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The Journal of Neuroscience, July 5, 2006, 26(27):7189-7200; doi:10.1523/JNEUROSCI.5474-05.2006

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Development/Plasticity/Repair
Altered Balance of Glutamatergic/GABAergic Synaptic Input and Associated Changes in Dendrite Morphology after BDNF Expression in BDNF-Deficient Hippocampal Neurons

B. Singh,¹ C. Henneberger,¹ D. Betances,¹ M. A. Arevalo,² A. Rodríguez-Tébar,² J. C. Meier,¹ and R. Grantyn¹

¹Developmental Physiology Group, Johannes Mueller Institute for Neurophysiology, University Medical School (Charité) of the Humboldt University, D-10117 Berlin, Germany, and ²Instituto de Neurobiología Cajal, Madrid, Spain

Correspondence should be addressed to Dr. Rosemarie Grantyn, Department of Sensory and Developmental Physiology, Johannes Mueller Center for Physiology, Humboldt University Medical School (Charité), Tucholskystrasse 2, D-10117 Berlin, Germany. Email: rosemarie.grantyn{at}charite.de

Cultured neurons from bdnf–/– mice display reduced densities of synaptic terminals, although in vivo these deficits are small or absent. Here we aimed at clarifying the local responses to postsynaptic brain-derived neurotrophic factor (BDNF). To this end, solitary enhanced green fluorescent protein (EGFP)-labeled hippocampal neurons from bdnf–/– mice were compared with bdnf–/– neurons after transfection with BDNF, bdnf–/– neurons after transient exposure to exogenous BDNF, and bdnf+/+ neurons in wild-type cultures. Synapse development was evaluated on the basis of presynaptic immunofluorescence and whole-cell patch-clamp recording of miniature postsynaptic currents. It was found that neurons expressing BDNF::EGFP for at least 16 h attracted a larger number of synaptic terminals than BDNF-deficient control neurons. Transfected BDNF formed clusters in the vicinity of glutamatergic terminals and produced a stronger upregulation of synaptic terminal numbers than high levels of ambient BDNF. Glutamatergic and GABAergic synapses reacted differently to postsynaptic BDNF: glutamatergic input increased, whereas GABAergic input decreased. BDNF::EGFP-expressing neurons also differed from BDNF-deficient neurons in their dendrite morphology: they exhibited weaker dendrite elongation and stronger dendrite initiation. The upregulation of glutamatergic synaptic input and the BDNF-induced downregulation of GABAergic synaptic terminal numbers by postsynaptic BDNF depended on tyrosine receptor kinase B activity, as deduced from the blocking effects of K252a. The suppression of dendrite elongation was also prevented by block of tyrosine receptor kinase B but required, in addition, glutamate receptor activity. Dendritic length decreased with the number of glutamatergic contacts. These results illuminate the role of BDNF as a retrograde synaptic regulator of synapse development and the dependence of dendrite elongation on glutamatergic input.

Key words: synaptogenesis; dendrite growth; E/I balance; bdnf knock-out; neuron transfection; retrograde messenger

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Received Dec. 21, 2005; revised April 16, 2006; accepted April 24, 2006.

Correspondence should be addressed to Dr. Rosemarie Grantyn, Department of Sensory and Developmental Physiology, Johannes Mueller Center for Physiology, Humboldt University Medical School (Charité), Tucholskystrasse 2, D-10117 Berlin, Germany. Email: rosemarie.grantyn{at}charite.de

This article has been cited by other articles:

				C. Henneberger, S. J. Redman, and R. Grantyn Cortical Efferent Control of Subcortical Sensory Neurons by Synaptic Disinhibition Cereb Cortex, September 1, 2007; 17(9): 2039 - 2049. [Abstract] [Full Text] [PDF]

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