DEVELOPMENT OF GLYCINERGIC SYNAPTIC TRANSMISSION TO RAT-BRAIN STEM MOTONEURONS

Citation
Jh. Singer et al., DEVELOPMENT OF GLYCINERGIC SYNAPTIC TRANSMISSION TO RAT-BRAIN STEM MOTONEURONS, Journal of neurophysiology, 80(5), 1998, pp. 2608-2620
Citations number
91
Categorie Soggetti
Neurosciences,Physiology
Journal title
ISSN journal
00223077
Volume
80
Issue
5
Year of publication
1998
Pages
2608 - 2620
Database
ISI
SICI code
0022-3077(1998)80:5<2608:DOGSTT>2.0.ZU;2-3
Abstract
Using an in vitro rat brain stem slice preparation, we examined the po stnatal 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: neona te (P0-3), intermediate (P5-8), and juvenile (P10-18). During the firs t two postnatal weeks, the decay time course of both unitary evoked IP SCs [mean decay time constant, tau(decay) = 17.0 +/- 1.6 (SE) ms in ne onates and 5.5 +/- 0.4 ms in juveniles] and spontaneous miniature IPSC s (tau(decay) = 14.2 +/- 2.4 ms in neonates and 6.3 +/- 0.7 ms in juve niles) became faster. As glycine uptake does not influence IPSC time c ourse at any postnatal age, this change most likely results from a dev elopmental alteration in glycine receptor (GlyR) subunit composition. We found that expression of fetal (alpha 2) GlyR subunit mRNA decrease d, whereas expression of adult (alpha 1) GlyR subunit mRNA increased p ostnatally. Single GlyR-channels recorded in outside-out patches excis ed 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 +/- 1 2 M Omega to 63 +/- 7 M Omega 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 s ynaptic currents were used to probe more closely the interaction betwe en IPSC time course and tau(m), and these simulations demonstrated tha t IPSP duration was reduced as a consequence of postnatal changes in b oth the kinetics of the underlying GlyR channel and the membrane prope rties that transform the IPSC into a postsynaptic potential. Additiona lly, gramicidin perforated-patch recordings of glycine-evoked currents reveal a postnatal change in reversal potential, which is shifted fro m -37 to -73 mV during this same period. Glycinergic PSPs are therefor e depolarizing and prolonged in neonate HMs and become faster and hype rpolarizing during the first two postnatal weeks.