Results 1 to 10 of about 1,055,671 (84)

Expression of hippocampal brain-derived neurotrophic factor and its receptors in Stanley consortium brains [PDF]

open access: yes, 2009
Several lines of evidence implicate BDNF in the pathophysiology of psychiatric illness. BDNF polymorphisms have also been associated with the risk of schizophrenia and mood disorders.
Dunham, Jason S.   +12 more
core   +1 more source

BDNF and its pro-peptide are stored in presynaptic dense core vesicles in brain neurons [PDF]

open access: yes, 2012
Although brain-derived neurotrophic factor (BDNF) regulates numerous and complex biological processes including memory retention, its extremely low levels in the mature central nervous system have greatly complicated attempts to reliably localize it ...
Ruben Deogracias   +24 more
core   +1 more source

和厚朴酚调节BDNF-TrkB-CREB信号通路对脑出血小鼠神经损伤和认知功能的影响 Effects of Honokiol on Neurological Injury and Cognitive Function in Mice with Intracerebral Hemorrhage by Regulating BDNF-TrkB-CREB Signaling Pathway

open access: yesZhongguo cuzhong zazhi
目的 探讨和厚朴酚对脑出血(intracerebral hemorrhage,ICH)小鼠神经损伤和认知功能的影响及其作用机制。 方法 将C57BL/6J小鼠随机分为假手术组,模型组,和厚朴酚低、中、高剂量组,以及和厚朴酚+抑制剂组。除假手术组外,其余组小鼠均通过自体血注入右侧基底神经节构建ICH模型。于ICH前15 min和ICH后1 h,和厚朴酚低、中、高剂量组分别腹腔注射10 mg/kg、20 mg/kg、40 mg/kg和厚朴酚,和厚朴酚+抑制剂组腹腔注射40 mg ...
李阳阳1,方建2,王晓雪1 (LI Yangyang1, FANG Jian2, WANG Xiaoxue1 )
doaj   +1 more source

针刺调节BDNF/TrkB信号通路改善中枢神经系统疾病的研究进展 [PDF]

open access: yes
BDNF/TrkB信号通路作为神经元生长、发育和突触可塑性的关键调节器,广泛参与中枢神经系统疾病的发生发展,如缺血性脑卒中、阿尔茨海默病、帕金森病和脊髓损伤等。研究表明针刺能调节BDNF/TrkB信号通路的活性,对以上疾病具有显著的治疗潜力,其作用机制与参与突触结构重塑,抑制神经细胞凋亡,促进神经发生和突触再生等有关。本文综述了BDNF/TrkB相关信号通路在中枢神经系统疾病中的作用以及针刺对该通路的调控机制,以期为临床治疗提供新思路。未来研究应深入探究针刺对BDNF/TrkB信号通路的精准调控 ...
白艳杰, 栗文静
core   +1 more source

Distinct requirements for TrkB and TrkC signaling in target innervation by sensory neurons

open access: yes, 2002
Signaling by brain-derived neurotrophic factor (BDNF) via the TrkB receptor, or by neurotrophin-3 (NT3) through the TrkC receptor support distinct populations of sensory neurons.
Schimmang, Thomas   +26 more
core   +1 more source

Role of neurotrophins and neuropeptides in Genetic Absence Epilepsy Rats from Strasbourg (GAERS) : a model for human generalized absence seizures [PDF]

open access: yes, 2010
Several studies have shown that neurotrophins and neuropeptides contribute to epileptogenesis but their impact on idiopathic generalized epilepsies is not yet elucidated.
Landweer, Svenja
core   +1 more source

Enlarged infarct volume and loss of BDNF mRNA induction following brain ischemia in mice lacking FGF-2

open access: yes, 2006
FGF-2, a potent multifunctional and neurotrophic growth factor, is widely expressed in the brain and upregulated in cerebral ischemia. Previous studies have shown that intraventricularly or systemically administered FGF-2 reduces the size of cerebral ...
Kiprianova, Irina   +6 more
core   +1 more source

Mutation at the TrkB PLC{gamma}-docking site affects hippocampal LTP and associative learning in conscious mice

open access: yes, 2007
Previous in vitro studies have characterized the electrophysiological properties and molecular events associated with long-term potentiation (LTP), but as yet there are no in vivo data from molecular-level dissection that directly identify LTP as the ...
Delgado-García, José M   +4 more
core   +1 more source

Ori activates the BDNF/TrkB/CREB signaling pathway in the hippocampus of AD mice.

open access: yes, 2016
(A) Western blotting for BDNF, p-TrkB, TrkB, p-CREB and CREB proteins. (B) Quantitative analysis of BDNF, p-TrkB and p-CREB expression. n = 5 mice per group and the experiment was performed for three times. Data are presented as the means ± SEM. *P1–42.
Xiaolei Zhu (325492)   +6 more
core   +1 more source

The BDNF–TrkB–CREB Signalling Pathway Is Involved in Bisphenol S-Induced Neurotoxicity in Male Mice by Regulating Methylation

open access: yes, 2022
Bisphenol S (BPS), the most common substitute for bisphenol A in manufacturing, is associated with neurotoxicity, but its molecular mechanisms are unclear.
Ya-Qi Kan   +11 more
core   +1 more source

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