Tyrosine hydroxylase in rat auditory midbrain: Distribution and changes following deafness

Tong, Ling; Altschuler, Richard A.; Holt, Avril Genene

doi:10.1016/j.heares.2005.03.006

Cited by 31 publications

(54 citation statements)

References 38 publications

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“…High doses of MDMA also cause neurotoxicity through increased glutamate levels (Sarkar & Schmued, 2010), oxidative stress (Fiaschi & Cerretani, 2010; Sarkar & Schmued, 2010), and ischemia/vasoconstriction (Baker et al, 2007; Bingham et al, 1998). Similarly, NIHL is associated with neural toxicity from reduced adenosine levels (Vlajkovic et al, 2009), reduced nicotinic acetylcholinergic activity (Elgoyhen et al, 2009), reduced glucocorticoid receptor activity (Jin et al, 2009), increased glutamate release (Le Prell et al, 2007), oxidative stress (Le Prell et al, 2007), ischemia in the stria vascularis (Le Prell et al, 2007), and serotonin and dopamine depletion (Lendvai et al, 2011; Papesh & Hurley, 2012; Tong et al, 2005). …”

Section: Discussionmentioning

confidence: 99%

“…Thus, using MDMA in combination with loud noise or other sensory trauma is likely to be a fruitful and insightful line of investigation, perhaps more so than studying the effects of MDMA alone. This is particularly true for studying MDMA’s depletion of serotonin and dopamine, because these neurotransmitters have inhibitory and possibly neural protective roles in the auditory system (Hurley & Hall, 2011; Papesh & Hurley, 2012; Tong et al, 2005) [however, see (Shah & Salamy, 1984)]. Thus, MDMA-induced depletion of these neurotransmitters should have adverse effects on auditory information processing and possibly sensory receptor and neural damage when combined with sensory trauma.…”

Section: Discussionmentioning

confidence: 99%

“…For example, MDMA can deplete the brain neurotransmitters serotonin and dopamine (Perrine et al, 2010; Sarkar & Schmued, 2010). Both of these neurotransmitters are believed to play a protective role against acoustic trauma (Lendvai et al, 2011; Papesh & Hurley, 2012; Tong et al, 2005). Second, both high-dose MDMA administration (Sarkar & Schmued, 2010) and noise trauma (Le Prell et al, 2007) induce neurotoxicity, often by similar mechanisms as described later (see Discussion).…”

Section: Introductionmentioning

confidence: 99%

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‘Ecstasy’ enhances noise-induced hearing loss

et al. 2013

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‘Ecstasy’ or 3,4-methylenedioxy-N-methamphetamine (MDMA) is an amphetamine abused for its euphoric, empathogenic, hallucinatory, and stimulant effects. It is also used to treat certain psychiatric disorders. Common settings for Ecstasy use are nightclubs and “rave” parties where participants consume MDMA and dance to loud music. One concern with the club setting is that exposure to loud sounds can cause permanent sensorineural hearing loss. Another concern is that consumption of MDMA may enhance such hearing loss. Whereas this latter possibility has not been investigated, this study tested the hypothesis that MDMA enhances noise-induced hearing loss (NIHL) by exposing rats to either MDMA, noise trauma, both MDMA and noise, or neither treatment. MDMA was given in a binge pattern of 5 mg/kg per intraperitoneal injections every 2 h for a total of four injections to animals in the two MDMA-treated groups (MDMA-only and Noise+MDMA). Saline injections were given to the animals in the two non-MDMA groups (Control and Noise-only). Following the final injection, noise trauma was induced by a 10 kHz tone at 120 dB SPL for 1 h to animals in the two noise trauma-treated groups (Noise-only and Noise+MDMA). Hearing loss was assessed by the auditory brainstem response (ABR) and cochlear histology. Results showed that MDMA enhanced NIHL compared to Noise-only and that MDMA alone caused no hearing loss. This implies that “clubbers” and “rave-goers” are exacerbating the amount of NIHL when they consume MDMA and listen to loud sounds. In contrast to earlier reports, the present study found that MDMA by itself caused no changes in the click-evoked ABR’s wave latencies or amplitudes.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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‘Ecstasy’ enhances noise-induced hearing loss

et al. 2013

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“…Social stimuli likely trigger activity in a range of neurochemical systems innervating the IC (Klepper and Herbert 1991;Tong et al 2005). Fast cyclic voltammetry, which relies on the shape of a voltammogram to distinguish neurochemicals, would therefore likely not allow us to focus on the serotonergic system during natural social behavior.…”

Section: Methodsmentioning

confidence: 99%

Socially induced serotonergic fluctuations in the male auditory midbrain correlate with female behavior during courtship

