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J Physiol Volume 586, Number 9, 2331-2343, May 1, 2008 DOI: 10.1113/jphysiol.2007.148916
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RESPIRATORY

Emergence of brain-derived neurotrophic factor-induced postsynaptic potentiation of NMDA currents during the postnatal maturation of the Kölliker–Fuse nucleus of rat

 Miriam Kron1,3, Julia Reuter1, Ellen Gerhardt2, Till Manzke1,2, Weiqi Zhang1,2 and Mathias Dutschmann1,3

1 Department of Neuro and Sensory Physiology, University Medicine Göttingen, Georg August University, Humboldtallee 23, 37073 Göttingen, Germany
2 Deutsche Forschungsgemeinschaft Research Center for Molecular Physiology of the Brain (CMPB), 37073 Göttingen, Germany
3 Bernstein Center for Computational Neurosciences (BCCN), 37073 Göttingen, Germany

The Kölliker–Fuse nucleus (KF) contributes essentially to respiratory pattern formation and adaptation of breathing to afferent information. Systems physiology suggests that these KF functions depend on NMDA receptors (NMDA-R). Recent investigations revealed postnatal changes in the modulation of glutamatergic neurotransmission by brain-derived neurotrophic factor (BDNF) in the KF. Therefore, we investigated postnatal changes in NMDA-R subunit composition and postsynaptic modulation of NMDA-R-mediated currents by BDNF in KF slice preparations derived from three age groups (neonatal: postnatal day (P) 1–5; intermediate: P6–13; juvenile: P14–21). Immunohistochemistry showed a developmental up-regulation of the NR2D subunit. This correlated with a developmental increase in decay time of NMDA currents and a decline of desensitization in response to repetitive exogenous NMDA applications. Thus, developmental up-regulation of the NR2D subunit, which reduces the Mg2+ block of NMDA-R, causes these specific changes in NMDA current characteristics. This may determine the NMDA-R-dependent function of the mature KF in the control of respiratory phase transition. Subsequent experiments revealed that bath-application of BDNF progressively potentiated these repetitively evoked NMDA currents only in intermediate and juvenile age groups. Pharmacological inhibition of protein kinase C (PKC), as a downstream component of the BDNF–tyrosine kinase B receptor (trkB) signalling, prevented BDNF-induced potentiation of NMDA currents. BDNF-induced potentiation of NMDA currents in later developmental stages might be essential for synaptic plasticity during the adaptation of the breathing pattern in response to peripheral/central commands. The lack of plasticity in neonatal neurones strengthens the hypothesis that the respiratory network becomes permissive for activity-dependent plasticity with ongoing postnatal development.

(Received 27 November 2007; accepted after revision 3 March 2008; first published online 13 March 2008)
Corresponding author M. Dutschmann: Department of Neuro and Sensory Physiology, University Medicine Göttingen, Georg August University, Humboldtallee 23, 37073 Göttingen, Germany. Email: mdutsch{at}gwdg.de

This paper has online supplemental material.






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