Deafness-related decreases in glycine-immunoreactive labeling in the rat cochlear nucleus

There is increasing evidence of activity-related plasticity in auditory pathways. The present study examined the effects of decreased activity on immunolocalization of the inhibitory neurotransmitter glycine in the cochlear nucleus of the rat after bilateral cochlear ablation. Specifically, glycine-immunoreactive puncta adjacent to somatic profiles were compared in normal hearing animals and animals deafened for 14 days. The number of glycine-immunoreactive puncta surrounding somatic profiles of spherical and globular bushy cells, glycine-immunoreactive type I stellate multipolar cells, radiate neurons (type II stellate multipolar cells), and fusiform cells decreased significantly. In addition, the number of glycine immunopositive tuberculoventral (vertical or corn) cells in the deep layer of the dorsal cochlear nucleus also decreased significantly. These results suggest that decreased inhibition reported in cochlear nucleus after deafness may be due to decreases in glycine. © 2005 Wiley-Liss, Inc.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/48685/1/20542_ftp.pd

Effects of Noise Exposure on the Vestibular System: A Systematic Review

Despite our understanding of the impact of noise-induced damage to the auditory system, much less is known about the impact of noise exposure on the vestibular system. In this article, we review the anatomical, physiological, and functional evidence for noise-induced damage to peripheral and central vestibular structures. Morphological studies in several animal models have demonstrated cellular damage throughout the peripheral vestibular system and particularly in the otolith organs; however, there is a paucity of data on the effect of noise exposure on human vestibular end organs. Physiological studies have corroborated morphological studies by demonstrating disruption across vestibular pathways with otolith-mediated pathways impacted more than semicircular canal-mediated pathways. Similar to the temporary threshold shifts observed in the auditory system, physiological studies in animals have suggested a capacity for recovery following noise-induced vestibular damage. Human studies have demonstrated that diminished sacculo-collic responses are related to the severity of noise-induced hearing loss, and dose-dependent vestibular deficits following noise exposure have been corroborated in animal models. Further work is needed to better understand the physiological and functional consequences of noise-induced vestibular impairment in animals and humans

Evidence of Key Tinnitus-Related Brain Regions Documented by a Unique Combination of Manganese-Enhanced MRI and Acoustic Startle Reflex Testing

Animal models continue to improve our understanding of tinnitus pathogenesis and aid in development of new treatments. However, there are no diagnostic biomarkers for tinnitus-related pathophysiology for use in awake, freely moving animals. To address this disparity, two complementary methods were combined to examine reliable tinnitus models (rats repeatedly administered salicylate or exposed to a single noise event): inhibition of acoustic startle and manganese-enhanced MRI. Salicylate-induced tinnitus resulted in wide spread supernormal manganese uptake compared to noise-induced tinnitus. Neither model demonstrated significant differences in the auditory cortex. Only in the dorsal cortex of the inferior colliculus (DCIC) did both models exhibit supernormal uptake. Therefore, abnormal membrane depolarization in the DCIC appears to be important in tinnitus-mediated activity. Our results provide the foundation for future studies correlating the severity and longevity of tinnitus with hearing loss and neuronal activity in specific brain regions and tools for evaluating treatment efficacy across paradigms

Immunocytochemical identification of met andleu enkephalin positive neurons within mating and agonistic relevant brain nuclei of the male Syrian hamster: Modulation by gonadal steroids and social behaviors.

Enkephalin plays a role in male cat, mouse, and rat, social behavior. No such correlation has been reported in the male hamster. However, several brain nuclei involved in male hamster social behaviors have been identified. We therefore asked: Are enkephalin immunoreactive (Enk-ir) cells found within brain nuclei previously implicated in male hamster social behaviors? Brains from male Syrian hamsters were processed for enkephalin immunoreactivity. Numerous brain regions involved in social behaviors contained Enk-ir cells. However, in most brain areas the number of Enk-ir cells varied between animals. This variability may be dependent upon the social status of the animal. Many enkephalinergic brain regions implicated in male hamster social behavior contain gonadal steroid receptors. Steroid receptors are also found within neurons expressing Fos protein following mating. Furthermore, the social behaviors mating and aggression are dependent upon the presence of gonadal steroids. We therefore hypothesized that Enk-ir neurons containing Fos increase following mating, that the number of Enk-ir neurons is altered following castration and hormonal manipulation, and that enkephalinergic neurons contain androgen receptors. Both social behaviors and castration resulted in decreased numbers of Enk-ir cells within several brain regions. Following mating, large percentages of the remaining enkephalinergic neurons contained Fos protein. The reduction following castration could be prevented by treatment with testosterone or estradiol, but not dihydrotestosterone. Surprisingly, only 12% of the Enk-ir neurons found within brain nuclei involved in aggression produce androgen receptors. Therefore we conclude enkephalin is a neuropeptide involved in male hamster social behaviors and warrants further study.PhDAnimal PhysiologyBiological SciencesNeurosciencesUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttp://deepblue.lib.umich.edu/bitstream/2027.42/130492/2/9732097.pd

