Key Spec Table
|Analytes Available||Species Reactivity||Key Applications||Detection Methods|
|Application||This ChemiKine Brain Derived Neurotrophic Factor, Sandwich ELISA is used to measure & quantify BDNF levels in Neuroscience research.|
|Safety Information according to GHS|
|Material Size||1 kit|
References | 24 Available | See All References
|Reference overview||Species||Pub Med ID|
|Expression and localization of brain-derived neurotrophic factor (BDNF) mRNA and protein in human submandibular gland. |
Juri Saruta,Kazuhiro Fujino,Masahiro To,Keiichi Tsukinoki
Acta histochemica et cytochemica 45 2012
Brain-derived neurotrophic factor (BDNF) promotes cell survival and differentiation in the central and peripheral nervous systems. Previously, we reported that BDNF is produced by salivary glands under acute immobilization stress in rats. However, expression of BDNF is poorly understood in humans, although salivary gland localization of BDNF in rodents has been demonstrated. In the present study, we investigated the expression and localization of BDNF in the human submandibular gland (HSG) using reverse transcription-polymerase chain reaction, western blot analysis, in situ hybridization (ISH), immunohistochemistry (IHC), and ELISA. BDNF was consistently localized in HSG serous and ductal cells, as detected by ISH and IHC, with reactivity being stronger in serous cells. In addition, immunoreactivity for BDNF was observed in the saliva matrix of ductal cavities. Western blotting detected one significant immunoreactive 14 kDa band in the HSG and saliva. Immunoreactivities for salivary BDNF measured by ELISA in humans were 40.76
|Various levels of plasma brain-derived neurotrophic factor in patients with tinnitus. |
Fumiyuki Goto,Juri Saruta,Sho Kanzaki,Masahiro To,Tomoko Tsutsumi,Keiichi Tsukinoki,Kaoru Ogawa
Neuroscience letters 510 2012
Thus far, no objective measure has been developed to evaluate tinnitus severity. There is a close relationship between tinnitus and depression, in which brain-derived neurotrophic factor (BDNF) has a pathophysiological role. To determine whether BDNF levels could be used to evaluate tinnitus severity, we evaluated plasma BDNF levels in patients with tinnitus.
|Decreased levels of brain-derived neurotrophic factor in the remitted state of unipolar depressive disorder. |
B J Hasselbalch,U Knorr,B Bennike,S G Hasselbalch,M H Greisen Søndergaard,L Vedel Kessing
Acta psychiatrica Scandinavica 126 2012
Hasselbalch BJ, Knorr U, Bennike B, Hasselbalch SG, Greisen Søndergaard MH, Vedel Kessing L. Decreased levels of brain-derived neurotrophic factor in the remitted state of unipolar depressive disorder. Objective: Decreased levels of peripheral brain-derived neurotrophic factor (BDNF) have been associated with depression. It is uncertain whether abnormally low levels of BDNF in blood are present beyond the depressive state and whether levels of BDNF are associated with the course of clinical illness. Method: Whole-blood BDNF levels were measured in blood samples from patients with unipolar disorder in a sustained state of clinical remission and in a healthy control group. Participants were recruited via Danish registers, a method that benefits from the opportunity to obtain well-matched community-based samples as well as providing a high diagnostic validity of the patient sample. Results: A total of 85 patients and 50 controls were included in the study. In multiple linear regression analyses, including the covariates age, gender, 17-item Hamilton Depression Rating Scale scores, body-mass index, education, smoking and physical exercise, patients with unipolar depressive disorder had decreased levels of BDNF compared to healthy control individuals [B = -7.4, 95% CI (-11.2, -3.7), = 0.21 P < 0.001]. No association between course of clinical illness and BDNF levels was present. Conclusion: Whole-blood BDNF levels seem to be decreased in patients remitted from unipolar depressive disorder, suggesting that neurotrophic changes may exist beyond the depressive state.
