High concentrations of divalent cations isolate monosynaptic inputs from local circuits in the auditory midbrain.
inferior colliculus; Animals; Mice; Acoustic Stimulation; Neural Inhibition/drug effects/*physiology; high divalents; local circuits; monosynaptic; first spike latency; Inferior Colliculi/drug effects/*physiology; Reaction Time/drug effects/physiology; Synapses/drug effects/*physiology; Cations; Divalent/*pharmacology
Hierarchical processing of sensory information occurs at multiple levels between the peripheral and central pathway. Different extents of convergence and divergence in top down and bottom up projections makes it difficult to separate the various components activated by a sensory input. In particular, hierarchical processing at sub-cortical levels is little understood. Here we have developed a method to isolate extrinsic inputs to the inferior colliculus (IC), a nucleus in the midbrain region of the auditory system, with extensive ascending and descending convergence. By applying a high concentration of divalent cations (HiDi) locally within the IC, we isolate a HiDi-sensitive from a HiDi-insensitive component of responses evoked by afferent input in brain slices and in vivo during a sound stimulus. Our results suggest that the HiDi-sensitive component is a monosynaptic input to the IC, while the HiDi-insensitive component is a local polysynaptic circuit. Monosynaptic inputs have short latencies, rapid rise times, and underlie first spike latencies. Local inputs have variable delays and evoke long-lasting excitation. In vivo, local circuits have variable onset times and temporal profiles. Our results suggest that high concentrations of divalent cations should prove to be a widely useful method of isolating extrinsic monosynaptic inputs from local circuits in vivo.
Sivaramakrishnan Shobhana; Sanchez Jason Tait; Grimsley Calum Alex
Frontiers in neural circuits
2013
1905-07
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.3389/fncir.2013.00175" target="_blank" rel="noreferrer noopener">10.3389/fncir.2013.00175</a>
Midbrain local circuits shape sound intensity codes.
inferior colliculus; Animals; Mice; Neurons/physiology; Acoustic Stimulation; Auditory Perception/*physiology; Inferior Colliculi/*physiology; Auditory Pathways/*physiology; Auditory Threshold/physiology; high divalents; local circuits; monosynaptic; Neural Inhibition/*physiology; sound intensity
Hierarchical processing of sensory information requires interaction at multiple levels along the peripheral to central pathway. Recent evidence suggests that interaction between driving and modulating components can shape both top down and bottom up processing of sensory information. Here we show that a component inherited from extrinsic sources combines with local components to code sound intensity. By applying high concentrations of divalent cations to neurons in the nucleus of the inferior colliculus in the auditory midbrain, we show that as sound intensity increases, the source of synaptic efficacy changes from inherited inputs to local circuits. In neurons with a wide dynamic range response to intensity, inherited inputs increase firing rates at low sound intensities but saturate at mid-to-high intensities. Local circuits activate at high sound intensities and widen dynamic range by continuously increasing their output gain with intensity. Inherited inputs are necessary and sufficient to evoke tuned responses, however local circuits change peak output. Push-pull driving inhibition and excitation create net excitatory drive to intensity-variant neurons and tune neurons to intensity. Our results reveal that dynamic range and tuning re-emerge in the auditory midbrain through local circuits that are themselves variable or tuned.
Grimsley Calum Alex; Sanchez Jason Tait; Sivaramakrishnan Shobhana
Frontiers in neural circuits
2013
1905-7
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
<a href="http://doi.org/10.3389/fncir.2013.00174" target="_blank" rel="noreferrer noopener">10.3389/fncir.2013.00174</a>