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The Journal of Neurophysiology Vol. 87 No. 5 May 2002, pp. 2297-2306
Copyright ©2002 by the American Physiological Society
The Vollum Institute, Oregon Health and Science University, Portland, Oregon 97201-3098
Leão, Ricardo M. and
Henrique Von
Gersdorff.
Noradrenaline Increases High-Frequency Firing at the Calyx of
Held Synapse During Development by Inhibiting Glutamate Release. J. Neurophysiol. 87: 2297-2306, 2002. The
mammalian auditory brain stem receives profuse adrenergic innervation,
whose function is poorly understood. Here we investigate, during
postnatal development, the effect of noradrenaline (NA) at the calyx of
Held synapse in the rat medial nucleus of the trapezoid body (MNTB). We
observed that NA inhibits the large glutamatergic EPSC, evoked by
afferent fiber stimulation, in a dose-dependent manner. The inhibition
was maximal (approximately 48%) at the concentration of 2 µM. It was
antagonized by yohimbine and mimicked by the 
2-adrenergic specific
agonist UK14304. Both AMPA and NMDA receptor-mediated EPSCs were
inhibited in parallel by NA, suggesting a presynaptic effect.
Presynaptic recordings showed that NA inhibits the action potential
(AP) generated Ca current by about 20%; however, NA did not
significantly affect the presynaptic AP waveform. We thus conclude that
the calyx of Held presynaptic terminal expresses 2-adrenergic
receptors that inhibit its Ca current and thus glutamate release.
Noradrenaline was effective in all cells tested from postnatal days 6 to 7 (P6-P7), and thereafter the number of responsive cells
diminished, although half of the P14 cells tested still had EPSCs that
were inhibited by NA. By contrast, activation by
L-2-amino-5-phosphonovaleric acid-sensitive metabotropic
glutamate receptors strongly inhibited the EPSCs of all cells tested
from P6 to P14. The effect of NA on postsynaptic action potential
firing was dependent on the stimulus frequency. At 10 Hz, NA had no
effect on firing probability; however, NA helped MNTB cells fire more
action potentials during a 100-Hz train of stimuli, even though it did
not increase the steady-state depressed EPSC, because it produced a
smaller N-methyl-D-aspartate (NMDA)
receptor-activated depolarizing plateau. We therefore suggest that the
reduction by NA of the first few EPSCs in a train leads to a smaller
NMDA depolarizing plateau and thus to increased firing probability at
100 Hz in young synapses. Surprisingly, the inhibition of glutamate
release by NA can thus actually increase the excitability of MNTB
neurons during early postnatal development.
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