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The Journal of Neurophysiology Vol. 88 No. 2 August 2002, pp. 595-603
Copyright ©2002 by the American Physiological Society
Developmental Physiology, Johannes Müller Institute of Physiology, Charité, D-10117 Berlin, Germany
Henneberger, Christian,
René Jüttner,
Thomas Rothe, and
Rosemarie Grantyn.
Postsynaptic Action of BDNF on GABAergic Synaptic Transmission in
the Superficial Layers of the Mouse Superior Colliculus. J. Neurophysiol. 88: 595-603, 2002. The
neurotrophin brain-derived neurotrophic factor (BDNF) is involved
in numerous aspects of synapse development and plasticity. The present
study was aimed at clarifying the significance of endogenous BDNF for
the synaptically driven spontaneous network activity and GABAergic
inhibition in the superficial layers of the mouse superior colliculus.
In this structure neuron survival is unaffected by the absence of BDNF.
Two experimental approaches were used: comparison of BDNF-deficient
(-/-) and wild-type (+/+) mice and blockade of BDNF receptor
signaling by the tyrosine kinase inhibitor K-252a. Patch-clamp
recordings were performed on horizontal slices during postnatal days 15 and 16. The lack of BDNF in -/- mice caused a significant reduction
of the spontaneous action potential frequency and an increase in the
pharmacologically induced disinhibition of spike discharge. This change
was accompanied by an increase in the amplitudes of GABAergic evoked,
spontaneous, and miniature inhibitory postsynaptic currents (IPSCs).
BDNF gene inactivation had no effect on the degree of paired-pulse
facilitation or the frequency of miniature IPSCs. The increase of IPSC
amplitudes by chronic BDNF deprivation was completely mimicked by acute
exposure to K-252a in +/+ animals. The enhancement of GABAergic IPSCs
in -/- animals was reversed by acute application of 100 ng/ml BDNF, but this rescue was completely prevented by blocking postsynaptic protein kinase C (PKC) activation with the PKC inhibitor peptide 19-31. From these results we conclude that BDNF increases spontaneous network activity by suppressing GABAergic inhibition, the site of
action of BDNF is predominantly postsynaptic, BDNF-induced suppression
of GABAergic synaptic transmission is caused by acute downregulation of
GABAA receptors, and BDNF effects are mediated by
its TrkB receptor and require PKC activation in the postsynaptic cell.
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