Timing of sound-evoked potentials and spike responses in the inferior colliculus of awake bats.
*Wakefulness; Acoustic Stimulation; Action Potentials/*physiology; Animals; Auditory Perception; Auditory/*physiology; Chiroptera/physiology; Electroencephalography; Evoked Potentials; Functional Laterality/physiology; Inferior Colliculi/*cytology; Neural Inhibition/physiology; Neurons/*physiology; Psychoacoustics; Reaction Time/*physiology/radiation effects
Neurons in the inferior colliculus (IC), one of the major integrative centers of the auditory system, process acoustic information converging from almost all nuclei of the auditory brain stem. During this integration, excitatory and inhibitory inputs arrive to auditory neurons at different time delays. Result of this integration determines timing of IC neuron firing. In the mammalian IC, the range of the first spike latencies is very large (5-50 ms). At present, a contribution of excitatory and inhibitory inputs in controlling neurons' firing in the IC is still under debate. In the present study we assess the role of excitation and inhibition in determining first spike response latency in the IC. Postsynaptic responses were recorded to pure tones presented at neuron's characteristic frequency or to downward frequency modulated sweeps in awake bats. There are three main results emerging from the present study: (1) the most common response pattern in the IC is hyperpolarization followed by depolarization followed by hyperpolarization, (2) latencies of depolarizing or hyperpolarizing responses to tonal stimuli are short (3-7 ms) whereas the first spike latencies may vary to a great extent (4-26 ms) from one neuron to another, and (3) high threshold hyperpolarization preceded long latency spikes in IC neurons exhibiting paradoxical latency shift. Our data also show that the onset hyperpolarizing potentials in the IC have very small jitter (\textless100 micros) across repeated stimulus presentations. The results of this study suggest that inhibition, arriving earlier than excitation, may play a role as a mechanism for delaying the first spike latency in IC neurons.
Voytenko S V; Galazyuk A V
Neuroscience
2008
2008-08
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/10.1016/j.neuroscience.2008.06.031" target="_blank" rel="noreferrer noopener">10.1016/j.neuroscience.2008.06.031</a>
Noise-induced cochlear synaptopathy: Past findings and future studies.
*Auditory Perception; *Hearing; *Hearing loss; *Molecular approach; *Preclinical model; *Spiral ganglion; *Synaptic loss; *Synaptic Transmission; Animals; Auditory; Hair Cells; Hearing Loss; Hearing Tests; Humans; Inner/*pathology; Noise-Induced/diagnosis/*pathology/physiopathology/psychology; Noise/*adverse effects; Predictive Value of Tests; Psychoacoustics; Spiral Ganglion/*pathology/physiopathology; Synapses/*pathology
For decades, we have presumed the death of hair cells and spiral ganglion neurons are the main cause of hearing loss and difficulties understanding speech in noise, but new findings suggest synapse loss may be the key contributor. Specifically, recent preclinical studies suggest that the synapses between inner hair cells and spiral ganglion neurons with low spontaneous rates and high thresholds are the most vulnerable subcellular structures, with respect to insults during aging and noise exposure. This cochlear synaptopathy can be "hidden" because this synaptic loss can occur without permanent hearing threshold shifts. This new discovery of synaptic loss opens doors to new research directions. Here, we review a number of recent studies and make suggestions in two critical future research directions. First, based on solid evidence of cochlear synaptopathy in animal models, it is time to apply molecular approaches to identify the underlying molecular mechanisms; improved understanding is necessary for developing rational, effective therapies against this cochlear synaptopathy. Second, in human studies, the data supporting cochlear synaptopathy are indirect although rapid progress has been made. To fully identify changes in function that are directly related this hidden synaptic damage, we argue that a battery of tests including both electrophysiological and behavior tests should be combined for diagnosis of "hidden hearing loss" in clinical studies. This new approach may provide a direct link between cochlear synaptopathy and perceptual difficulties.
Kobel Megan; Le Prell Colleen G; Liu Jennifer; Hawks John W; Bao Jianxin
Hearing research
2017
2017-06
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/10.1016/j.heares.2016.12.008" target="_blank" rel="noreferrer noopener">10.1016/j.heares.2016.12.008</a>