999 ◽  
Vol 9 ◽  
pp. 184-185 ◽  
Author(s):  
O. Guillin ◽  
L. Damier ◽  
N. Griffon ◽  
J. Diaz ◽  
P. Carroll ◽  
...  
Keyword(s):  
Neurotrophic Factor ◽  
Brain Derived Neurotrophic Factor ◽  
Receptor Expression ◽  
D3 Receptor

The role of brain-derived neurotrophic factor in the pathophysiology of adolescent suicidal behavior

2011 ◽  
Vol 23 (3) ◽  
Author(s):  
Leo Sher
Keyword(s):  
At Risk ◽  
Psychiatric Disorders ◽  
Suicidal Behavior ◽  
Neurotrophic Factor ◽  
Adolescent Suicide ◽  
Developmental Change ◽  
Brain Derived Neurotrophic Factor ◽  
Childhood And Adolescence ◽  
Compulsive Disorder

Abstract Adolescent suicide research has mostly focused on demographic risk factors. Such studies focus on who is at risk, but do not explain why certain adolescents are at risk for suicide. Studies of the neurobiology of adolescent suicide could clarify why some youths are more suicidal than others and help to find biological markers of suicidal behavior in teenagers. Over the past decade the role of brain-derived neurotrophic factor (BDNF) in the pathophysiology of suicidal behavior has attracted significant attention of scientists. BDNF is involved in the pathophysiology of many psychiatric disorders associated with suicidal behavior including depression, post-traumatic stress disorder, schizophrenia, and obsessive-compulsive disorder. BDNF dysregulation could be associated with increased suicidality independently of psychiatric diagnoses. BDNF plays an important role in the regulation and growth of neurons during childhood and adolescence. Prominent among the brain regions undergoing developmental change during adolescence are stressor-sensitive areas. The serotonin dysfunction found in adolescent and adult suicidal behavior could be related to the low level of BDNF, which impedes the normal development of serotonin neurons during brain development. BDNF dysfunction could play a more significant role in the pathophysiology of psychiatric disorders and suicidal behavior in adolescents than in adults. Treatment-induced enhancement in the BDNF function could reduce suicidal behavior secondary to the improvement in psychiatric pathology or independently of improvement in psychiatric disorders. It is interesting to hypothesize that BDNF could be a biological marker of suicidal behavior in adolescents or in certain adolescent populations.

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