Scientific Foundations of Audiology: Perspectives from Physics, Biology, Modeling, and Medicine

With advancements across various scientific and medical fields, professionals in audiology are in a unique position to integrate cutting-edge technology with real-world situations. Scientific Foundations of Audiology provides a strong basis and philosophical framework for understanding various domains of hearing science in the context of contemporary developments in genetics, gene expression, bioengineering, neuroimaging, neurochemistry, cochlear and mid-brain implants, associated speech processing and understanding, molecular biology, physics, modeling, medicine, and clinical practice. Key features of this text include: - Highly technical information presented in a cohesive and understandable manner (i.e., concepts without complex equations) - Discussion of integrating newly developed technology within the clinical practice of audiology - State-of-the-art contributions from a stellar array of international, world-class experts Scientific Foundations of Audiology is geared toward doctoral students in audiology, physics, and engineering; residents in otolaryngology, neurology, neurosurgery, and pediatrics; and those intermediaries between innovation and clinical reality

Effects of salicyate and noise exposure on MEMRI measured signal intensity in the inferior colliculus after three days of salicylate administration and 48 hrs post noise exposure.

<p>Signal intensity was compared across groups (A–D). In the salicylate group, manganese accumulation was supernormal in the central nucleus of the inferior colliculus (B; CNIC; 174. 20±3.60; p = 0.03), as well as the dorsal cortex (C; DCIC; 195. 21±4.96; p = 0.005) and external cortex (D; ECIC; 186. 52±2.35; p = 0.02) when compared to controls. In the noise exposed group, only the DCIC had increased signal intensity (186. 35±2.17; p = 0.03). Asterisks denote significance, p≤0.05; error bars equal StDev, C – control, S – salicylate, N - noise exposed.</p

Salicyate increases MEMRI measured signal intensity in the DCN but not the VCN.

<p>In the dorsal cochlear nucleus (DCN) a significant increase in signal intensity was observed (<b>A–B</b>) in the salicylate treated group (242. 37±12.08; p = 0.02) when compared to controls (210.26±6.76), but no change was observed in the VCN (<b>A, C</b>). Noise exposure does not change MEMRI measured signal intensity in the DCN (209. 90±5.22; p = 0.02) or VCN (187. 41±9.02; p = 0.02) 48 hrs post noise exposure (A–C). Signal intensity is calculated as a percentage of nearby muscle. Asterisk denotes significance, p≤0.05; error bars equal StDev, C – control, S – salicylate, N - noise exposed In MRI panels white arrows indicate VCN, green arrows indicate DCN, and blue arrows indicate ventricular space.</p

Salicylate results in a decreased ability to blunt the acoustic startle response (ASR) under conditions of gap inhibition.

<p>Performance during ASR testing was recorded before treatment (Baseline), 1 hr following the second day of salicylate administration (Post Treatment 1) and seven hrs following the third day of salicylate administration (Post Treatment 2). Relative to a full startle response (100%), untreated rats detected the gap and prepulse and could suppress the startle reflex across all frequencies (baseline in <b>A</b>). Across all frequencies significant decreases in pASR were observed relative to baseline both one hour following salicylate administration (Post Treatment 1) and seven hours after treatment (Post Treatment 2) (<b>A</b>). When compared to baseline, p = 0.0001 for both Post Treatment 1 and 2 (compare a–b and a–c). Post Treatment 1 and 2 were also significantly different from one another (b–c; p = 0.0004). At 12 kHz the % sound off startle initially changed by 12% (p = 0.05) from Baseline to Post Treatment 1, but was not significantly different from Baseline during Post Treatment 2 testing (<b>B</b>). Differing letters denote significance across time points, p≤0.05 was significant; error bars equal SEM.</p

Summary graph of gap ASR comparing experimental groups (control, salicylate, noise) at three different time points (baseline, post treatment 1 and post treatment 2).

<p>For control animals the percent inhibition of startle remains constant. For the salicylate group post treatment 1 testing resulted in decreased inhibition of gASR, but by post treatment 2 testing, gASR had returned to normal levels. The 10 kHz noise group demonstrated a decreased ability to inhibit gASR at both time points following noise exposure when compared to baseline. Error bars equal SEM.</p

Effects of salicylate and noise exposure on neuronal activity in different brain regions as measured by manganese enhanced MRI.

a<p>Bold text indicates beginning of new brain region.</p>b<p>Signal intensity, expressed as the percentage of adjacent muscle; arbitrary units (a.u.).</p>c<p>Significance p≤0.05.</p>d<p>Error (±) is expressed as SEM.</p