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1 Graduate Program in Neurobiology and Behavior, University of Washington, Seattle, Seattle, WA, USA; Department of Physiology and Biophysics, University of Washington, Seattle, Seattle, WA, USA
2 Department of Physiology and Biophysics, University of Washington, Seattle, Seattle, WA, USA
* To whom correspondence should be addressed. E-mail: sebe{at}u.washington.edu.
Neurons within the intact respiratory network produce bursts of action potentials that cause inspiration or expiration. Within inspiratory bursts, activity is synchronized on a shorter time-scale to generate clusters of action potentials that occur in a set frequency range and are called synchronous oscillations. We investigated how GABA and glycine modulate synchronous oscillations and respiratory rhythm over postnatal development. We recorded inspiratory activity from hypoglossal nerves using the in vitro rhythmically active mouse medullary slice preparation from P0-11 mice. Average oscillation frequency increased with postnatal development, from 17 ± 12 Hz in P0-6 mice (n=15) to 38 ± 7 Hz in P7-11 mice (n=37) (P<0.0001). Bath application of GABAA and GlyR antagonists significantly reduced oscillation power in neonates (P0-6) and juveniles (P7-10) and increased peak integrated activity in both age groups. To test whether elevating slice excitability, is sufficient to reduce oscillation power, Substance P was bath applied alone. Substance P, while increasing peak integrated activity, had no significant effect on oscillation power. Prolonging the time course of GABAergic synaptic currents with zolpidem decreased the median oscillation frequency in P9-10 mouse slices. These data demonstrate that oscillation frequency increases with postnatal development and that both GABAergic and glycinergic transmission contribute to synchronization of activity. Further, the time course of synaptic GABAergic currents is a determinant of oscillation frequency.
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