Inhibitory inputs to avian ITD circuits.
Paula T Kuokkanen, Z Mehnoush Faghani, Ira Kraemer and 2 others
Blocking GABA and glycine receptors in the barn owl's auditory brainstem increased the synaptic signal without shifting its timing sensitivity.
The inhibition widens the dynamic range of what the circuit can detect, rather than retuning which timing differences it picks up.
Key findings
1Blocking GABA-A receptors (gabazine) or glycine receptors (strychnine) in the nucleus laminaris increased the low-pass filtered synaptic signal at both stimulus onset and offset, but did not alter the ITD tuning of the high-frequency neurophonic component.
2The glycinergic component was larger than the GABAergic component at both onset and offset, and simultaneous blockade of both receptor types produced a supra-linear effect greater than the sum of the two drugs applied independently.
3The superior olivary nucleus contains both GABAergic and glycinergic neurons in two morphological size classes, projects ipsilaterally to the nucleus laminaris, and only about 21% of its recorded neurons showed ITD sensitivity.
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How it was doneWhat they found
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What it does not show
Fourteen barn owls total, with different subsets used for anatomy, SON physiology, and NL pharmacology; the simultaneous drug experiment was possible in only one animal because of its duration. Washout after strychnine did not always return to baseline, so only the initial control condition was used as reference. The authors could not determine whether individual SON neurons co-expressed GABA and glycine because double labeling was not performed. It was not possible to identify which specific SON response types project to NL, so the source of the inhibitory input remains uncertain. The postsynaptic ITD tuning of NL neurons could not be isolated from the field potential, so the effect of inhibition on single-neuron ITD tuning was not directly tested. Small, inconsistent phase shifts in the neurophonic (up to 50 μs) occurred over hours of recording, attributed to possible electrode drift relative to the delay-line axons.
Declared interests
Funded by NSF (CRCNS IOS1516357), NIDCD (DC00436, DC019341), the German BMBF (01GQ1505A, 01GQ1505B), and the DFG (502188599). The authors declared no potential conflicts of interest.
The easy way to misread this
This is a basic neuroscience study in barn owls describing how inhibitory synapses shape the auditory brainstem circuit. It does not report on human hearing, hearing loss, or any clinical intervention, and its findings about GABA and glycine in the owl nucleus laminaris cannot be read as evidence for or against any therapeutic approach in human auditory or speech disorders.
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