|BDNF as an effect modifier for gender effects on pain thresholds in healthy subjects. |
Luciana Cadore Stefani,Iraci Lucena da Silva Torres,Izabel Cristina Custodio de Souza,Joanna Ripoll Rozisky,Felipe Fregni,Wolnei Caumo
Neuroscience letters 514 2012
BDNF is an important marker of neuronal plasticity. It has also been associated with pain processing. Increased BDNF levels are observed in chronic pain syndromes. In order to understand the role of BDNF associated with other factors such as gender on experimental pain we aimed to determine whether experimental heat or pressure pain threshold is correlated with brain derived neurotrophic factor (BDNF) level, gender and age. Heat pain threshold and pressure pain threshold were measured in 49 healthy volunteers (27 females). The multivariate linear regression models (on heat and pressure pain thresholds) revealed a significant effect of gender (p=0.001 for both models), serum BDNF (p<0.004 for both models) and interaction between BDNF and gender (<0.001 for both models). In fact, when adjusting for BDNF levels and age, heat and pressure pain thresholds were significantly reduced in women as compared to men (p<0.001 for both models). These effects were not observed when gender was analyzed alone. These finding suggests that experimental heat and pressure pain threshold is gender-related and BDNF dependent. In fact BDNF has a facilitatory effect on pain threshold in females but has an opposite effect in males; supporting the notion that BDNF is an effect modifier of the gender effects on pain threshold in healthy subjects.
|Propofol interacts with stimulus intensities of electroconvulsive shock to regulate behavior and hippocampal BDNF in a rat model of depression. |
Jie Luo,Su Min,Ke Wei,Junfang Zhang,Yuanyuan Liu
Psychiatry research 198 2012
As a psychiatric treatment, modern electroconvulsive therapy (ECT) requires anesthesia to enhance safety, but anesthetics may weaken its efficacy. Previous studies have provided inconsistent results and lack satisfactory details of the influence of anesthetics on ECT efficacy, which partially complicates the clinical selection of ECT protocols. To test our hypothesis that anesthetics interact with the intrinsic parameters of ECT to differentially regulate its therapeutic efficacy, we investigated the effects of the anesthetic propofol and the stimulus intensities of ECT on behavior and hippocampal brain-derived neurotrophic factor (BDNF) in a rodent model of depression. After treatment with chronic unpredictable mild stresses to produce the model, the depressed rats received anesthesia with propofol or normal saline, i.p., and electroconvulsive shock (ECS, an analog of ECT to animals) with different stimulus intensities. The sucrose preference and open field tests were performed to assess behavior, and BDNF level in hippocampus was measured with ELISA. We found that propofol regulated the efficacy of ECS differently at different stimulus intensities in both the behavioral and molecular levels. At medium intensities (120 and 180 mC), propofol enhanced the anti-depressant efficacy of ECS without largely compromising the recovering efficacy of ECS on spontaneous exploratory activities. The results indicated that propofol and ECS stimulus intensities interacted and resulted in different regulating efficacies at different intensities. Medium stimulus intensities were optimal for ECS efficacy under propofol anesthesia.
|Prolonged therapeutic hypothermia does not adversely impact neuroplasticity after global ischemia in rats. |
Gergely Silasi,Ana C Klahr,Mark J Hackett,Angela M Auriat,Helen Nichol,Frederick Colbourne
Journal of cerebral blood flow and metabolism : official journal of the International Society of Cerebral Blood Flow and Metabolism 32 2012
Hypothermia improves clinical outcome after cardiac arrest in adults. Animal data show that a day or more of cooling optimally reduces edema and tissue injury after cerebral ischemia, especially after longer intervention delays. Lengthy treatments, however, may inhibit repair processes (e.g., synaptogenesis). Thus, we evaluated whether unilateral brain hypothermia (∼33°C) affects neuroplasticity in the rat 2-vessel occlusion model. In the first experiment, we cooled starting 1 hour after ischemia for 2, 4, or 7 days. Another group was cooled for 2 days starting 48 hours after ischemia. One group remained normothermic throughout. All hypothermia treatments started 1 hour after ischemia equally reduced hippocampal CA1 injury in the cooled hemisphere compared with the normothermic side and the normothermic group. Cooling only on days 3 and 4 was not beneficial. Importantly, no treatment influenced neurogenesis (Ki67/Doublecortin (DCX) staining), synapse formation (synaptophysin), or brain-derived neurotropic factor (BDNF) immunohistochemistry. A second experiment confirmed that BDNF levels (ELISA) were equivalent in normothermic and 7-day cooled rats. Last, we measured zinc (Zn), which is important in plasticity, with X-ray fluorescence imaging in normothermic and 7-day cooled rats. Hypothermia did not alter the postischemic distribution of Zn within the hippocampus. In summary, cooling significantly mitigates injury without compromising neuroplasticity.
