In contrast, in the avian cochlear nucleus involved in the timing pathway, nucleus magnocellularis (NM), nerve terminals exhibit pronounced short-term synaptic depression. In the avian cochlear nucleus involved in the intensity pathway, nucleus angularis (NA), nerve terminals exhibit a mixture of short-term synaptic facilitation and depression that allows the transmission of rate-encoded intensity information important for interaural level difference coding ( MacLeod et al. Recently, short-term synaptic plasticity has been proposed to be another distinguishing property between the two pathways ( MacLeod and Carr 2007 MacLeod et al. Numerous well-studied morphological and intrinsic properties distinguish the parallel neural pathways that encode timing and intensity information ( Oertel 1999 Trussell 1999). We investigated the short-term plasticity in the avian cochlear nuclei, the first relays of auditory information arriving via the auditory nerve. The auditory brainstem contains circuits with a rich diversity of functionality, offering an opportunity to relate short-term plasticity to specific sensory transformations. Synapses that differ in the specific time- and activity-dependence of their filtering properties process information differently, such that the same presynaptic spike train can drive multiple postsynaptic targets differently. 2002 Trussell 2002 von Gersdorff and Borst 2002 Abbott and Regehr 2004 Blitz et al. The rapid, activity-dependent alteration of the strength of synapses, known as short-term synaptic plasticity, contributes to neural coding by acting as a filter through which the information contained in the presynaptic spike train must pass ( O’Donovan and Rinzel 1997 Markram et al. We propose that the rapid recovery following depression allows improved coding of natural auditory signals that often consist of sound bursts separated by short gaps. We tested whether a previously proposed model of synaptic transmission based on vesicle depletion and sequential steps of vesicle replenishment could account for the recovery responses, and found it was insufficient, suggesting an activity-dependent feedback mechanism is present. We also show that the recorded recovery in the intensity pathway differs from similar recordings in the timing pathway, specifically the cochlear nucleus magnocellularis, in two ways: (1) a fast recovery that was not due to recovery from postsynaptic receptor desensitization and (2) a recovery trajectory that was characterized by a non-monotonic bump that may be due in part to facilitation mechanisms more prevalent in the intensity pathway. These synaptic responses showed a very rapid recovery, following a bi-exponential time course with a fast time constant of ~40 ms and a dependence on the presynaptic activity levels, resulting in a crossing over of the recovery trajectories following high-rate versus low-rate stimulation trains. To identify key differences in the plasticity properties, we made patch-clamp recordings from neurons in the cochlear nucleus responsible for intensity coding, nucleus angularis, and measured the time course of the recovery of excitatory postsynaptic currents following short-term synaptic depression. In the avian auditory brainstem, specific forms of plasticity are expressed at different terminals of the same auditory nerve fibers and contribute to the divergence of acoustic timing and intensity information. Short-term synaptic plasticity acts as a time- and firing rate-dependent filter that mediates the transmission of information across synapses.

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