The presence of opioid receptors in rat inner ear

Jongkamonwiwat, Nopporn; Phansuwan‐Pujito, Pansiri; Sarapoke, P; Chetsawang, Banthit; Casalotti, Stefano O.; Forge, Andrew; Dodson, H.C.; Govitrapong, Piyarat

doi:10.1016/s0378-5955(03)00175-8

Cited by 45 publications

(43 citation statements)

References 51 publications

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“…Therefore, it is unlikely that opioid receptors exist at or near the large medial efferent olivocochlear terminals located near the bases of the outer hair cells. It is more plausible that opioid κ-receptors in the chinchilla are anatomically positioned within Type I auditory dendrites found near the bases of the inner hair cells, similar to that reported in the rat (Jongkamonwiwat et al, 2003) and guinea pig cochlea (Jongkamonwiwat et al, 2006). Consequently, the available evidence suggests a κ-opioidinduced neural modulatory role for endogenous LEOC dynorphins in the mammalian cochlea.…”

Section: Discussionmentioning

confidence: 52%

“…There is direct evidence that κ-opioid receptors exist in the cochlea of the rat (Jongkamonwiwat et al, 2003) and guinea pig (Jongkamonwiwat et al, 2006). In both species, κ-opioid receptor immunoreactivity was detected on the sensory Type I auditory dendrites that are anatomically positioned at the bases of the cochlear inner hair cells.…”

Section: Introductionmentioning

confidence: 99%

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Bi-phasic intensity-dependent opioid-mediated neural amplitude changes in the chinchilla cochlea: Partial blockade by an N-Methyl-d-Aspartate (NMDA)-receptor antagonist

Sahley

Anderson

Chernicky

2008

European Journal of Pharmacology

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Dynorphins, glutamate, and glutamate-sensitive N-Methyl-D-Aspartate (NMDA) receptors exist in the mammalian cochlea. Dynorphins produce neural excitation and excitotoxic effects in the spinal cord through a κ-opioid facilitation of NMDA receptor sensitivity to glutamate. The κ-opioid receptor drug agonists N-dimethylallyl-normetazocine [(-)-pentazocine (50 mmol)] and trans-3,4-dichloro-N-methyl-N-[2-(1-pyrrolidinyl)-cyclohexyl]-benzeneacetamide [U-50488H (100 mmol)] were administered across the cochlear round window membrane in the chinchilla. Each drug produced significant post-baseline amplitude changes in the click-evoked auditory nerve compound action potential. Amplitude changes at threshold amounted to increases in sensitivity that ranged from 4-8 decibels, measured in sound pressure level (dB SPL). The large neural amplitude increases at threshold were accompanied by progressively smaller amplitude changes at 5 and 10 dB above threshold (dB SL). However, at stimulus intensities ≥ 20dB SL, post-baseline neural amplitudes were suppressed to levels below baseline and control values. These bi-phasic intensity-dependent neural amplitude changes have never before been observed following i.v. administered (-)-pentazocine in this species. Finally, the bi-phasic neural amplitude changes in U-50488H-treated (100 mmol) animals were partially blocked (except at 20dB SL), following a round window pretreatment with the NMDA receptor drug antagonist, dizocilpine hydrogen maleate [(+)-MK-801 (8 mmol)]. Our data suggests that endogenous dynorphins within lateral efferent olivocochlear neurons differentially modulate auditory neural excitation, possibly through cochlear NMDA receptors and glutamate. The role played by lateral efferent opioid neuromodulation at cochlear NMDA receptors, is discussed.

