Synaptic depression and short-term habituation are located in the sensory part of the mammalian startle pathway

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. Concordant with this, short-term habituation of the acoustic startle response in behavioral experiments did not influence tactile startle response amplitudes and vice versa. Further electrophysiological analysis showed that the passive properties of the postsynaptic neuron were unchanged but revealed some alterations in short-term plasticity during depression. Moreover, depression was induced only by trains of presynaptic action potentials and not by single pulses. There was no evidence for transmitter receptor desensitization. In summary, the data indicates that the synaptic depression mechanism is located presynaptically.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. Our results further corroborate the link between synaptic depression and short-term habituation of the startle response.The mammalian startle response is a protective response that results in the contraction of skeletal and facial muscles in response to a sudden acoustic, tactile or vestibular stimulus. This response is modulated by elementary forms of learning such as sensitization [1,2] and habituation [3,4]. Short-term habituation is an attenuation of the startle response upon repeated presentation of startle stimuli within one session that is reversible within several minutes [5,6]. The degree of attenuation varies between different animal species and different mouse strains [7,8].The startle response is mediated by a short, well-described primary pathway [for review see [9]], which is depicted in figure 1. A relatively small population of giant neurons in the PnC represents the sensorimotor inte