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J Neurophysiol 80: 2608-2620, 1998;
0022-3077/98 $5.00
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The Journal of Neurophysiology Vol. 80 No. 5 November 1998, pp. 2608-2620
Copyright ©1998 The American Physiological Society

Development of Glycinergic Synaptic Transmission to Rat Brain Stem Motoneurons

Joshua H. Singer1, Edmund M. Talley2, Douglas A. Bayliss2, and Albert J. Berger1

1 Department of Physiology and Biophysics, University of Washington School of Medicine, Seattle, Washington 98195-7290; and 2 Department of Pharmacology, University of Virginia School of Medicine, Charlottesville, Virginia 22908

Singer, Joshua H., Edmund M. Talley, Douglas A. Bayliss, and Albert J. Berger. Development of glycinergic synaptic transmission to rat brain stem motoneurons. J. Neurophysiol. 80: 2608-2620, 1998. Using an in vitro rat brain stem slice preparation, we examined the postnatal changes in glycinergic inhibitory postsynaptic currents (IPSCs) and passive membrane properties that underlie a developmental change in inhibitory postsynaptic potentials (IPSPs) recorded in hypoglossal motoneurons (HMs). Motoneurons were placed in three age groups: neonate (P0-3), intermediate (P5-8), and juvenile (P10-18). During the first two postnatal weeks, the decay time course of both unitary evoked IPSCs [mean decay time constant, tau decay = 17.0 ± 1.6 (SE) ms in neonates and 5.5 ± 0.4 ms in juveniles] and spontaneous miniature IPSCs (tau decay = 14.2 ± 2.4 ms in neonates and 6.3 ± 0.7 ms in juveniles) became faster. As glycine uptake does not influence IPSC time course at any postnatal age, this change most likely results from a developmental alteration in glycine receptor (GlyR) subunit composition. We found that expression of fetal (alpha 2) GlyR subunit mRNA decreased, whereas expression of adult (alpha 1) GlyR subunit mRNA increased postnatally. Single GlyR-channels recorded in outside-out patches excised from neonate motoneurons had longer mean burst durations than those from juveniles (18.3 vs. 11.1 ms). Concurrently, HM input resistance (RN) and membrane time constant (tau m) decreased (RN from 153 ± 12 MOmega to 63 ± 7 MOmega and tau m from 21.5 ± 2.7 ms to 9.1 ± 1.0 ms, neonates and juveniles, respectively), and the time course of unitary evoked IPSPs also became faster (tau decay = 22.4 ± 1.8 and 7.7 ± 0.9 ms, neonates vs. juveniles, respectively). Simulated synaptic currents were used to probe more closely the interaction between IPSC time course and tau m, and these simulations demonstrated that IPSP duration was reduced as a consequence of postnatal changes in both the kinetics of the underlying GlyR channel and the membrane properties that transform the IPSC into a postsynaptic potential. Additionally, gramicidin perforated-patch recordings of glycine-evoked currents reveal a postnatal change in reversal potential, which is shifted from -37 to -73 mV during this same period. Glycinergic PSPs are therefore depolarizing and prolonged in neonate HMs and become faster and hyperpolarizing during the first two postnatal weeks.




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