A:Paired pulses applied with 50 ms interstimulus intervals (ISI) to the auditory pathway in rat brain slices revealed paired pulse facilitation (ppf). Short-term plasticity is altered during synaptic depression. cEPSCs for each cell were normalized to the first evoked cEPSC of the respective cell. C: cEPSC amplitudes in PnC giant neurons evoked by 100 bursts applied to auditory fibers ( top) and trigeminal fibers ( bottom) in rat slices exponentially decreased to 56 % and 60 % of the respective initial value (n = 29 for auditory and n = 44 for trigeminal stimulation). Original traces of the first and the 100 th cEPSC of one sequence are shown the horizontal bar indicates 25 ms, the vertical bar 50 pA. The maximum amplitude of the cEPSC decreased upon repeated activation. B: Stimulation of auditory afferents with a short train of four pulses (within 12 ms) evoked a compound EPSC (cEPSC) in PnC giant neurons of rats, since single responses strongly summated. VCN: ventral cochlear nucleus, LSO: lateral superior olive, 8n: root of the auditory nerve, 7n: 7th nerve, Pr5: principal nucleus of the 5th nerve, PnC: caudal pontine reticular nucleus. Filled circles indicate the positions of the concentric bipolar extracellular stimulation electrodes. from the root of the 8 th nerve and/or the VCN) and from trigeminal neurons (emerging from the most ventral part of the Pr5) are plotted. Fibers of the secondary auditory neurons (emerging e.g. A: Scheme of a rat brainstem slice at bregma -9.8 and interaural -0.8. Our results further corroborate the link between synaptic depression and short-term habituation of the startle response. Our electrophysiological and behavioral data strongly indicate that synaptic depression in the PnC as well as short-term habituation are located in the sensory part of the startle pathway, namely at the axon terminals of sensory afferents in the PnC. In summary, the data indicates that the synaptic depression mechanism is located presynaptically. There was no evidence for transmitter receptor desensitization. Moreover, depression was induced only by trains of presynaptic action potentials and not by single pulses. Further electrophysiological analysis showed that the passive properties of the postsynaptic neuron were unchanged but revealed some alterations in short-term plasticity during depression. Concordant with this, short-term habituation of the acoustic startle response in behavioral experiments did not influence tactile startle response amplitudes and vice versa. Patch-clamp recordings in vitro were combined with behavioral experiments synaptic depression was specific for the input pathway stimulated and did not affect signals elicited by other sensory afferents. If this is confirmed, it would imply that these processes take place prior to multimodal signal integration, rather than occurring at postsynaptic sites on PnC giant neurons that directly drive motor neurons. We address here the question whether both this synaptic depression and the short-term habituation of the startle response are localized at the presynaptic terminals of sensory afferents.

Short trains of action potentials in sensory afferent fibers induce depression of synaptic responses in PnC giant neurons, a phenomenon that has been proposed to be the cellular correlate for short-term habituation.

The underlying mechanism is located within the primary startle pathway, presumably at sensory synapses on giant neurons in the caudal pontine reticular nucleus (PnC).

Short-term habituation of the startle response represents an elementary form of learning in mammals.

Imail 2006