RT Journal Article
SR Electronic
T1 Inhibitory Control at a Synaptic Relay
JF The Journal of Neuroscience
JO J. Neurosci.
FD Society for Neuroscience
SP 2643
OP 2647
DO 10.1523/JNEUROSCI.5144-03.2004
VO 24
IS 11
A1 Awatramani, Gautam B.
A1 Turecek, Rostislav
A1 Trussell, Laurence O.
YR 2004
UL http://www.jneurosci.org/content/24/11/2643.abstract
AB The mammalian medial nucleus of the trapezoid body (MNTB) harbors one of the most powerful terminals in the CNS, the calyx of Held. The mechanisms known to regulate this synaptic relay are relatively ineffective. Here, we report the presence of a remarkably robust and fast-acting glycinergic inhibitory system capable of suppressing calyceal transmission. Evoked glycinergic IPSCs were relatively small in 2-week-old rats, an age by which calyceal maturation has reportedly neared completion. However, by postnatal day 25 (P25), glycinergic transmission had undergone a vigorous transformation, resulting in peak synaptic conductances as high as 280 nS. These are comparable with glutamatergic conductances activated by calyceal inputs. Decay kinetics for IPSCs were severalfold faster than for glycinergic synaptic events reported previously. At physiological temperatures in P25 rats, IPSCs decayed in ∼1 msec and could be elicited at frequencies up to 500 Hz. Moreover, EPSPs triggered by glutamatergic signals derived from the calyx or simulated by conductance clamp were suppressed when preceded by simulated glycinergic IPSPs. The matching of excitatory transmission in the calyx of Held by a powerful, precision inhibitory system suggests that the relay function of the MNTB may be rapidly modified during sound localization.