Keesom

Hurley

2016

Journal of Neurophysiology

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Keesom SM, Hurley LM. Socially induced serotonergic fluctuations in the male auditory midbrain correlate with female behavior during courtship. J Neurophysiol 115: 1786 -1796, 2016. First published January 20, 2016 doi:10.1152/jn.00742.2015.-Cues from social partners trigger the activation of socially responsive neuromodulatory systems, priming brain regions including sensory systems to process these cues appropriately. The fidelity with which neuromodulators reflect the qualities of ongoing social interactions in sensory regions is unclear. We addressed this issue by using voltammetry to monitor serotonergic fluctuations in an auditory midbrain nucleus, the inferior colliculus (IC), of male mice (Mus musculus) paired with females, and by concurrently measuring behaviors of both social partners. Serotonergic activity strongly increased in male mice as they courted females, relative to serotonergic activity in the same males during trials with no social partners. Across individual males, average changes in serotonergic activity were negatively correlated with behaviors exhibited by female partners, including broadband squeaks, which relate to rejection of males. In contrast, serotonergic activity did not correlate with male behaviors, including ultrasonic vocalizations. These findings suggest that during courtship, the level of serotonergic activity in the IC of males reflects the valence of the social interaction from the perspective of the male (i.e., whether the female rejects the male or not). As a result, our findings are consistent with the hypothesis that neuromodulatory effects on neural responses in the IC may reflect the reception, rather than the production, of vocal signals.

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“…This robust pattern of TH-ir in TS appears to be consistent across teleosts and is likely a mixture of DA and NAergic input, as there are reports of DBH, TH, and DA-ir fibers and terminals in this area across a variety of species (e.g., Adrio et al, 2002;Batten et al, 1993;Corio et al, 1991;Ekstrom et al, 1990;Ekstrom et al, 1986;Hornby and Piekut, 1990;Kaslin and Panula, 2001;Ma, 1994;Roberts et al, 1989;Sas et al, 1990;Vetillard et al, 2002). Furthermore, the amphibian TS, mammalian inferior colliculus (IC, TS homolog; Bass et al, 2005) and dorsal lateral mesencephalic nucleus in birds (MLd, IC homolog; Karten, 1967) all receive substantial CAergic input (Appeltants et al, 2001;Endepols et al, 2000;Kitahama et al, 1996;Klepper and Herbert, 1991;Mello et al, 1998;Tong et al, 2005), which suggests a conserved pattern and modulatory role of CAs on central auditory processing across vertebrates. The primary source of NAergic fibers is likely the LC (Ma, 1994) as is the case in mammals (Hormigo et al, 2012;Klepper and Herbert, 1991) and birds (Kitt and Brauth, 1986a) since projection patterns of NAergic neurons are highly conserved (Smeets and Gonzalez, 2000;Tay et al, 2011).…”

Section: Th-ir Innervation Of Central Auditory Circuitry-likementioning

confidence: 99%

Catecholaminergic connectivity to the inner ear, central auditory, and vocal motor circuitry in the plainfin midshipman fish porichthys notatus

Forlano

Kim

Krzyminska

et al. 2014

J of Comparative Neurology

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Although the neuroanatomical distribution of catecholaminergic (CA) neurons has been well documented across all vertebrate classes, few studies have examined CA connectivity to physiologically and anatomically identified neural circuitry that controls behavior. The goal of this study was to characterize CA distribution in the brain and inner ear of the plainfin midshipman fish (Porichthys notatus) with particular emphasis on their relationship with anatomically labeled circuitry that both produces and encodes social acoustic signals in this species. Neurobiotin labeling of the main auditory endorgan, the saccule, combined with tyrosine hydroxylase immunofluorescence (TH-ir) revealed a strong CA innervation of both the peripheral and central auditory system. Diencephalic TH-ir neurons in the periventricular posterior tuberculum, known to be dopaminergic, send ascending projections to the ventral telencephalon and prominent descending projections to vocal-acoustic integration sites, notably the hindbrain octavolateralis efferent nucleus, as well as onto the base of hair cells in the saccule via nerve VIII. Neurobiotin backfills of the vocal nerve in combination with TH-ir revealed CA terminals on all components of the vocal pattern generator which appears to largely originate from local TH-ir neurons but may include diencephalic projections as well. This study provides strong evidence for catecholamines

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Tyrosine hydroxylase in rat auditory midbrain: Distribution and changes following deafness

Cited by 31 publications

References 38 publications

‘Ecstasy’ enhances noise-induced hearing loss

‘Ecstasy’ enhances noise-induced hearing loss

Socially induced serotonergic fluctuations in the male auditory midbrain correlate with female behavior during courtship

Catecholaminergic connectivity to the inner ear, central auditory, and vocal motor circuitry in the plainfin midshipman fish porichthys notatus

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