Functional organisation of a corollary discharge mechanism

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A fundamental problem in sensory neuroscience is the processing of self-generated sensory information and information from the environment that occurs in the same pathway. For example how can animals like crickets, which repetitively generate very loud acoustic signals for intraspecific communication, prevent their auditory pathways from desensitisation or distinguish their own sound signals from the sound of singing rivals? As a solution to this problem neuroscientists proposed a corollary discharge mechanism that is activated by the animals own motor activity and that is mediated to sensory areas to interfere with the processing of self-generated signals. The evidence for corollary discharges is compelling but the cellular basis of this principle of neural processing has been demonstrated only in weakly electric fish, tadpole swimming, crayfish escape behaviour and in singing crickets. In crickets we recently identified a corollary discharge interneurone (CDI), that is activated in the phase of sound production and that inhibits auditory afferents and interneurons, whenever the animals produce a sound pulse during singing. As a consequence their responses to self-generated sound pulses are distinctly reduced and the sensitivity of the auditory pathway is maintained. To complement this picture of the corollary discharge mechanism we now want to progress in three areas. 1. How is CDI activated? Evidence points towards the motor network that generates the singing activity. This network however, has not yet been studied in any detail. We will therefore identify the interneurons of this motor network by intracellular recordings, dye injection and current injection experiments, which demonstrate the functional importance of neurons for pattern recognition. Then we will use simultaneous recordings of the motor network interneurons and of CDI to analyse any synaptic connections between them. These experiments will tell how the corollary discharge is generated in the first place. We expect that interneurons of the motor network, which are active in phase with sound production, drive CDI with excitatory postsynaptic potentials. This would lead to a comprehensive cellular understanding of the corollary discharge mechanisms. 2. Furthermore we want to analyse if CDI affects sensory pathways other than the auditory pathway. This is important for our understanding of the organisation of corollary discharge pathways. CDI has profuse axonal output arborisation in the auditory neuropil but other axonal collaterals project into the mechanosensory neuropils of all ganglia. The arborisation pattern of CDI is therefore suited to modulate other sensory pathways as well - so is it a local or a global corollary discharge pathway? We will analyse neural processing in a wind-sensitive and vibration-sensitive pathway. These pathways are activated by self-generated stimuli during singing but at the same time also have to mediate escape responses. A problem of sensory processing that is most similar to the processing of auditory signals. We will stimulate these pathways with wind puffs or vibration stimuli and we will record the activity of the primary afferents and interneurons to reveal any signs of inhibition during singing. If the experiments demonstrate that sensory processing is modulated by a corollary discharge we will again use double intracellular recordings to analyse the synaptic interaction between CDI and afferents and interneurons of these pathways. Our experiments will reveal, if CDI globally modulates sensory processing during singing, as it is indicated by its structure. 3. Finally, we will analyse the details of CDI's arborisation pattern with histological sections. This will show the overlap of its axonal arborisations with mechanosensory neuropils. We also will use immunohistochemistry to demonstrate if GABA is the transmitter of the interneurone that mediates the inhibitory postsynaptic synaptic potentials.