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Neurotrophins improve neuromuscular transmission in adult but not early postnatal diaphragm
Author(s) -
Mantilla Carlos B,
Ermilov Leonid G,
Zhan WenZhi,
Sieck Gary C
Publication year - 2011
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.25.1_supplement.653.8
In the adult rat diaphragm muscle (DIAm), the neurotrophin brain‐derived neurotrophic factor (BDNF) enhances neuromuscular transmission via activation of TrkB receptors. During postnatal development there are significant differences in DIAm activation, being near maximal at birth and becoming progressively submaximal afterwards. We hypothesized that BDNF contributes to enhanced synaptic transmission during early postnatal development and thus to the increased motor unit activation necessary for ventilatory behaviors. In rats, neuromuscular transmission failure (NMTF) was assessed in DIAm‐phrenic nerve preparations as the difference in force developed during repetitive phrenic nerve stimulation (0.2 ms pulses, 40 Hz, 330‐ms trains for 2 min) and the force developed by intermittent (every 15 s) direct DIAm stimulation (two trains of 2 ms pulses, 40 Hz, 330‐ms). Exogenous BDNF treatment significantly improved neuromuscular transmission in the adult DIAm, but not in 7‐day and 14‐day old rats. In adults, inhibition of TrkB signaling worsened neuromuscular transmission significantly, but this effect was not present in early postnatal DIAm. These results demonstrate that in the postnatal rat diaphragm muscle, BDNF does not contribute to the increased motor unit activation necessary for sustaining near maximal activation during ventilatory behaviors. Supported by NIH grants AR051173 and HL096750.