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Developmental changes in the BDNF‐induced modulation of inhibitory synaptic transmission in the Kölliker–Fuse nucleus of rat
Author(s) -
Kron Miriam,
Zhang Weiqi,
Dutschmann Mathias
Publication year - 2007
Publication title -
european journal of neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.346
H-Index - 206
eISSN - 1460-9568
pISSN - 0953-816X
DOI - 10.1111/j.1460-9568.2007.05960.x
Subject(s) - inhibitory postsynaptic potential , neuroscience , neurotransmission , excitatory postsynaptic potential , biology , neurotrophic factors , postsynaptic current , brain derived neurotrophic factor , synapse , receptor , biochemistry
The Kölliker–Fuse nucleus (KF), part of the pontine respiratory group, is involved in the control of respiratory phase duration, and receives both excitatory and inhibitory afferent input from various other brain regions. There is evidence for developmental changes in the modulation of excitatory inputs to the KF by the neurotrophin brain‐derived neurotrophic factor (BDNF). In the present study we investigated if BDNF exerts developmental effects on inhibitory synaptic transmission in the KF. Recordings of inhibitory postsynaptic currents (IPSCs) in KF neurons in a pontine slice preparation revealed general developmental changes. Recording of spontaneous and evoked IPSCs (sIPSCs, eIPSCS) revealed that neonatally the γ‐aminobutyric acid (GABA)ergic fraction of IPSCs was predominant, while in later developmental stages glycinergic neurotransmission significantly increased. Bath‐application of BDNF significantly reduced sIPSC frequency in all developmental stages, while BDNF‐mediated modulation on eIPSCs showed developmental differences. The eIPSCs mean amplitude was uniformly and significantly reduced following BDNF application only in neurons from rats younger than postnatal day 10. At later postnatal stages the response pattern became heterogeneous, and both augmentations and reductions of eIPSC amplitudes occurred. All BDNF effects on eIPSCs and sIPSCs were reversed with the tyrosine kinase receptor‐B inhibitor K252a. We conclude that developmental changes in inhibitory neurotransmission, including the BDNF‐mediated modulation of eIPSCs, relate to the postnatal maturation of the KF. The changes in BDNF‐mediated modulation of IPSCs in the KF may have strong implications for developmental changes in synaptic plasticity and the adaptation of the breathing pattern to afferent inputs.