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Cerebral Cortex Advance Access published online on July 6, 2004
Cerebral Cortex, doi:10.1093/cercor/bhh130
© 2004 by Oxford University Press
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Article

BDNF Locally Potentiates GABAergic Presynaptic Machineries: Target-selective Circuit Inhibition

Shizu Ohba 1, Takamitsu Ikeda 1, Yuji Ikegaya 1, Nobuyoshi Nishiyama 1, Norio Matsuki 1, Maki K. Yamada 1*

1 Laboratory of Chemical Pharmacology, Graduate School of Pharmaceutical Sciences, The University of Tokyo, Hongo, Bunkyo-ku, Tokyo, Japan

* To whom correspondence should be addressed. E-mail: maki{at}mol.f.u-tokyo.ac.jp.


  Abstract

Inhibitory neurotransmission is critical for neuronal circuit formation. To examine whether inhibitory neurotransmission receives target-selective modulation in the long term, we expressed the cDNA of brain-derived neurotrophic factor (BDNF), which has been shown to induce the augmentation of GABAergic synapses in vivo and in vitro, in a small population of cultured hippocampal neurons. At 48 h after transfection, the expression level of glutamic acid decarboxylase 65 (GAD65), a GABA synthetic enzyme that resides mainly in GABAergic terminals, was selectively enhanced around the BDNF-expressing neurons, in comparison with the neighboring control neurons interposed between the BDNF-expressing neurons and inhibitory neurons. Exogenous BDNF application for 48 h also increased the GAD level and enhanced the GABA release probability. These potentiating effects were attenuated in inhibitory synapses on neurons expressing a dominant negative form of the BDNF receptor (tTrkB). This suggests that postsynaptic BDNF-TrkB signaling contributes to the target-selective potentiation of inhibitory presynaptic machineries. Since BDNF is expressed in an activity-dependent manner in vivo, this selectivity may be one of the key mechanisms by which the independence of functional neuronal circuits is maintained.

Keywords: GABA; GAD; hippocampus; independence; inhibitory synapse; plasticity.
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