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BDNF antibody [EPR1292]

RRID:AB_10862052

Antibody ID

AB_10862052

Target Antigen

BDNF antibody [EPR1292] mouse, human, rat, human, mouse, rat

Proper Citation

(Abcam Cat# ab108319, RRID:AB_10862052)

Clonality

monoclonal antibody

Comments

validation status unknown, seller recommendations provided in 2012: IHC-P, WB; Immunohistochemistry; Immunohistochemistry - fixed; Western Blot

Host Organism

rabbit

Vendor

Abcam

BDNF infusion into the MPN mag is sufficient to restore copulatory behavior in the castrated Syrian hamster.

  • Brague JC
  • Horm Behav
  • 2018 May 12

Literature context:


Abstract:

Testosterone plays a key role in the expression of male sex behavior by influencing cellular activity and synapses within the magnocellular medial preoptic nucleus (MPN mag), a sub-nucleus of the medial preoptic area (MPOA) in the Syrian hamster. Although the mechanisms underlying hormonally-induced synaptic plasticity in this region remain elusive, the data suggests that an increase in synaptic density may mediate testosterone's effects on copulation. As brain derived neurotrophic factor (BDNF) plays an integral role in regulating synaptic plasticity and gonadal steroids regulate the levels of BDNF, we hypothesize that BDNF may mediate the effects of gonadal hormones on copulatory behavior. To test this hypothesis, we infused BDNF or controls into the MPN mag of long-term castrates. Our results indicate that BDNF, but not the controls, restored copulatory behavior in castrated male Syrian hamsters. Furthermore, the rise of BDNF expression in the MPOA preceded the rise of synaptophysin following testosterone replacement in castrated males. These data are consistent with our hypothesis, implicating a role for BDNF in mediating testosterone's action on copulation and suggest that the delay in testosterone's restoration of copulation is, in part, due to the delay in the increase of BDNF and synaptophysin.

Funding information:
  • NIAMS NIH HHS - R01 AR031062-27(United States)

β2 Adrenergic-Neurotrophin Feedforward Loop Promotes Pancreatic Cancer.

  • Renz BW
  • Cancer Cell
  • 2018 Jan 8

Literature context:


Abstract:

Catecholamines stimulate epithelial proliferation, but the role of sympathetic nerve signaling in pancreatic ductal adenocarcinoma (PDAC) is poorly understood. Catecholamines promoted ADRB2-dependent PDAC development, nerve growth factor (NGF) secretion, and pancreatic nerve density. Pancreatic Ngf overexpression accelerated tumor development in LSL-Kras+/G12D;Pdx1-Cre (KC) mice. ADRB2 blockade together with gemcitabine reduced NGF expression and nerve density, and increased survival of LSL-Kras+/G12D;LSL-Trp53+/R172H;Pdx1-Cre (KPC) mice. Therapy with a Trk inhibitor together with gemcitabine also increased survival of KPC mice. Analysis of PDAC patient cohorts revealed a correlation between brain-derived neurotrophic factor (BDNF) expression, nerve density, and increased survival of patients on nonselective β-blockers. These findings suggest that catecholamines drive a feedforward loop, whereby upregulation of neurotrophins increases sympathetic innervation and local norepinephrine accumulation.

Funding information:
  • NCI NIH HHS - P30 CA013696()
  • NCI NIH HHS - R35 CA210088()
  • NCRR NIH HHS - S10 RR025686()
  • NIDDK NIH HHS - DK053904(United States)

Regulation and effects of neurotrophic factors after neural stem cell transplantation in a transgenic mouse model of Alzheimer disease.

  • Li B
  • J. Neurosci. Res.
  • 2017 Nov 9

Literature context:


Abstract:

According to much research, neurodegeneration and cognitive decline in Alzheimer disease (AD) are correlated with alternations of neurotrophic factors such as nerve growth factor, brain-derived neurotrophic factor, and glial cell-derived neurotrophic factor. The experimental illumination of neural stem cell (NSC) transplantation to eliminate AD symptoms is being explored frequently, and we have acknowledged that neurotrophic factors may play a pivotal role in cognitive improvement. However, the relation between the reversal of cognitive deficits after NSC transplantation and directed alternations of neurotrophic factors is not clearly expounded. Meanwhile, reduced inflammatory response, promoted vessel density, and vascular endothelial growth factor (VEGF) can be reflections of improvement in cerebrovascular function. Three weeks after NSC transplantation, spatial learning and memory function in NSC-injected (Tg-NSC) mice were significantly improved compared with vehicle-injected (Tg-Veh) mice. Meanwhile, results obtained by immunofluorescence and Western blot analyses demonstrated that the levels of neurotrophic factors, VEGF, and vessel density in the cortex of Tg-NSC mice were significantly enhanced compared with Tg-Veh mice, while the levels of proinflammatory cytokines interleukin (IL)-1β, tumor necrosis factor-α, and IL-6 were significantly decreased. Our results suggest that elevated concentrations of neurotrophic factors probably play a critical role in rescuing cognitive dysfunction in APP/PS1 transgenic mice after NSC transplantation, and neurotrophic factors may improve cerebrovascular function by means such as reducing inflammatory response and promoting angiogenesis.

Chronic lithium treatment elicits its antimanic effects via BDNF-TrkB dependent synaptic downscaling.

  • Gideons ES
  • Elife
  • 2017 Jun 16

Literature context:


Abstract:

Lithium is widely used as a treatment for Bipolar Disorder although the molecular mechanisms that underlie its therapeutic effects are under debate. In this study, we show brain-derived neurotrophic factor (BDNF) is required for the antimanic-like effects of lithium but not the antidepressant-like effects in mice. We performed whole cell patch clamp recordings of hippocampal neurons to determine the impact of lithium on synaptic transmission that may underlie the behavioral effects. Lithium produced a significant decrease in α-amino-3-hydroxyl-5-methyl-4-isoxazolepropionic acid receptor (AMPAR)-mediated miniature excitatory postsynaptic current (mEPSC) amplitudes due to postsynaptic homeostatic plasticity that was dependent on BDNF and its receptor tropomyosin receptor kinase B (TrkB). The decrease in AMPAR function was due to reduced surface expression of GluA1 subunits through dynamin-dependent endocytosis. Collectively, these findings demonstrate a requirement for BDNF in the antimanic action of lithium and identify enhanced dynamin-dependent endocytosis of AMPARs as a potential mechanism underlying the therapeutic effects of lithium.