|Serum MIP-1 alpha level: a biomarker for the follow-up of lentiviral therapy in mucopolysaccharidosis IIIB mice. |
Paola Di Natale,Carmela Di Domenico,Daniele Di Napoli
Journal of inherited metabolic disease 33 2010
Mucopolysaccharidosis (MPS) IIIB is an inherited lysosomal storage disorder caused by deficiency of alpha-N-acetylglucosaminidase (NAGLU). The disease is characterized by mild somatic features and severe neurological involvement, with high mortality rates. Although some therapeutic approaches have been applied to the murine model of the disease, no effective therapy is available. Moreover, assessing therapeutic efficacy is challenged by the lack of markers to for progression and severity. In this study, we examined the effect of brain-directed lentiviral (LV) gene therapy on serum levels of macrophage inflammatory protein 1 alpha (MIP-1alpha) and brain-derived neurotrophic factor (BDNF) proteins in the murine model of MPS IIIB to identify novel serum biomarkers. The cytokine MIP-1alpha was elevated in MPS IIIB mouse serum, and following gene therapy, it was reduced to normal levels. For neurotrophin BDNF, the difference in serum levels between MPS IIIB and normal mice was not statistically significant; after LV gene therapy, an increase in protein was found in treated mice, although the values were not statistically significant. Our studies suggest MIP-1alpha as the first serum biomarker that could be used to monitor disease progression and treatment for MPS IIIB disease.
|Increase in brain-derived neurotrophic factor in first episode psychotic patients after treatment with atypical antipsychotics. |
González-Pintoa A, Mosquera F, Palomino A, Alberich S, Gutiérrez A, Haidar K, Vega P, Barbeito S, Ortiz A, Matute C
Int Clin Psychopharmacol 25 241-5. 2010
Some preclinical and postmortem studies suggest that the effects of atypical antipsychotics could be mediated by brain-derived neurotrophic factor (BDNF). Olanzapine is an atypical antipsychotic with shown efficacy in psychosis treatment. The aim of this study was to compare plasma BDNF levels at baseline and after 1 year of olanzapine treatment in 18 drug-naive patients who experienced a first psychotic episode with those of 18 healthy control participants matched by age, sex, and socioeconomic level. Plasma BDNF levels were measured in patients at the index episode and at 1, 6, and 12 months of follow-up using an enzyme-linked immunosorbent assay. Symptoms and functioning of patients and controls were assessed with the Positive and Negative Symptom Scale and Global Assessment of Function Scale. BDNF levels of patients at onset were significantly lower than controls but increased toward control values during olanzapine treatment. There was a significant positive correlation between BDNF levels and functioning (Global Assessment of Function Scale). BDNF levels were also negatively correlated with positive symptoms, but not with negative symptoms or general psychopathology. Results suggest that olanzapine can offset the low BDNF levels at the onset of first psychotic episodes, and improving psychotic symptoms. The increase in BDNF levels may be its mechanism of action in improving positive symptoms.
|IFATS collection: The conditioned media of adipose stromal cells protect against hypoxia-ischemia-induced brain damage in neonatal rats. |
Xing Wei, Zhimei Du, Liming Zhao, Dongni Feng, Gang Wei, Yongzheng He, Jiangning Tan, Wei-Hui Lee, Harald Hampel, Richard Dodel, Brian H Johnstone, Keith L March, Martin R Farlow, Yansheng Du
Stem cells (Dayton, Ohio) 27 478-88 2009
Adipose tissue stroma contains a population of mesenchymal stem cells, which support repair when administered to damaged tissues, in large part through secreted trophic factors. We directly tested the ability of media collected from cultured adipose-derived stem cells (ASCs) to protect neurons in a rat model of brain hypoxic-ischemic (HI) injury. Concentrated conditioned medium from cultured rat ASCs (ASC-CM) or control medium was infused through the jugular vein of neonatal Sprague-Dawley rats subjected to HI injury. The ASC-CM was administered either 1 hour before or 24 hours after induction of injury. Analysis at 1 week indicated that administration at both time points significantly protected against hippocampal and cortical volume loss. Analysis of parallel groups for behavioral and learning changes at 2 months postischemia demonstrated that both treated groups performed significantly better than the controls in Morris water maze functional tests. Subsequent post-mortem evaluation of brain damage at the 2-month time point confirmed neuronal loss to be similar to that observed at 1 week for all groups. We have identified several neurotrophic factors in ASC-CM, particularly insulin-like growth factor-1 and brain-derived neurotrophic factor, which are important factors that could contribute to the protective effects of ASCs observed in studies with both in vitro and in vivo neuronal injury models. These data suggest that delivery of the milieu of factors secreted by ASCs may be a viable therapeutic option for treatment of HI, as well as other brain injuries.
