Neuroscience
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The central auditory system shows a remarkable ability to rescale its neural representation of loudness following long-term, low-level acoustic exposures; even when the noise is presented intermittently. Circadian rhythms exert potent biological effects, but it remains unclear if acoustic exposures occurring during the light or dark cycle affect the neurophysiological changes involved in loudness rescaling. ⋯ However, neural activity in the inferior colliculus demonstrated negative gain in a frequency- and intensity-specific manner compared to unexposed controls; the magnitude and direction of the neuroplastic changes in the inferior colliculus were largely the same regardless of whether the 12-h noise exposures occurred during the light or dark phase of the circadian cycle. These neuroplastic changes could become relevant for low-level sound therapies used to treat hyperacusis.
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Debilitating perceptual disorders including tinnitus, hyperacusis, phantom limb pain and visual release hallucinations may reflect aberrant patterns of neural activity in central sensory pathways following a loss of peripheral sensory input. Here, we explore short- and long-term changes in gene expression that may contribute to hyperexcitability following a sudden, profound loss of auditory input from one ear. We used fluorescence in situ hybridization to quantify mRNA levels for genes encoding AMPA and GABAA receptor subunits (Gria2 and Gabra1, respectively) in single neurons from the inferior colliculus (IC) and auditory cortex (ACtx). ⋯ By contrast to the opposing, synergistic shifts in Gria2 and Gabra1 observed 30 days after hearing loss, we found that transcription levels for both genes were equivalently reduced after 5 days of hearing loss, producing no net change in the excitatory/inhibitory transcriptional balance. Opposing transcriptional shifts in AMPA and GABA receptor genes that emerge several weeks after a peripheral insult could promote both sensitization and disinhibition to support a homeostatic recovery of neural activity following auditory deprivation. Imprecise transcriptional changes could also drive the system toward perceptual hypersensitivity, degraded temporal processing and the irrepressible perception of non-existent environmental stimuli, a trio of perceptual impairments that often accompany chronic sensory deprivation.
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Previous studies suggest that envelope-following responses (EFRs) reveal important differences in temporal coding fidelity amongst listeners who have normal hearing thresholds, consistent with these listeners differing in the degree to which they suffer from cochlear synaptopathy. Like conventional hearing loss, the severity of cochlear synaptopathy may vary along the cochlea. A number of earlier studies have suggested methods for estimating EFRs driven by specific frequency regions of the cochlea, which would allow synaptopathy to be estimated as a function of cochlear place. ⋯ Other results suggested that while off-frequency contributions to EFRs driven by narrowband signals (due to spread of excitation) can add destructively to the on frequency response, these interactions were small compared to EFR magnitude. Overall, our results point to the utility of using multi-band complex tone stimuli to estimate the profile of temporal coding fidelity, and thus the degree of synaptopathy, as a function of cochlear place. This article is part of a Special Issue entitled: Hearing Loss, Tinnitus, Hyperacusis, Central Gain.
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Substantia nigra pars reticulata is the output station in basal ganglia; its GABAergic neurons control the activity of thalamo-cortical premotor nuclei, thus controlling motor behavior. D1-like and D2-like presynaptic dopamine receptors on subthalamo-nigral afferents by modulation of glutamate release change the firing rate of nigral neurons; however, their relative contribution to the control of glutamate release and their pharmacological properties have not been studied. This is important since the prevalence of the inhibition or stimulation of release determines the firing rate of nigral neurons, therefore motor activity. ⋯ We also co-activated these to test their interaction; an antagonist interaction of D1-like with D2 and D3R, and an additive between D2 and D3R were found. Pharmacological receptor antagonist effects in release from reserpinized vs. non-reserpinized slices were similar, suggesting that endogenous dopamine stimulates receptors in the same way. These findings suggest differences in the control of glutamate release by different dopamine receptors in the substantia nigra, which could contribute to explaining the effect of dopamine and its agonists on motor behavior.