Medical Journals

Regulation of Glycinergic and Gabaergic Synaptogenesis by Brain-derived Neurotrophic Factor in Developing Spinal Neurons.

Authors:
  • Carrasco M A
  • Castro P
  • Sepulveda F J
  • Tapia J C
  • Gatica K
  • Davis M I
  • Aguayo L G

From: Laboratory of Neurophysiology, Department of Physiology, University of Concepción, P.O. Box 160-C, Concepción, Chile.

Neuroscience

  • Publish Date: Mar 2007
  • ISSN: 0306-4522
  • Volume: 145
  • Issue: 2
  • Pages: 484-94
  • Medium: Print
  • Language: English
  • Citation (JAMA): Carrasco M A, Castro P, Sepulveda F J, et al. Regulation of Glycinergic and Gabaergic Synaptogenesis by Brain-derived Neurotrophic Factor in Developing Spinal Neurons.. Neuroscience Mar 2007;145:484-94

Abstract

Brain-derived neurotrophic factor (BDNF) effects on the establishment of glycinergic and GABAergic transmissions in mouse spinal neurons were examined using combined electrophysiological and calcium imaging techniques. BDNF (10 ng/ml) caused a significant acceleration in the onset of synaptogenesis without large effects on the survival of these neurons. Amplitude and frequency of spontaneous inhibitory postsynaptic currents (sIPSCs) and miniature inhibitory postsynaptic currents (mIPSCs) associated to activation of glycine and GABA(A) receptors were augmented in neurons cultured with BDNF. The neurotrophin effect was blocked by long term tetrodotoxin (TTX) addition suggesting a dependence on neuronal activity. In addition, BDNF caused a significant increase in glycine- and GABA-evoked current densities that partly explains the increase in synaptic transmission. Presynaptic mechanisms were also involved in BDNF effects since triethylammonium(propyl)-4-(2-(4-dibutylamino-phenyl)vinyl)pyridinium (FM1-43) destaining with high K(+) was augmented in neurons incubated with the neurotrophin. The effects of BDNF were mediated by receptor tyrosine kinase B (TrkB) and mitogen-activated protein kinase kinase (MEK) activation since culturing neurons with either (9S,10R,12R)-2,3,9,10,11,12-hexahydro-10-hydroxy-9-methyl-1-oxo-9,12-epoxy-1H-diindolo[1,2,3-fg:3’,2’,1’- kl]pyrrolo[3,4-i][1,6]benzodiazocine-10-carboxylic acid methyl ester (K252a) or 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one (PD98059) blocked the augmentation in synaptic activity induced by the neurotrophin.

Mesh Headings (Keywords): Animals, Brain-Derived Neurotrophic Factor, Cell Differentiation, Cells, Cultured, Enzyme Inhibitors, Glycine, Inhibitory Postsynaptic Potentials, MAP Kinase Kinase 1, Mice, Mice, Inbred C57BL, Neural Inhibition, Neural Pathways, Neuronal Plasticity, Neurons, Pyridinium Compounds, Quaternary Ammonium Compounds, Receptor, trkB, Receptors, GABA-A, Receptors, Glycine, Sodium Channel Blockers, Spinal Cord, Synapses, Synaptic Transmission, gamma-Aminobutyric Acid


Check for Full Text / PubMed Unique Identifier (PMID): 17306467


This abstract is part of PubMed, a service of the U.S. National Library of Medicine. PubMed includes more than 17 million citations from MEDLINE and other life science journals for biomedical articles. See Copyright and Disclaimers.

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