|The differential regulation of BDNF and TrkB levels in juvenile rats after four days of escitalopram and desipramine treatment. |
Megan E Kozisek, David Middlemas, David B Bylund
Neuropharmacology 54 251-7 2008
Major depressive disorder is a major health problem in adults and is now recognized as a substantial problem in children as well. Tricyclic antidepressants, including desipramine (DMI), are no better than placebo in treating childhood and adolescent depression, but are effective in treating adult depression. Several studies have suggested that normal BDNF (brain-derived neurotrophic factor) signaling is necessary for antidepressant drug action. Antidepressant drugs induce several plastic changes in the rodent brain which may be associated with changes in BDNF levels and/or with BDNF function. In the present study we report parallel measurements of BDNF mRNA and protein in the frontal cortex and hippocampus after four days of twice daily treatments with escitalopram, a selective serotonin reuptake inhibitor, and desipramine, a tricyclic antidepressant. Post-natal day 13, 21, 28 and adult rats were used in this study. TrkB (the primary receptor for BDNF) mRNA levels were also examined under the same treatment conditions. BDNF mRNA and protein levels, as well as TrkB mRNA levels, were increased significantly in post-natal day 13 pups after escitalopram treatment as compared to control, but desipramine failed to increase either BDNF or TrkB. The failure of desipramine to increase BDNF and TrkB levels in juvenile rats is consistent with the lack of efficacy of desipramine in children and adolescents. The serotonergic nervous system matures earlier than the noradrenergic system, which may explain why escitalopram, but not desipramine, increases BDNF and TrkB levels.
|An analysis of time-dependent changes of neurotrophic factors (BDNF, CNTF) in traumatic facial nerve injury of a nerve-cut and nerve-crush model in rats. |
Sertac Yetiser,Erkan Kahraman
Otology & neurotology : official publication of the American Otological Society, American Neurotology Society [and] European Academy of Otology and Neurotology 29 2008
To investigate neurotrophic changes in the injured facial nerve in rats.
|Apoptosis time course in the limbic system after myocardial infarction in the rat. |
Kaloustian, S, et al.
Brain Res., 1216: 87-91 (2008) 2008
|Dietary restriction started after spinal cord injury improves functional recovery. |
Ward T Plunet, Femke Streijger, Clarrie K Lam, Jae H T Lee, Jie Liu, Wolfram Tetzlaff
Experimental neurology 213 28-35 2008
Spinal cord injury typically results in limited functional recovery. Here we investigated whether therapeutic dietary restriction, a multi-faceted, safe, and clinically-feasible treatment, can improve outcome from cervical spinal cord injury. The well-established notion that dietary restriction increases longevity has kindled interest in its potential benefits in injury and disease. When followed for several months prior to insult, prophylactic dietary restriction triggers multiple molecular responses and improves outcome in animal models of stroke and myocardial infarction. However, the efficacy of the clinically-relevant treatment of post-injury dietary restriction is unknown. Here we report that every-other-day fasting (EODF), a form of dietary restriction, implemented after rat cervical spinal cord injury was neuroprotective, promoted plasticity, and improved behavioral recovery. Without causing weight loss, EODF improved gait-pattern, forelimb function during ladder-crossing, and vertical exploration. In agreement, EODF preserved neuronal integrity, dramatically reduced lesion volume by >50%, and increased sprouting of corticospinal axons. As expected, blood beta-hydroxybutyrate levels, a ketone known to be neuroprotective, were increased by 2-3 fold on the fasting days. In addition, we found increased ratios of full-length to truncated trkB (receptor for brain-derived neurotrophic factor) in the spinal cord by 2-6 folds at both 5 days (lesion site) and 3 weeks after injury (caudal to lesion site) which may further enhance neuroprotection and plasticity. Because EODF is a safe, non-invasive, and low-cost treatment, it could be readily translated into the clinical setting of spinal cord injury and possibly other insults.