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Section: Discussionmentioning

confidence: 52%

Section: Introductionmentioning

confidence: 99%

Bi-phasic intensity-dependent opioid-mediated neural amplitude changes in the chinchilla cochlea: Partial blockade by an N-Methyl-d-Aspartate (NMDA)-receptor antagonist

Sahley

Anderson

Chernicky

2008

European Journal of Pharmacology

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“…The hypothesis is based on dynorphin and enkephalin-like opioids that are co-distributed within lateral efferent brainstem nuclei. Also enkephalin-and dynorphin-positive lateral efferent fibers have been described in inner and outer spiral bundle in the cochlea of species such as the guinea pig and rat (Abou-Madi et al, 1987;Altschuler et al, 1988;Jongkamonwiwat et al, 2003Jongkamonwiwat et al, , 2006. Furthermore, elevated levels of Met5-enkephalin-like opioid peptides after exposure to intense, stressful noise were described (Drescher et al, 1983;Drescher and Drescher, 1985).…”

Section: Salicylate-and Acoustic Trauma-induced Molecular Events On Tmentioning

confidence: 98%

Molecular aspects of tinnitus

2010

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“…Intense sounds are not only perceived as painfully loud (Ades et al, 1959), but can also induce pain sensations in around the external ear (otalgia; Dominguez et al, 2006; Hebert et al, 2013; Henry et al, 2014; Kaltenbach et al, 2000; Knipper et al, 2013; McFerran and Baguley, 2007; Norena, 2011; Pienkowski et al, 2014; Tyler et al, 2014a; Van Campen et al, 1999; Westcott et al, 2013). Pain transmitting neuropeptides and receptors are present in the CN and auditory nerve (Aguilar et al, 2004; Bauer et al, 2007b; Jongkamonwiwat et al, 2003; Nguyen et al, 2014; Phansuwan-Pujito et al, 2003; Tongjaroenbuangam et al, 2006), raising the possibility that loud sounds may trigger the perception of pain through these signaling pathways.…”

Section: Introductionmentioning

confidence: 99%

Noise-induced hearing loss: Neuropathic pain via Ntrk1 signaling

Manohar

Dahar

Adler

et al. 2016

Molecular and Cellular Neuroscience

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Severe noise-induced damage to the inner ear leads to auditory nerve fiber degeneration thereby reducing the neural input to the cochlear nucleus (CN). Paradoxically, this leads to a significant increase in spontaneous activity in the CN which has been linked to tinnitus, hyperacusis and ear pain. The biological mechanisms that lead to an increased spontaneous activity are largely unknown, but could arise from changes in glutamatergic or GABAergic neurotransmission or neuroinflammation. To test this hypothesis, we unilaterally exposed rats for 2 h to a 126 dB SPL narrow band noise centered at 12 kHz. Hearing loss measured by auditory brainstem responses exceeded 55 dB from 6 to 32 kHz. The mRNA from the exposed CN was harvested at 14 or 28 days post-exposure and qRT-PCR analysis was performed on 168 genes involved in neural inflammation, neuropathic pain and glutamatergic or GABAergic neurotransmission. Expression levels of mRNA of Slc17a6 and Gabrg3, involved in excitation and inhibition respectively, were significantly increased at 28 days post-exposure, suggesting a possible role in the CN spontaneous hyperactivity associated with tinnitus and hyperacusis. In the pain and inflammatory array, noise exposure up-regulated mRNA expression levels of four pain/inflammatory genes, Tlr2, Oprd1, Kcnq3 and Ntrk1 and decreased mRNA expression levels of two more genes, Ccl12 and Il1β. Pain/inflammatory gene expression changes via Ntrk1 signaling may induce sterile inflammation, neuropathic pain, microglial activation and migration of nerve fibers from the trigeminal nerve and cuneate and vestibular nuclei into the CN. These changes could contribute to somatic tinnitus, hyperacusis and otalgia.

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The presence of opioid receptors in rat inner ear

Cited by 45 publications

References 51 publications

Bi-phasic intensity-dependent opioid-mediated neural amplitude changes in the chinchilla cochlea: Partial blockade by an N-Methyl-d-Aspartate (NMDA)-receptor antagonist

Bi-phasic intensity-dependent opioid-mediated neural amplitude changes in the chinchilla cochlea: Partial blockade by an N-Methyl-d-Aspartate (NMDA)-receptor antagonist

Molecular aspects of tinnitus

Noise-induced hearing loss: Neuropathic pain via Ntrk1 signaling

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