Title: Did Kant Suffer from misophonia?
Arnaud Norena, Frontiers in Psychology
Abstract: Misophonia is a disorder of decreased tolerance to specific sounds, often produced by humans but not always, which can trigger intense emotional reactions (anger, disgust etc.). This relatively prevalent disorder can cause a reduction in the quality of life. The causes of misophonia are still unclear. In this article, we develop a hypothesis suggesting that misophonia can be caused by a failure in the organization of the perceived world. The perceived world is the result of both the structure of human thought and the many conditioning factors that punctuate human life, particularly social conditioning. It is made up of abstract symbols that map the world and help humans to orient himself in a potentially dangerous environment. In this context, the role of social rules acquired throughout life is considerable. Table manners, for example, are a set of deeply regulated and controlled behaviors (it’s considered impolite to eat with the mouth open and to make noise while eating), which contribute to shape the way the perceived world is organized. So it’s not surprising to find sounds from the mouth (chewing etc.) among the most common misophonic sound triggers. Politeness can be seen as an act of obedience to moral rules or courtesy, which is a prerequisite for peaceful social relations. Beyond this example, we also argue that any sound can become a misophonic trigger as long as it is not integrated into the perceived ordered and harmonious world, because it is considered an “anomaly,” i.e., a disorder, an immorality or a vulgarity. Article ici.
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Title: The effect of acute and chronic noise trauma on stimulus evoked activity across primary auditory cortex layers
Vinay Parameshwarappa, Arnaud Norena, Journal of Neurophysiology
Abstract: Our study shows that cortical activity is enhanced after trauma and that the sequence of cortical column activation during stimulus-evoked response is altered, i.e. the supragranular layer becomes a major input recipient. We speculate that these large cortical changes may play a key role in the auditory hypersensitivity (hyperacusis) that can be triggered after noise trauma in human subjects. Article ici
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Title: Noise-induced hearing loss alters potassium-chloride cotransporter KCC2 and GABA inhibition in the auditory centers
V. Parameshwarappa, M. Siponen, I. Watabe **, A. Karkaba , A. Galazyuk , A. Noreña. Scientific Reports
** Technicienne, Equipe STECHBIO, CRPN.
Abstract: Abstract Homeostatic plasticity, the ability of neurons to maintain their averaged activity constant around a set point value, is thought to account for the central hyperactivity after hearing loss. Here, we investigated the putative role of GABAergic neurotransmission in this mechanism after a noise-induced hearing loss larger than 50 dB in high frequencies in guinea pigs. The effect of GABAergic inhibition is linked to the normal functioning of K + –Cl– co-transporter isoform 2 (KCC2) which maintains a low intracellular concentration of chloride. The expression of membrane KCC2 were investigated before and after noise trauma in the ventral and dorsal cochlear nucleus (VCN and DCN, respectively) and in the inferior colliculus (IC). Moreover, the effect of gabazine (GBZ), a GABA antagonist, was also studied on the neural activity in IC. We show that KCC2 is downregulated in VCN, DCN and IC 3 days after noise trauma, and in DCN and IC 30 days after the trauma. As expected, GBZ application in the IC of control animals resulted in an increase of spontaneous and stimulus-evoked activity. In the noise exposed animals, on the other hand, GBZ application decreased the stimulus-evoked activity in IC neurons. The functional implications of these central changes are discussed. Article ici