scholarly journals EFFECTS OF AGMATINE ON ACOUSTIC STARTLE REFLEX AND AUDITORY SYSTEM IN RATS

2021 ◽  
Vol 7 (2) ◽  
pp. 85-92
Author(s):  
Özlem Saatci ◽  
Burcu Çevreli ◽  
Tayfun Uzbay

Background: A polyamine, agmatine, has been proposed as a new neurotransmitter in the brain. Objective: The aim of this study was to evaluate the effects of acute and chronic agmatine treatment on the rat auditory system. Methods: Male Wistar albino rats weighing between 280-330 grams were used. Animals were divided into four groups (n= 8 for each group). Acute and chronic agmatine (160 mg/kg) was administered to rats. Prepulse inhibition (PPI) of the acoustic startle reflex (ASR), distortion product otoacoustic emissions (DPOAEs), auditory brainstem responses (ABR) were evaluated in all groups. Results: Both acute and chronic agmatine treatments also significantly disrupted PPI. Chronic but not acute treatment with agmatine produced some DPOAE and ABR changes in rats. Conclusion: Our results suggested that chronic agmatine treatment for seven days resulted in some significant negative changes in cochlear function. Because the PPI of the ASR is also used as an indicator for psychoses, such as schizophrenia, in human and experimental animal studies, our findings also imply that the DPOAE and ABR tests may also be considered in the diagnosis and follow-up of patients with psychoses.

1997 ◽  
Vol 111 (3) ◽  
pp. 218-222 ◽  
Author(s):  
William W. Qiu ◽  
Shengguang S. Yin ◽  
Fred J. Stucker ◽  
Mardjohan Hardjasudarma

AbstractGlomus tumours involving the middle ear and the cerebellopontine angle are reported with emphasis on audiological findings. Magnetic resonance imaging (MRI), angiographic and pathological results are presented. Audiological tests, including impedance audiometry, evoked otoacoustic emissions and auditory brainstem responses, are valuable in evaluation of the effect of glomus tumours on the auditory system as well as their pathological extent.


2006 ◽  
Vol 17 (09) ◽  
pp. 667-676 ◽  
Author(s):  
Ashley W. Harkrider ◽  
Joanna W. Tampas

Studies of acceptable noise level (ANL) consistently report large intersubject variability in acceptance of background noise while listening to speech. This variability is not related to age, gender, hearing sensitivity, type of background noise, speech perception in noise performance, or efferent activity of the medial olivocochlear pathway. An exploratory study was conducted to determine if differences in aggregate responses from the peripheral and central auditory system can account for intersubject variability in ANL. Click-evoked otoacoustic emissions (CEOAEs), binaural auditory brainstem responses (ABRs), and middle latency responses (MLRs) were measured in females with normal hearing with low (n = 6) versus high (n = 7) ANLs. Results of this preliminary study indicate no differences between the groups for CEOAEs or waves I or III of the ABR. Differences between the two groups emerge for the amplitudes of wave V of the ABR and for the Na-Pa component of the MLR, suggesting that physiological variations arising from more central regions of the auditory system may mediate background noise acceptance.


2020 ◽  
Author(s):  
Angela Ballesteros ◽  
Tracy S. Fitzgerald ◽  
Kenton J. Swartz

AbstractThe reporter mT/mG mice expressing a membrane-targeted fluorescent protein are becoming widely used to study the auditory and vestibular system due to its versatility. Here we show that high expression levels of the fluorescent mtdTomato reporter affect the function of the sensory hair cells and the auditory performance of mT/mG transgenic mice. Auditory brainstem responses and distortion product otoacoustic emissions revealed that adult mT/mG homozygous mice are profoundly deaf, whereas heterozygous mice present high frequency loss. We explore whether this line would be useful for studying and visualizing the membrane of auditory hair cells by airyscan super-resolution confocal microscopy. Membrane localization of the reporter was observed in hair cells of the cochlea, facilitating imaging of both cell bodies and stereocilia bundles without altering cellular architecture or the expression of the integral membrane motor protein prestin. Remarkably, hair cells from mT/mG homozygous mice failed to uptake the FM1-43 dye and to locate TMC1 at the stereocilia, indicating defective mechanoelectrical transduction machinery. Our work emphasizes that precautions must be considered when working with reporter mice and highlights the potential role of the cellular membrane in maintaining functional hair cells and ensuring proper hearing.


2009 ◽  
Vol 75 (4) ◽  
pp. 476-484 ◽  
Author(s):  
Marcos Rabelo de Freitas ◽  
Viviane Carvalho da Silva ◽  
Gerly Anne de Castro Brito ◽  
José Valdir de Carvalho Junior ◽  
Raimundo Martins Gomes Junior ◽  
...  

2011 ◽  
Vol 125 (7) ◽  
pp. 668-672 ◽  
Author(s):  
S Singh ◽  
S K Munjal ◽  
N K Panda

AbstractIntroduction:Tinnitus is a disturbing symptom and is often the main reason for otology referral. It is usually associated with hearing loss of varying aetiology, and is thought to begin in the cochlea, with later abnormal central activity. We hypothesise that tinnitus without hearing loss may be caused by central and subcortical abnormalities and altered outer hair cell function.Aim:To compare the auditory brainstem responses, middle latency responses and otoacoustic emissions in normal-hearing individuals with and without tinnitus.Methodology:The audiological test results of 25 normal hearing subjects with tinnitus (age 18–45 years) were determined, and compared with those of a control group.Results:A statistically significant difference was found between study group tinnitus ears vs control group ears, as regards wave I latency prolongation, shortening of wave V and absolute I–III and I–V interpeak latency, enlargement of wave Na and Pa amplitude, and distortion product and transient evoked otoacoustic emission signal-to-noise ratios. There was no statistically significant difference between unilateral vs bilateral tinnitus ears.Conclusion:The pathogenesis and optimum management of tinnitus are still unclear. It often occurs with primary ear disease, usually associated with hearing loss, but may occur in patients with normal hearing. Observed changes in auditory brainstem and middle latency responses indicate central auditory alterations. Tinnitus involves both peripheral and central activity, and complete audiological and neurophysiological investigation is required. Management should be based on both audiological and neurophysiological findings.


