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Donald M. Caspary

Researcher at Southern Illinois University School of Medicine

Publications -  121
Citations -  9226

Donald M. Caspary is an academic researcher from Southern Illinois University School of Medicine. The author has contributed to research in topics: Inferior colliculus & GABAA receptor. The author has an hindex of 55, co-authored 118 publications receiving 8582 citations. Previous affiliations of Donald M. Caspary include Southern Illinois University Carbondale & New York University.

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Ringing Ears: The Neuroscience of Tinnitus

TL;DR: Evidence is considered that deafferentation of tonotopically organized central auditory structures leads to increased neuron spontaneous firing rates and neural synchrony in the hearing loss region, which covers the frequency spectrum of tinnitus sounds.
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Inhibitory Neurotransmission, Plasticity and Aging in the Mammalian Central Auditory System

TL;DR: Findings of age-related inhibitory changes within mammalian auditory circuits are similar to age and deafferentation plasticity changes observed in other sensory systems.
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Elevated Fusiform Cell Activity in the Dorsal Cochlear Nucleus of Chinchillas with Psychophysical Evidence of Tinnitus

TL;DR: Chinchillas with psychophysical evidence of chronic tinnitus were shown to have significantly elevated spontaneous activity and stimulus-evoked responses in putative fusiform cells of the dorsal cochlear nuclei (DCN), consistent with the hypothesis that chronic tonal tinnusitus is associated with, and may result from, trauma-induced elevation of activity of DCN fuses.
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Gap detection deficits in rats with tinnitus: A potential novel screening tool.

TL;DR: It is suggested that gap detection reflex procedures might be effective for rapid tinnitus screening in rats when the gap was embedded in a background similar to their tinnitis.
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Central auditory aging: GABA changes in the inferior colliculus

TL;DR: Age-related alterations in neural circuits involved in the processing of acoustic information could reflect changes in the synthesis, degradation, uptake, release, and receptor sensitivity of neurotransmitters, perhaps secondary to cell loss and/or progressive deafferentation.