The effect of quinine on outer hair cell shape, compliance and force

Jarboe, John K; Hallworth, Richard

doi:10.1016/s0378-5955(99)00031-3

Cited by 20 publications

(10 citation statements)

References 33 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Salicylate has been shown to reduce OHC motility following acute administration (45-47). Quinine has been shown to effect OHC morphology and function; (48) however no recovery of DPOAEs was observed in this group after the suspension of quinine treatment. Despite the fact that DPOAE had not fully recovered following quinine treatment, the ABR showed no changes in threshold 14 days after quinine or salicylate treatments.…”

Section: Discussionmentioning

confidence: 64%

Comparison of Salicylate- and Quinine-Induced Tinnitus in Rats

Ralli¹,

Lobariñas²,

Fetoni³

et al. 2010

Otology &Amp; Neurotology

View full text Add to dashboard Cite

Background-Salicylate and quinine have been shown to reliably induce short-term tinnitus when administered at high doses. The present study compared salicylate and quinine induced tinnitus in rats using the gap prepulse inhibition of acoustic startle (GPIAS).Methods-Twenty-four rats were divided into 2 groups; the first group (n=12) was injected with salicylate (300 mg/kg/d), the second (n=12) was treated with quinine orally at a dose of 200 mg/kg/ d. Animals were treated daily for 4 consecutive days. All rats were tested for tinnitus and hearing loss before and 2, 24, 48, 72, 96 hours after the first drug administration. Tinnitus was assessed using GPIAS; hearing function was measured with DPOAEs and ABR.Results-Salicylate treatment induced transient tinnitus with a pitch near 16 kHz starting 2 h posttreatment, persisting over the 4-day treatment period and disappearing 24 h later. Animals in the quinine group showed GPIAS changes at a higher pitch (20 kHz); however, changes were more variable among animals and the mean data were not statistically significant. Hearing function varied across treatments. In the salicylate group, high-level DPOAEs were slightly affected; most changes occurred 2 h post-treatment. Low-level DPOAEs were affected at all frequencies with a progressive dose-dependent effect. In the quinine group, only high-level DPOAEs were affected, mainly at 16 kHz.Conclusion-The present study highlights the similarities and differences in the frequency and the time course of tinnitus and hypoacusis induced by salicylate and quinine. Transient tinnitus was reliably induced pharmacologically with salicylate while hearing loss remained subclinical with only minor changes in DPOAEs.

show abstract

Section: Discussionmentioning

confidence: 64%

Comparison of Salicylate- and Quinine-Induced Tinnitus in Rats

Ralli¹,

Lobariñas²,

Fetoni³

et al. 2010

Otology &Amp; Neurotology

View full text Add to dashboard Cite

show abstract

“…However, a few cells did not exhibit the motility-dependent variation in cell shortening and lengthening as attributed to the kinetics of K + channels [16,26,27] prior to treatment. Quinine, another ototoxic agent with properties similar to heavy metals, applied in vitro on OHC at a concentration of 5.0 mM, substantially decreased active forces of cell elongation and shortening [19]. These results are indicative that Pb 2 + perhaps has different actions on cell membrane properties and motility mechanisms than that of quinine.…”

Section: Discussionmentioning

confidence: 86%

Lead (Pb2+) modulation of potassium currents of guinea pig outer hair cells

Guihua

Järlebark

Ulfendahl

et al. 2004

Neurotoxicology and Teratology

View full text Add to dashboard Cite

Outer hair cells (OHC) are mechanosensitive sensory cells of the inner ear cochlea and are involved in modulating the activity of inner hair cells in the transduction of an acoustic stimulus. Potassium (K + ) currents play an important role in the sensory transduction process. K + currents were recorded from acutely dissociated OHC obtained from the guinea pig organ of Corti. The whole-cell patch clamp technique was employed. We identified a channel that exhibited outward current of the delayed rectifier type (Kv). Kv channels mediating inward currents carried by potassium ions were also identified and took on the appearance of a previously described inwardly rectifying current. Lead (Pb 2 + ) acetate at concentrations of 0.1, 1.0, 10, and 100 AM was bath applied. Time to activation for outward-going current was not affected by Pb 2 + . The time course of Pb 2 + effects was seen as a dose-dependent reduction of K + current over time, with very little or no recovery after washout. Pb 2 + inhibited the outward Kv relative current with values of 0.10, 0.14, 0.18, and 0.30 at 0.1, 1.0, 10, and 100 AM, respectively. Pb 2 + did not modulate time to activation, peak current, or inactivation of inward I K . The effects of Pb 2 + on the potassium currents of OHC are not remarkable and therefore OHC are probably not a major cause of purported peripheral hearing loss observed in Pb 2 + -exposed animals and humans. D

show abstract

“…Quinoline derivatives cause a substantial but usually reversible sensorineural hearing loss at middle to high frequencies accompanied by tinnitus and vertigo (Jung et al, 1993). The mechanism of ototoxicity may involve different levels of the auditory system (Eggermont and Kenmochi, 1998;Jarboe and Hallworth, 1999). However, there is considerable evidence showing that the auditory periphery is the primary location underlying the hearing loss induced by quinine (Puel et al, 1990;Lin et al, 1998).…”

Section: Discussionmentioning

confidence: 99%

Effects of Quinine, Quinidine, and Chloroquine on α9α10 Nicotinic Cholinergic Receptors

et al. 2005

View full text Add to dashboard Cite

In this study, we report the effects of the quinoline derivatives quinine, its optical isomer quinidine, and chloroquine on ␣9␣10-containing nicotinic acetylcholine receptors (nAChRs). The compounds blocked acetylcholine (ACh)-evoked responses in ␣9␣10-injected Xenopus laevis oocytes in a concentration-dependent manner, with a rank order of potency of chloroquine (IC 50 ϭ 0.39 M) Ͼ quinine (IC 50 ϭ 0.97 M) ϳ quinidine (IC 50 ϭ 1.37 M). Moreover, chloroquine blocked ACh-evoked responses on rat cochlear inner hair cells with an IC 50 value of 0.13 M, which is within the same range as that observed for recombinant receptors. Block by chloroquine was purely competitive, whereas quinine inhibited ACh currents in a mixed competitive and noncompetitive manner. The competitive nature of the blockage produced by the three compounds was confirmed by equilibrium binding experiments using [ 3 H]methyllycaconitine. Binding affinities (K i values) were 2.3, 5.5, and 13.0 M for chloroquine, quinine, and quinidine, respectively. Block by quinine was found to be only slightly voltage-dependent, thus precluding open-channel block as the main mechanism of interaction of quinine with ␣9␣10 nAChRs. The present results add to the pharmacological characterization of ␣9␣10-containing nicotinic receptors and indicate that the efferent olivocochlear system that innervates the cochlear hair cells is a target of these ototoxic antimalarial compounds.

show abstract

The effect of quinine on outer hair cell shape, compliance and force

Cited by 20 publications

References 33 publications

Comparison of Salicylate- and Quinine-Induced Tinnitus in Rats

Comparison of Salicylate- and Quinine-Induced Tinnitus in Rats

Lead (Pb2+) modulation of potassium currents of guinea pig outer hair cells

Effects of Quinine, Quinidine, and Chloroquine on α9α10 Nicotinic Cholinergic Receptors

Contact Info

Product

Resources

About