Alterations in brain-derived neurotrophic factor (BDNF) and its precursor proBDNF in the brain regions of a learned helplessness rat model and the antidepressant effects of a TrkB agonist and antagonist

@article{Shirayama2015AlterationsIB,
  title={Alterations in brain-derived neurotrophic factor (BDNF) and its precursor proBDNF in the brain regions of a learned helplessness rat model and the antidepressant effects of a TrkB agonist and antagonist},
  author={Yukihiko Shirayama and Chun Yang and Ji-chun Zhang and Qian Ren and Wei Yao and Kenji Hashimoto},
  journal={European Neuropsychopharmacology},
  year={2015},
  volume={25},
  pages={2449-2458}
}
Brain-derived neurotrophic factor-TrkB signaling in the medial prefrontal cortex plays a role in the anhedonia-like phenotype after spared nerve injury
  • X. Fang, Chun Yang, A. Luo
  • Biology, Psychology
    European Archives of Psychiatry and Clinical Neuroscience
  • 2018
TLDR
It is suggested that reduced BDNF-TrkB signaling in the mPFC might contribute to neuropathic pain-induced anhedonia, and that TrkB agonists could be potential therapeutic drugs for pain- inducedAnhedonia.
Regional differences in the expression of brain-derived neurotrophic factor (BDNF) pro-peptide, proBDNF and preproBDNF in the brain confer stress resilience
TLDR
This study suggests that regional differences in conversion of BDNF precursors into BDNF and BDNF pro-peptide by proteolytic cleavage may contribute to stress resilience.
Regulation of glutamate transporter 1 via BDNF-TrkB signaling plays a role in the anti-apoptotic and antidepressant effects of ketamine in chronic unpredictable stress model of depression
TLDR
The findings suggest that regulation of GLT-1 on astrocytes, responsible for 90 % of glutamate reuptake from the synapse, through BDNF-TrkB signaling is involved in mediation of the therapeutic effects of ketamine on behavioral abnormalities and morphological changes in the hippocampus of the CUS-exposed rats.
Brain-derived Neurotrophic Factor (BDNF)-TrkB Signaling in Inflammation-related Depression and Potential Therapeutic Targets
TLDR
An overview of the tryptophan-kynurenine pathway and BDNF-TrkB signaling in the pathophysiology of inflammation-induced depression, and mechanistic actions for potential therapeutic agents are proposed.
Ibogaine Modifies GDNF, BDNF and NGF Expression in Brain Regions Involved in Mesocorticolimbic and Nigral Dopaminergic Circuits
TLDR
Examination of the effect of ibogaine acute administration on the expression of neurotrophic factors in distinct regions containing dopaminergic neurons found that NGF was found to be upregulated in all regions after I40, while a selective upregulation was found in PFC and VTA for the I20 treatment.
Injection of Anti-proBDNF in Anterior Cingulate Cortex (ACC) Reverses Chronic Stress-Induced Adverse Mood Behaviors in Mice
TLDR
Bilateral ACC treatment with anti-proBDNF microinjection not only reversed depressive activity but also significantly increased the amount of foraged food and BDNF mRNA in the brain.
The alterations of glutamate transporter 1 and glutamine synthetase in the rat brain of a learned helplessness model of depression
TLDR
The results suggest that the LH rats experienced up-regulations of GLT-1 and GS in the CA-1, CA-3, DG, mPF, and NAc and a down-regulation of GS inThe amygdala and it is possible that the effects of theGLT- 1 and GS levels on astrocytes in theCA-3 are critical for the differentiation of resilience from vulnerability.
Depression-like phenotype by deletion of α7 nicotinic acetylcholine receptor: Role of BDNF-TrkB in nucleus accumbens
TLDR
Findings suggest that increased BDNF-TrkB signaling and synaptogenesis in the NAc by deletion of α7 nAChR plays a key role in depression.
...
...

References

SHOWING 1-10 OF 62 REFERENCES
Antidepressant Effects of TrkB Ligands on Depression-Like Behavior and Dendritic Changes in Mice After Inflammation
TLDR
It is suggested that LPS-induced inflammation may cause depression-like behavior by altering BDNF and spine density in the CA3, DG, PFC, and NAc, which may be involved in the antidepressant effects of 7,8-DHF and ANA-12, respectively.
Brain-derived neurotrophic factor in the ventral midbrain–nucleus accumbens pathway: a role in depression
Brain-Derived Neurotrophic Factor Produces Antidepressant Effects in Behavioral Models of Depression
TLDR
The hypothesis that BDNF in the hippocampus produces an antidepressant effect in behavioral models of depression, the learned helplessness (LH) and forced swim test (FST) paradigms is tested and provides further support for the hypothesis thatBDNF contributes to the therapeutic action of antidepressant treatment.
Infralimbic BDNF/TrkB Enhancement of GluN2B Currents Facilitates Extinction of a Cocaine-Conditioned Place Preference
TLDR
It is demonstrated that activation of a primary BDNF target, the tropomyosin-related kinase B (TrkB) receptor, enhances the amplitude and prolongs the decay kinetics of N-methyl-d-aspartate receptor (NMDAR) currents in male rat infralimbic prefrontal pyramidal neurons, and that TrkB receptor activation enhances extinction of cocaine-CPP via GluN2B-containing NMDARs.
Hippocampal astrocytes are necessary for antidepressant treatment of learned helplessness rats
TLDR
Results indicate that astrocytes are responsive to the antidepressant‐like effect of imipramine in the dentate gyrus and CA3 region of the hippocampus, which is a major component of the neural network and plays a role in brain function.
Activation of the TrkB Neurotrophin Receptor Is Induced by Antidepressant Drugs and Is Required for Antidepressant-Induced Behavioral Effects
TLDR
The data suggest that antidepressants acutely increase trkB signaling in a BDNF-dependent manner in cerebral cortex and that this signaling is required for the behavioral effects typical of antidepressant drugs.
Regional Differences in Brain-Derived Neurotrophic Factor Levels and Dendritic Spine Density Confer Resilience to Inescapable Stress
TLDR
The results suggest that regional differences in BDNF levels and spine density in rat brain may contribute to resilience to inescapable stress.
Neurotrophins and depression.
  • C. Altar
  • Biology, Psychology
    Trends in pharmacological sciences
  • 1999
Infusions of allopregnanolone into the hippocampus and amygdala, but not into the nucleus accumbens and medial prefrontal cortex, produce antidepressant effects on the learned helplessness rats
TLDR
It is suggested that ALLO exerts antidepressant‐like effects in the CA3 region of hippocampus through the GABA system and in the central region of amygdala, dependently on the activation of the glutamatergic mechanisms.
Antidepressant Drugs Transactivate TrkB Neurotrophin Receptors in the Adult Rodent Brain Independently of BDNF and Monoamine Transporter Blockade
TLDR
The present findings suggest that ADs transactivate brain TrkB receptors independently of BDNF and monoamine reuptake blockade and emphasize the need of an intact tissue context for the ability of ADs to induce TrkB activity in brain.
...
...