Abstract
Feed-forward inhibition (FFI) represents a powerful mechanism by which control of the timing and fidelity of action potentials in local synaptic circuits of various brain regions is achieved. In the cochlear nucleus, the auditory nerve provides excitation to both principal neurons and inhibitory interneurons. Here, we investigated the synaptic circuit associated with fusiform cells (FCs), principal neurons of the dorsal cochlear nucleus (DCN) that receive excitation from auditory nerve fibers and inhibition from tuberculoventral cells (TVCs) on their basal dendrites in the deep layer of DCN. Despite the importance of these inputs in regulating fusiform cell firing behavior, the mechanisms determining the balance of excitation and FFI in this circuit are not well understood. Therefore, we examined the timing and plasticity of auditory nerve driven FFI onto FCs. We find that in some FCs, excitatory and inhibitory components of FFI had the same stimulation thresholds indicating they could be triggered by activation of the same fibers. In other FCs, excitation and inhibition exhibit different stimulus thresholds, suggesting FCs and TVCs might be activated by different sets of fibers. In addition, we find that during repetitive activation, synapses formed by the auditory nerve onto TVCs and FCs exhibit distinct modes of short-term plasticity. Feed-forward inhibitory post-synaptic currents (IPSCs) in FCs exhibit short-term depression because of prominent synaptic depression at the auditory nerve-TVC synapse. Depression of this feedforward inhibitory input causes a shift in the balance of fusiform cell synaptic input towards greater excitation and suggests that fusiform cell spike output will be enhanced by physiological patterns of auditory nerve activity.
Highlights
To further investigate the roles of synaptic excitation and inhibition in auditory processing by Fusiform cells (FCs), we used parasagittal slices of the cochlear nucleus that preserve components of the synaptic circuit associated with the fusiform cell basal dendrites (Figure 1)
The membrane potential of the fusiform cell was clamped at −40 mV, which is above the reversal potential for inhibitory synaptic currents (ECl, ∼−60 mV) and below the reversal for excitatory synaptic currents (EGlu, ∼0 mV)
In the current study, we investigated the properties and mechanisms of feed-forward inhibition (FFI) in the dorsal cochlear nucleus (DCN) driven by the auditory nerve
Summary
In many regions of the mammalian brain, feed-forward inhibition (FFI) represents a complex synaptic arrangement in neuronal networks that results from parallel activation of principal cells and inhibitory interneurons by the same excitatory input (Buzsaki, 1984; Pouille and Scanziani, 2001; Blitz and Regehr, 2005; Gabernet et al, 2005; Mittmann et al, 2005; Cruikshank et al, 2007; Torborg et al, 2010; Ellender et al, 2011; Kuo and Trussell, 2011; Najac et al, 2011; Zhou et al, 2012). Fusiform cells (FCs) are the principal neurons of the DCN that integrate multiple excitatory and inhibitory synaptic inputs onto their apical and basal dendrites (Voigt and Young, 1980, 1990; Blackstad et al, 1984; Oertel and Wu, 1989; Berrebi and Mugnaini, 1991; Zhang and Oertel, 1994). Excitatory inputs contacting apical dendrites of FCs come from granule cell parallel fibers located in the superficial molecular layer. These fibers innervate cartwheel cells, local glycinergic interneurons that provide inhibition to FC apical dendrites (Roberts and Trussell, 2010; Kuo and Trussell, 2011).
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