Effects of a dopaminergic agonist in the guinea pig cochlea

D'Aldin, Christine; Puel, Jean–Luc; Leducq, Régine; Crambes, O.; Eybalin, Michel; Pujol, Rémy

doi:10.1016/0378-5955(95)00167-5

Cited by 86 publications

(58 citation statements)

References 16 publications

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“…The D 1 agonist CAPB and the D 2 agonist QUI modulated the frequency of afferent discharge in the range of 50-100 M . Sensitivity of bath-applied DOP agonists obtained in the present experiments corresponds well to results reported on the inhibitory effects of DOP agonists in the mammalian cochlea [14][15][16] . Interestingly, the dose-response curves of DOP agonists were quite similar to each other in one important respect: without stimulation, the vestibular organs demonstrated ongoing transmitter release as shown by the continuous afferent discharge.…”

Section: Discussionsupporting

confidence: 78%

“…The action of DOP and its agonists on the chemically induced activity of afferent nerve fibers could be blocked by the D 1 and D 2 antagonists. Electrophysiological data from piribedil, a dopaminergic D 2 /D 3 agonist, clearly demonstrated the modulatory action of this substance on radial afferent dendrites [16] . Moreover, this agonist was shown to play an immediate protective role in the prevention of dendrite damage under pathophysiological conditions resulting from an excitotoxic effect from L -Glu during acoustic trauma or ischemia.…”

Section: Introductionmentioning

confidence: 99%

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Dopaminergic Modulation of Afferent Synaptic Transmission in the Semicircular Canals of Frogs

Andrianov

Ryzhova²,

Tobias³

2009

Neurosignals

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Using multiunit recording of action potentials from the whole nerve with the aid of external perfusion, we investigated the effects of dopamine (DOP) agonists that are involved in modulatory actions on synaptic transmission in the isolated labyrinth preparations of frogs. The external application of DOP (0.1–1 mM), the D₁ agonist chloro-APB hydrobromide (CAPB, 50–100 μM) and the D₂ agonist quinerolane (QUI, 50–100 μM) induced a dose-dependent and reversible decline in the resting discharge frequency. In this concentration range, the potency of applied CAPB considerably exceeded that of QUI. AMPA, NMDA and ACPD responses were inhibited by the D₁ and D₂ agonists, implicating both subtypes of DOP receptors in the modulation of both ionotropic and metabotropic glutamate receptors. The inhibitory action of the DOP agonists on L-glutamate responses persisted in a high Mg²⁺ solution in conditions of selective activation of the postsynaptic membrane. The results obtained suggest that DOP may interact with both D₁ and D₂ receptor subtypes, most likely located postsynaptically on the afferent nerve fibers. This dopaminergic control mechanism may result in the reduction of the activated firing rate, thus preventing over-excitation and excitotoxic injury of the afferent dendrites after the external application of L-glutamate and excessive receptor stimulation.

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Section: Discussionsupporting

confidence: 78%

Section: Introductionmentioning

confidence: 99%

Dopaminergic Modulation of Afferent Synaptic Transmission in the Semicircular Canals of Frogs

Andrianov

Ryzhova²,

Tobias³

2009

Neurosignals

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“…Binding by mineralocorticoid receptors results (among other effects) in an activation of the enzyme sodium-potassiumATPase, which may contribute to restoration of disturbed cellular osmolarity, electro-chemical gradients, and neuronal conduction. At this point we have to remind that dAldin et al [34] and Puel et al [35] demonstrated that dendritic damage at the base of inner hair cells, the latter representing the site of CAP generation, accounts for half the contribution to acute hearing loss after acoustic trauma (especially in case of continuous noise exposure). In the long term study of d'Aldin et al [36], when the first injection of corticoid is given 1 h or 24 hours after exposure to noise, noise-induced threshold shift is decreased, recovery is faster, and less hair cell damage is observed (noise-induced hearing loss observed one day after corticoid administration: 25 dB, is almost equivalent to that observed 14 days after exposure in untreated animals: 20 dB).…”

Section: Hyperbaric Oxygen Therapymentioning

confidence: 99%

“…Synaptic repair can occur in 5 days [35], but most hair cell damage remains which is probably responsible for the long-term threshold shifts. It has also been demonstrated that dendrite damage could be prevented by perfusing a glutamate antagonist [35], or a dopaminergic agonist [34], into the cochlea during the noise exposure. However, it is essential to find curative drugs to treat patients who underwent acoustic trauma and to address both the hair cell injuries and the dendrite damage.…”

Section: Hearing Damage From Noisementioning

confidence: 99%

“…It is well known that intense sound exposure induces two major types of damage : (i) injuries occurring first in the first row of outer hair cells (OHC), then in the inner hair cells (IHC), and subsequently in the second and third rows of OHC [30], and (ii) massive destruction of the dendrites of the primary auditory neurons below the IHC [31,32,33]. It has been demonstrated that after acoustic trauma, the acute hearing losses are due both to hair cell injuries and to dendrite damage [34]. Synaptic repair can occur in 5 days [35], but most hair cell damage remains which is probably responsible for the long-term threshold shifts.…”

Section: Hearing Damage From Noisementioning

confidence: 99%

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Damage Risk from Impulse Noise. (les Risques auditifs et extra auditifs des bruits impulsionnels)

H¹,

Johnson²,

Buck³

et al. 2000

PsycEXTRA Dataset

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Persistence, distribution, and impact of distinctly segmented microparticles on cochlear health following in vivo infusion

Ross

Rahmani

Prieskorn

et al. 2016

J Biomedical Materials Res

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Delivery of pharmaceuticals to the cochleae of patients with auditory dysfunction could potentially have many benefits from enhancing auditory nerve survival to protecting remaining sensory cells and their neuronal connections. Treatment would require platforms to enable drug delivery directly to the cochlea and increase the potential efficacy of intervention. Cochlear implant recipients are a specific patient subset that could benefit from local drug delivery as more candidates have residual hearing; and since residual hearing directly contributes to post-implantation hearing outcomes, it requires protection from implant insertion-induced trauma. This study assessed the feasibility of utilizing microparticles for drug delivery into cochlear fluids, testing persistence, distribution, biocompatibility, and drug release characteristics. To allow for delivery of multiple therapeutics, particles were composed of two distinct compartments; one containing polylactide-co-glycolide (PLGA), and one composed of acetal-modified dextran and PLGA. Following in vivo infusion, image analysis revealed microparticle persistence in the cochlea for at least 7 days post-infusion, primarily in the first and second turns. The majority of subjects maintained or had only slight elevation in auditory brainstem response thresholds at 7 days post-infusion compared to pre-infusion baselines. There was only minor to limited loss of cochlear hair cells and negligible immune response based on CD45+ immunolabling. When Piribedil-loaded microparticles were infused, Piribedil was detectable within the cochlear fluids at 7 days post-infusion. These results indicate that segmented microparticles are relatively inert, can persist, release their contents, and be functionally and biologically compatible with cochlear function and therefore are promising vehicles for cochlear drug delivery.

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Effects of a dopaminergic agonist in the guinea pig cochlea

Cited by 86 publications

References 16 publications

Dopaminergic Modulation of Afferent Synaptic Transmission in the Semicircular Canals of Frogs

Dopaminergic Modulation of Afferent Synaptic Transmission in the Semicircular Canals of Frogs

Damage Risk from Impulse Noise. (les Risques auditifs et extra auditifs des bruits impulsionnels)

Persistence, distribution, and impact of distinctly segmented microparticles on cochlear health following in vivo infusion

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