Brain-derived neurotrophic factor facilitates glutamate and inhibits GABA release from hippocampal synaptosomes through different mechanisms

Autor: Joaquim A. Ribeiro, Nuno Canas, Inês Tomás Pereira, Ana M. Sebastião
Přispěvatelé: Repositório da Universidade de Lisboa
Rok vydání: 2004
Předmět:
Male
Nipecotic Acids
Tropomyosin receptor kinase B
Hippocampus
Indole Alkaloids
chemistry.chemical_compound
Cadmium Chloride
Synaptosome
Drug Interactions
γ-Aminobutyric acid
Enzyme Inhibitors
gamma-Aminobutyric Acid
Neurons
Voltage-dependent calcium channel
General Neuroscience
Glutamate receptor
Calcium Channel Blockers
Excitatory postsynaptic potential
SKF-89976A
Glutamate
medicine.medical_specialty
GABA Agents
Carbazoles
Glutamic Acid
In Vitro Techniques
Biology
Tritium
Inhibitory postsynaptic potential
Brain-derived neurotrophic factor
Internal medicine
medicine
Animals
Rats
Wistar
Molecular Biology
Analysis of Variance
Dose-Response Relationship
Drug
Brain-Derived Neurotrophic Factor
Rats
Endocrinology
nervous system
chemistry
Potassium
Brain-derived neurotrophic factor (BDNF)
Calcium
Neurology (clinical)
Synaptosomes
Developmental Biology
Zdroj: Repositório Científico de Acesso Aberto de Portugal
Repositório Científico de Acesso Aberto de Portugal (RCAAP)
instacron:RCAAP
ISSN: 0006-8993
DOI: 10.1016/j.brainres.2004.04.070
Popis: © 2004 Elsevier B.V.
Brain-derived neurotrophic factor (BDNF) has an acute excitatory effect on rat hippocampal synaptic transmission. To compare the action of BDNF upon the release of excitatory and inhibitory neurotransmitters in the hippocampus, we studied the effect of acutely applied BDNF on the K+ -evoked glutamate and on the K+ -evoked y-aminobutyric acid (GABA) release from rat hippocampal nerve terminals (synaptosomes). The acute application of BDNF (30–100 ng/ml) enhanced the K+ -evoked [3H]glutamate release. This effect involved tyrosine-kinase B (TrkB) receptor phosphorylation and Ca2 + entry into synaptosomes through voltage-sensitive calcium channels, since it was abolished by K252a (200 nM), which prevents TrkB-mediated phosphorylation, and by CdCl2 (0.2 mM), a blocker of voltage-sensitive calcium channels. In contrast, BDNF (3–100 ng/ml) inhibited K+-evoked [3H]GABA release from hippocampal synaptosomes. This action was also mediated by phosphorylation of the TrkB receptor, but was independent of Ca2 + entry into synaptosomes through voltage-sensitive calcium channels. Blockade of transport of GABA with SKF 89976a (20 AM) prevented the inhibitory action of BDNF upon GABA release, indicating that BDNF influences the activity of GABA transporters. It is concluded that BDNF influences in an opposite way, through distinct mechanisms, the release of glutamate and the release of GABA from hippocampal synaptosomes.
Work supported by FCT and EU (POCTI/37398/NSE/2001). ITP is in award of a FCT fellowship.
Databáze: OpenAIRE
Externí odkaz: