دورية أكاديمية
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BDNF-induced nitric oxide signals in cultured rat hippocampal neurons: time course, mechanism of generation, and effect on neurotrophin secretion.

التفاصيل البيبلوغرافية
العنوان: BDNF-induced nitric oxide signals in cultured rat hippocampal neurons: time course, mechanism of generation, and effect on neurotrophin secretion.
المؤلفون: Kolarow R; Medical Faculty, Institute of Physiology, Otto-von-Guericke-University Magdeburg, Germany ; University Medical Center, Institute of Physiology, Johannes Gutenberg-University Mainz Mainz, Germany., Kuhlmann CR; University Medical Center, Institute of Physiology, Johannes Gutenberg-University Mainz Mainz, Germany., Munsch T; Medical Faculty, Institute of Physiology, Otto-von-Guericke-University Magdeburg, Germany., Zehendner C; University Medical Center, Institute of Physiology, Johannes Gutenberg-University Mainz Mainz, Germany., Brigadski T; Medical Faculty, Institute of Physiology, Otto-von-Guericke-University Magdeburg, Germany ; University Medical Center, Institute of Physiology, Johannes Gutenberg-University Mainz Mainz, Germany., Luhmann HJ; University Medical Center, Institute of Physiology, Johannes Gutenberg-University Mainz Mainz, Germany., Lessmann V; Medical Faculty, Institute of Physiology, Otto-von-Guericke-University Magdeburg, Germany ; University Medical Center, Institute of Physiology, Johannes Gutenberg-University Mainz Mainz, Germany.
المصدر: Frontiers in cellular neuroscience [Front Cell Neurosci] 2014 Nov 07; Vol. 8, pp. 323. Date of Electronic Publication: 2014 Nov 07 (Print Publication: 2014).
نوع المنشور: Journal Article
اللغة: English
بيانات الدورية: Publisher: Frontiers Research Foundation Country of Publication: Switzerland NLM ID: 101477935 Publication Model: eCollection Cited Medium: Print ISSN: 1662-5102 (Print) Linking ISSN: 16625102 NLM ISO Abbreviation: Front Cell Neurosci Subsets: PubMed not MEDLINE
أسماء مطبوعة: Original Publication: Lausanne, Switzerland : Frontiers Research Foundation, 2007-
مستخلص: BDNF and nitric oxide signaling both contribute to plasticity at glutamatergic synapses. However, the role of combined signaling of both pathways at the same synapse is largely unknown. Using NO imaging with diaminofluoresceine in cultured hippocampal neurons we analyzed the time course of neurotrophin-induced NO signals. Application of exogenous BDNF, NT-4, and NT-3 (but not NGF) induced NO signals in the soma and in proximal dendrites of hippocampal neurons that were sensitive to NO synthase activity, TrkB signaling, and intracellular calcium elevation. The effect of NO signaling on neurotrophin secretion was analyzed in BDNF-GFP, and NT-3-GFP transfected hippocampal neurons. Exogenous application of the NO donor sodium-nitroprusside markedly inhibited neurotrophin secretion. However, endogenously generated NO in response to depolarization and neurotrophin stimulation, both did not result in a negative feedback on neurotrophin secretion. These results suggest that a negative feedback of NO signaling on synaptic secretion of neurotrophins operates only at high intracellular levels of nitric oxide that are under physiological conditions not reached by depolarization or BDNF signaling.
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فهرسة مساهمة: Keywords: BDNF; PSD95; TrkB; neurotrophins; nitric oxide; peptide secretion; synaptic plasticity
تواريخ الأحداث: Date Created: 20141127 Date Completed: 20141126 Latest Revision: 20200930
رمز التحديث: 20231215
مُعرف محوري في PubMed: PMC4224130
DOI: 10.3389/fncel.2014.00323
PMID: 25426021
قاعدة البيانات: MEDLINE
الوصف
تدمد:1662-5102
DOI:10.3389/fncel.2014.00323