|Spontaneous glutamatergic activity induces a BDNF-dependent potentiation of GABAergic synapses in the newborn rat hippocampus. |
Kuczewski, Nicola, et al.
J. Physiol. (Lond.), 586: 5119-28 (2008) 2008
|Val66met polymorphism and serum brain-derived neurotrophic factor levels in bipolar disorder. |
Tramontina, J, et al.
Mol. Psychiatry, 12: 230-1 (2007) 2007
|Spontaneous expression of neural phenotype and NGF, TrkA, TrkB genes in marrow stromal cells. |
Na Li, Hui Yang, Lingling Lu, Chunli Duan, Chunli Zhao, Huanying Zhao
Biochemical and biophysical research communications 356 561-8 2007
Marrow stromal cells (MSCs) have the ability to provide growth factors and differentiate into neural-like cells on treating with EGF, bFGF and other factors. We wanted to explore whether growth factors secreted by MSCs itself could induce self-differentiation into neural-like cells. Here, we show that even in the absence of inducing factors, rMSCs spontaneously differentiate into neural-like cells expressing neural markers, such as nestin, beta-tubulin III, Doublecortin (DCX), microtubule-associated protein 2 (MAP2) and neuron-specific enolase (NSE). Furthermore, some cells become neurosphere-like growing in suspension. Compared with control and neural-like rMSCs induced by epidermal growth factor (EGF) and basic fibroblast growth factor (bFGF), we found using real-time PCR that self-differentiating rMSCs (SDrMSCs) expressed significantly higher levels of neurotrophic high-affinity receptors (TrkA and TrkB). Coincident with neural marker expression, nerve growth factor (NGF) mRNA was significantly higher than controls despite lower protein levels in the supernatant. Our study suggests that rMSCs have the potential to differentiate into neural cells spontaneously in culture and may contribute towards the natural function of MSCs for neural system in vivo.
|Measurements of brain-derived neurotrophic factor: methodological aspects and demographical data. |
Viktorija Trajkovska,Anders B Marcussen,Maj Vinberg,Per Hartvig,Susana Aznar,Gitte M Knudsen
Brain research bulletin 73 2007
Although numerous studies have dealt with changes in blood brain-derived neurotrophic factor (BDNF), methodological issues about BDNF measurements have only been incompletely resolved. We validated BDNF ELISA with respect to accuracy, reproducibility and the effect of storage and repeated freezing cycles on BDNF concentrations. Additionally, the effect of demographic characteristics in healthy subjects on BDNF was verified. Whole blood and serum was collected from 206 healthy subjects and a subgroup was genotyped for BDNF Val66Met polymorphism. The effect of age, gender, BDNF genotype and thrombocyte count on whole blood BDNF was assessed. The BDNF ELISA measurement was accurate, 91.6+/-3.0%, and showed high reproducibility, whereas inter-assay and intra-subject variations were modest, 8.4+/-5.2% and 17.5+/-14.1%, respectively. Storage of whole blood samples at 4 degrees C significantly decreased BDNF concentration, while repeated freezing cycles and storage at -20 degrees C was without any effect. Storage at -20 degrees C of serum, but not whole blood, was associated with a significant decrease in BDNF concentration. Women had significantly higher whole blood BDNF concentrations than men (18.6+/-1.3 ng/ml versus 16.5+/-1.4 ng/ml), and showed a right-skewed BDNF concentration distribution. No association between whole blood BDNF concentrations and thrombocyte count, age, or BDNF genotype was found. In conclusion, the BDNF ELISA assay determines whole blood BDNF accurately and with high reproducibility. Female gender is associated with higher whole blood BDNF concentrations whereas age, thrombocyte count and BDNF Val66Met polymorphism were un-associated.
|Increased BDNF serum concentration in fibromyalgia with or without depression or antidepressants |
Laske, Christoph, et al.