2009 ◽  
Vol 75 (4) ◽  
pp. 476-484
Author(s):  
Marcos Rabelo de Freitas ◽  
Viviane Carvalho da Silva ◽  
Gerly Anne de Castro Brito ◽  
José Valdir de Carvalho ◽  
Raimundo Martins Gomes ◽  
...  

2018 ◽  
Vol 159 (2) ◽  
pp. 343-346 ◽  
Author(s):  
Katie Spielbauer ◽  
Lisa Cunningham ◽  
Nicole Schmitt

Immune checkpoint inhibition used in combination with standard cisplatin-based chemotherapy regimens is currently under evaluation in clinical trials for head and neck squamous cell carcinoma (HNSCC). The impact of anti–PD-1 therapy on cisplatin-induced ototoxicity and nephrotoxicity has not been established. Here we use a murine model of cisplatin-induced hearing loss to investigate the impact of anti–PD-1 immunotherapy on auditory brainstem responses (ABRs), distortion product otoacoustic emissions (DPOAEs), serum creatinine, and hair cell and renal histology. We demonstrate only mild worsening of DPOAEs at 14.4 and 16 kHz as well as a mild increase in serum creatinine. Renal and hair cell histology as well as ABR measures were unchanged by PD-1 inhibition. Thus, our data suggest that the use of PD-1 inhibition in conjunction with cisplatin results in toxicities that are similar to those of cisplatin alone.


2012 ◽  
Vol 126 (5) ◽  
pp. 464-469 ◽  
Author(s):  
S Alıcura Tokgöz ◽  
E Vuralkan ◽  
N D Sonbay ◽  
M Çalişkan ◽  
C Saka ◽  
...  

AbstractObjective:This experimental study aimed to investigate the effects of vitamins E, B and C and l-carnitine in preventing cisplatin-induced ototoxicity.Methods:Twenty-five adult, male, Wistar albino rats were randomly allocated to receive intraperitoneal cisplatin either alone or preceded by vitamins B, E or C or l-carnitine. Auditory brainstem response (i.e. hearing thresholds and wave I–IV intervals) and distortion product otoacoustic emissions (i.e. signal-to-noise ratios) were recorded before and 72 hours after cisplatin administration.Results:The following statistically significant differences were seen: control group pre- vs post-treatment wave I–IV interval values (p < 0.05); control vs vitamin E and B groups' I–IV interval values (p < 0.05); control vs other groups' hearing thresholds; vitamin E vs vitamin B and C and l-carnitine groups' hearing thresholds (p < 0.05); and vitamin B vs vitamin C and l-carnitine groups' hearing thresholds (p < 0.05). Statistically significant decreases were seen when comparing the initial and final signal-to-noise ratios in the control, vitamin B and l-carnitine groups (2000 and 3000 Hz; p < 0.01), and the initial and final signal-to-noise ratios in the control group (at 4000 Hz; p < 0.01).Conclusion:Vitamins B, E and C and l-carnitine appear to reduce cisplatin-induced ototoxicity in rats. The use of such additional treatments to decrease cisplatin-induced ototoxicity in humans is still under discussion.


2016 ◽  
Vol 27 (01) ◽  
pp. 049-061 ◽  
Author(s):  
O'neil W. Guthrie

Background: Permanent loss of outer hair cell (OHC) amplification may occur within days of acoustic overexposure. This loss of sensory function typically results in an immediate loss of neural sensitivity although neurodegeneration occurs months or years after damage to OHCs. This delay in neurodegeneration might provide an opportunity to preserve neural sensitivity although OHC amplification is permanently lost. Purpose: To test the hypothesis that neural functions can be preserved after permanent and severe loss of OHC amplification. To begin to address this possibility, an animal model of severe permanent loss of both OHC and neural functions was established. Research Design: This research employed a 4 × 4 split-plot factorial design, with four levels of the within-subject factor (time: baseline, 1-day, 1-week, and 1-mo postnoise exposure) and four levels of the between-subject factor (experimental groups: control, noise exposed, therapy, and noise exposed + therapy). Study Sample: Twenty-six hooded male Long-Evans rats (263 ± 63 g) served as subjects for this experiment. All animals exhibited baseline auditory function that approximated normative values for rats of the same strain. Data Collection and Analysis: Distortion product otoacoustic emissions and auditory brainstem responses were used to assay and differentiate OHC versus neural functions. Factorial analysis of variances was computed to identify statistically significant main effects and Dunnett testing was employed in post hoc computations. Intervention: To rescue neural function after permanent loss of OHC amplification, small molecular weight carboxy alkyl esters were employed after noise injury. Results: The results revealed that in the presence of permanent loss of OHC amplification, the loss of neural sensitivity could be rescued. In addition, auditory brainstem response wave I amplitudes at suprathreshold levels were rescued from noise-induced depletion into the biologic noise floor. Conclusion: Since mammalian OHCs do not regenerate after damage, these results encourage further experiments aimed at preserving neural functions following noise injury.


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