Scopolamine, Morphine, and Brain-stem Auditory Evoked Potentials in Awake Monkeys

Samra, Satwant K.; Krutak-Krol, H.; Pohorecki, Roman; Domino, Edward F.

doi:10.1097/00000542-198504000-00011

Cited by 16 publications

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“…Morphine and fentanyl induced an increase in the amplitude of PI and PII waves of the ABR, so we inferred that this opioid would be exerting its function both in the cochlea and in the cochlear nucleus, where the presence of the MOR has been demonstrated by in situ hybridization studies (Mansour et al, ). These results differ from that reported in the literature regarding the absence of effects on the components of early ABRs, in response to opioids administered systemically in other animal models such as the guinea pig (Sahley et al, ) or the macaque Rhesus (Samra, Krutak‐Krol, Pohorecki, & Domino, ). This is probably because the experiments were done using different anesthetics and routes of opioid administration.…”

Section: Discussioncontrasting

confidence: 99%

Opioid modulation of cochlear auditory responses in the rat inner ear

Ramírez

Soto

Vega

2019

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| INTRODUC TI ONThe primary neurotransmitter released by the efferent terminals of the olivocochlear pathway is acetylcholine (ACh), which binds to nicotinic ACh α9-α10 located at the base of the outer hair cell (OHC) (Taranda et al., 2009), and M2 and M4 muscarinic receptors, in the synaptic complex of both the lateral olivocochlear pathway (LOC) and the medial olivocochlear pathway (MOC) (Maison et al., 2010). ACh and the calcitonin gene-related peptide co-localize in the efferent neurons of the OC bundle. Immunoreactivity to γ-aminobutyric acid was also detected in the OC cochlear efferents, although it seems to be limited to the apex of the cochlea (Maison, Adams, & Liberman, 2003; Maison, Casanova, AbstractThe auditory system has an extensive efferent innervation, which contributes to processes of control and regulation of the afferent input. The expression of receptors to various neurotransmitters and neuropeptides in the inner ear has been described, among which endogenous opioid receptors are found. The role of opioid receptors in the cochlea is not yet fully defined, it has been reported that opioid agonists and antagonists modulate the response to auditory stimuli and in clinical practice, multiple cases have been reported in which the consumption of opioid derivatives induce sensorineural hearing loss. In this work, we evaluated the effects of acute treatment with morphine, fentanyl, tramadol, and naloxone, in the auditory brain stem potentials (ABR), the compound action potential (CAP), and distortion products otacoustic emissions (DPOAE), across a wide range of stimulus frequencies and amplitudes.Adult Long-Evans rats of the strain CII/ZV weighing 180-220 g were used. For the ABR recording drugs were administered intraperitoneally or intravenously. For the CAP and DPOAE drugs were applied by direct perfusion in the middle ear. The opioid agonists produced a consistent increase in the amplitude of the PI component of the ABR and of the N1-P1 amplitude of the CAP. Naloxone produced no significant changes in the ABR and a reduction of the CAP N1-P1 amplitude. Also, opioid agonists induced a decrease in the amplitude of the DPOAE. These results show that the opioid receptor activation modulates both the afferent response at both the afferent response to acoustic stimuli, and also at the cochlear mechanics as revealed by DPOAE changes. These results present a significant step in understanding how opioid modulation of auditory responses may contribute to the auditory processing and to sensorineural hearing loss produced by opioids. K E Y W O R D Sauditory loss, drug abuse, fentanyl, morphine, tramadol

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Section: Discussioncontrasting

confidence: 99%

Opioid modulation of cochlear auditory responses in the rat inner ear

Ramírez

Soto

Vega

2019

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“…With regard to the ABR, general anesthetics such as barbiturates (Shapiro et al, 1984;Drummond et al, 1985;Church and Shucard, 1987), ketamine (Church and Gritzke, 1987) and the halogenated volatiles (Dubois et al, 1982;Sainz et al, 1987;Santarelli et al, 2003) typically increase its latency, especially of later peaks, without affecting the amplitude. Nitrous oxide (Manninen et al, 1985), and the opioids morphine and fentanyl (Samra et al, 1984(Samra et al, , 1985 do not affect the ABR. Effects of general anesthetics on the peripheral auditory system are less well characterized and reported effects are variable.…”

Section: Introductionmentioning

confidence: 95%

Effects of isoflurane on auditory evoked potentials in the cochlea and brainstem of guinea pigs

2010

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“…Further support for the resistance of ABRs to be modulated pharmacologically comes from human and nonhuman primate studies which allow awake ABRs experiments. In this context, Samra et al showed in awake rhesus monkeys that neither Scopolamine nor Morphine intravenous injection could modulate the ABRs waves 70 . In addition, studies in humans report no effects of anesthetics agents, and drugs such as Benzodiazepines, Propofol, and ketamine on ABRs 2,71 .…”

Section: Discussionmentioning

confidence: 99%

Auditory brainstem responses are resistant to pharmacological modulation in Sprague Dawley wildtype and Neurexin1α knockout rats

Marashli

Janz

Redondo

2023

Preprint

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Sensory processing in the auditory brainstem can be studied with auditory brainstem responses (ABRs) across species. Although ABRs have been widely utilized to evaluate abnormalities in auditory brainstem physiology, there is limited understanding if ABRs can be useful tools to assess the effect of pharmacological interventions. Therefore, we set out to understand how pharmacological agents that target key transmitter systems of the auditory brainstem circuitry affect ABR physiology in rats. Given previous studies, demonstrating that Nrxn1α KO Sprague Dawley rats show substantial auditory processing deficits and altered sensitivity to GABAergic modulators, we used both Nrxn1α KO and wildtype littermates in our study. First, we probed how different commonly used anesthetics (isoflurane, ketamine/xylazine, medetomidine) affect ABRs waveforms. In the next step, we assessed the effects of different pharmacological compounds (diazepam, gaboxadol, retigabine, nicotine, baclofen, and bitopertin) either under isoflurane or medetomidine anesthesia. We found that under our experimental conditions, ABRs are largely unaffected by diverse pharmacological modulation. Significant modulation was observed with i.) nicotine, affecting the late ABR components at 90 dB stimulus intensity under isoflurane anesthesia in both genotypes and ii.) retigabine, showing a slight decrease in late ABRs deflections at 80 dB stimulus intensity, mainly in isoflurane-anesthetized Nrxn1α KO rats. Our study suggests that ABRs in anesthetized rats are resistant to a wide range of pharmacological modulators, which has important implications for the applicability of ABRs to study auditory brainstem physiology.

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Scopolamine, Morphine, and Brain-stem Auditory Evoked Potentials in Awake Monkeys

Cited by 16 publications

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Opioid modulation of cochlear auditory responses in the rat inner ear

Opioid modulation of cochlear auditory responses in the rat inner ear

Effects of isoflurane on auditory evoked potentials in the cochlea and brainstem of guinea pigs

Auditory brainstem responses are resistant to pharmacological modulation in Sprague Dawley wildtype and Neurexin1α knockout rats

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