Journal of psychiatric research, 41:600-605 (2007) 2007
|Effects of castration on the expression of brain-derived neurotrophic factor (BDNF) in the vas deferens and male accessory genital glands of the rat. |
Mirabella, Nicola, et al.
Cell Tissue Res., 323: 513-22 (2006) 2006
|Acute BDNF and cortisol response to low intensity exercise and following ramp incremental exercise to exhaustion in humans |
Rojas Vega, Sandra, et al
Brain Res, 1121:59-65 (2006) 2006
|Peripheral levels of BDNF and NGF in primary headaches. |
F Blandini, L Rinaldi, C Tassorelli, G Sances, M Motta, A Samuele, R Fancellu, G Nappi, A Leon
Cephalalgia : an international journal of headache 26 136-42 2006
Neurotrophins, such as brain-derived neurotrophic factor (BDNF) and nerve growth factor (NGF), have been implicated in the generation and modulation of pain. To investigate whether alterations in neurotrophin levels can be detected in subjects suffering from nociceptive disorders, such as primary headaches, we determined the peripheral (platelet and plasma) levels of BDNF and NGF in patients suffering from migraine, with or without aura, or cluster headache (CH), in the interictal phase, and in healthy volunteers. All primary headaches patients studied showed significantly decreased platelet levels of BDNF (migraine vs. controls P0.001; CH vs. controls P0.01), while a selective reduction of platelet NGF was observed in migraine sufferers and not in CH patients compared with control subjects (migraine vs. controls P0.001). These changes were not accompanied by significant modifications of neurotrophin plasma levels. Our findings show for the first time that changes in peripheral levels of neurotrophines (BDNF and NGF) occur in patients suffering from different types of primary headaches, suggesting a potential involvement of BDNF and NGF in the pathophysiology of these disorders, and raising the possibility that differences in peripheral neurotrophins may help to distinguish migraine biologically from CH.
|Increased adult hippocampal brain-derived neurotrophic factor and normal levels of neurogenesis in maternal separation rats. |
Mia H Greisen, C Anthony Altar, Tom G Bolwig, Richard Whitehead, Gitta Wörtwein
Journal of neuroscience research 79 772-8 2005
Repeated maternal separation of rat pups during the early postnatal period may affect brain-derived neurotrophic factor (BDNF) or neurons in brain areas that are compromised by chronic stress. In the present study, a highly significant increase in hippocampal BDNF protein concentration was found in adult rats that as neonates had been subjected to 180 min of daily separation compared with handled rats separated for 15 min daily. BDNF protein was unchanged in the frontal cortex and hypothalamus/paraventricular nucleus. Expression of BDNF mRNA in the CA1, CA3, or dentate gyrus of the hippocampus or in the paraventricular hypothalamic nucleus was not affected by maternal separation. All animals displayed similar behavioral patterns in a forced-swim paradigm, which did not affect BDNF protein concentration in the hippocampus or hypothalamus. Repeated administration of bromodeoxyuridine revealed equal numbers of surviving, newly generated granule cells in the dentate gyrus of adult rats from the 15 min or 180 min groups. The age-dependent decline in neurogenesis from 3 months to 7 months of age did not differ between the groups. Insofar as BDNF can stimulate neurogenesis and repair, we propose that the elevated hippocampal protein concentration found in maternally deprived rats might be a compensatory reaction to separation during the neonatal period, maintaining adult neurogenesis at levels equal to those of the handled rats.
|Effects of tryptophan depletion on serum levels of brain-derived neurotrophic factor in unmedicated patients with remitted depression and healthy subjects |
Neumeister, Alexander, et al.
The American journal of psychiatry, 162:805-807 (2005) 2005
|BDNF-induced white matter neuroprotection and stage-dependent neuronal survival following a neonatal excitotoxic challenge. |
Husson, Isabelle, et al.
Cereb. Cortex, 15: 250-61 (2005) 2005
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|ChemiKineTM Brain Derived Neurotrophic Factor (BDNF) Sandwich ELISA Kit|
|ChemiKineTM Brain Derived Neurotrophic Factor (BDNF)|